Добірка наукової літератури з теми "LNK"
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Статті в журналах з теми "LNK"
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Takaki, Satoshi, Julian D. Watts, Katherine A. Forbush, Nhan T. Nguyen, Jun Hayashi, Jose Alberola-Ila, Ruedi Aebersold, and Roger M. Perlmutter. "Characterization of Lnk." Journal of Biological Chemistry 272, no. 23 (June 6, 1997): 14562–70. http://dx.doi.org/10.1074/jbc.272.23.14562.
Повний текст джерела
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koren-Michowitz, Maya, Sigal Gery, Daniel Nowak, Arnon Nagler, Aiko Matsubara, Takayuki Tabayashi, Seishi Ogawa, and H. Phillip Koeffler. "Adaptor Protein LNK Binds to and Is Phosphorylated by JAK3 and May Serve as a Scaffold for JAK3 Autophosphorylation In the Absence of An Appropriate Cytokine Receptor." Blood 116, no. 21 (November 19, 2010): 2785. http://dx.doi.org/10.1182/blood.v116.21.2785.2785.
Повний текст джерелаАнотація:
Abstract Abstract 2785 The adaptor protein LNK has an important role during the development and maturation of cells in the hematopoietic system. LNK KO mice have an expansion of hematopoietic stem cells (HSCS) and an increase in circulating neutrophils, platelets, as well as immature B cells. On the other hand, overexpression of WT LNK under the control of a lymphocyte-specific expression vector results in an impaired expansion of lymphoid precursor cells and altered mature B cell subpopulations. Recently, LNK PH domain mutations were described in myeloproliferative neoplasms (MPN). The non-receptor tyrosine kinase JAK3 is expressed mainly in hematopoietic cells and together with JAK1, transmits signals from cytokine receptors of the IL-2 family. While JAK3 loss of function causes severe combined immune deficiency (SCID), JAK3 activating mutations were described in AML, particularly in acute megakaryocytic leukemia (AMKL). The importance of both LNK and JAK3 in lymphopoiesis, coupled with the finding that LNK binds to another JAK family member (JAK2), has led us to study whether LNK and JAK3 interact. LNK and JAK3 co- immunoprecipitated (co-IP) in the following leukemic cell lines- HEL, NALM6 (containing both LNK and WT JAK3), CMK (containing both LNK and an activating JAK3 mutant) and not in K562 (no JAK3). WT-JAK3 and WT LNK also co-IP when overexpressed in 293T cells, and this binding was associated with phosphorylation of LNK. To determine which domain of LNK is responsible for JAK3 binding, WT JAK3 was overexpressed in 293T cells with the following LNK mutants: 1. point mutation in the SH2 domain (R392E); 2. Deletion of the SH2 domain (del SH2); 3. Deletion of the PH and SH2 (del SH2/PH) domains; 4. Point mutation in the PH domain, recently found in a patient with a JAK2 V617F negative MPN (E208Q); 5. LNK SNP (rs3184504) described in GWAS to associate with an increased risk of autoimmune disease and which also causes an amino acid change in the LNK PH domain (W262R). LNK binding was retained in the E208Q and W262R mutants, markedly reduced in the R392E and del SH2 mutants and completely abolished with the del SH2/PH mutant, suggesting that LNK SH2 domain is important for the binding of LNK and WT-JAK3, although some binding may occur even in its absence. The effect of the LNK mutants R392E, E208Q and W262R on WT-JAK3 and LNK phosphorylation was also studied in 293T cells. Notably, WT-JAK3 was phosphorylated in the presence of WT-LNK and the E208Q and W262R mutants and not in the presence of the R392E mutant or an empty vector; also, the WT-LNK, LNK E208Q and W262R were phophorylated and the LNK R392E was not. These results suggest that WT-JAK3 phosphorylates LNK and that the LNK SH2 domain is important for this to occur. Interestingly, we found that the LNK PH domain mutant (E208Q) was much more phosphorylated than the WT- LNK when co-expressed with WT-JAK3. A similar result was obtained when LNK E208Q was co-expressed in 293T cells with vectors expressing an activating JAK3 mutant- A572V and the JAK2 V617F mutant but not when it was co-expressed with a BCR-ABL vector. This, again, supports the fact that direct binding underlines LNK phosphorylation by JAK3, as was previously shown for JAK2, while the BCR-ABL kinase does not bind LNK. The LNK PH domain mutation E208Q may cause a conformational change in LNK, allowing better access to tyrosine residues, or a change in LNK localization. The finding in 293T cells that WT-JAK3 is phophorylated only in the presence of LNK that retains a PH domain is intriguing. The other LNK family members- SH2B1 and APS were previously shown to homo- and heterodimerize. LNK contains a dimerization domain and we speculate that LNK homodimerization may serve as a scaffold for WT-JAK3 in the absence of a cytokine receptor, enabling JAK3 autophosphorylation. Since LNK PH domain mutations were recently described in MPN and may involve activation of the JAK2-STAT pathway we hypothesized that similar mutations might be found in lymphoma cases where JAK3 is reported to be activated. We, therefore, sequenced LNK PH domain in 147 lymphoma samples including- mantle cell lymphoma, peripheral T cell lymphoma (PTCL) and adult T cell leukemia/lymphoma cases but could not detect any mutations. In summary- we found that JAK3 binds and phosphorylates both WT-LNK and to a greater extent, the LNK PH domain mutant E208Q and in the absence of a cytokine receptor can lead to JAK3 phosphorylation. Taken together, LNK may likely control JAK3 activity. Disclosures: No relevant conflicts of interest to declare.
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Dou, Huijuan, Andriana Kotini, Wenli Liu, Trevor Fidler, Kaori Endo-Umeda, Xiaoli Sun, Malgorzata Olszewska, et al. "Oxidized Phospholipids Promote NETosis and Arterial Thrombosis in LNK(SH2B3) Deficiency." Circulation 144, no. 24 (December 14, 2021): 1940–54. http://dx.doi.org/10.1161/circulationaha.121.056414.
Повний текст джерелаАнотація:
Background: LNK/SH2B3 inhibits Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling by hematopoietic cytokine receptors. Genome-wide association studies have shown association of a common single nucleotide polymorphism in LNK (R262W, T allele) with neutrophilia, thrombocytosis, and coronary artery disease. We have shown that LNK(TT ) reduces LNK function and that LNK-deficient mice display prominent platelet–neutrophil aggregates, accelerated atherosclerosis, and thrombosis. Platelet–neutrophil interactions can promote neutrophil extracellular trap (NET) formation. The goals of this study were to assess the role of NETs in atherosclerosis and thrombosis in mice with hematopoietic Lnk deficiency. Methods: We bred mice with combined deficiency of Lnk and the NETosis-essential enzyme PAD4 (peptidyl arginine deiminase 4) and transplanted their bone marrow into Ldlr –/– mice. We evaluated the role of LNK in atherothrombosis in humans and mice bearing a gain of function variant in JAK2 (JAK2 V617F ). Results: Lnk -deficient mice displayed accelerated carotid artery thrombosis with prominent NETosis that was completely reversed by PAD4 deficiency. Thrombin-activated Lnk –/– platelets promoted increased NETosis when incubated with Lnk –/– neutrophils compared with wild-type platelets or wild-type neutrophils. This involved increased surface exposure and release of oxidized phospholipids (OxPL) from Lnk –/– platelets, as well as increased priming and response of Lnk –/– neutrophils to OxPL. To counteract the effects of OxPL, we introduced a transgene expressing the single-chain variable fragment of E06 (E06-scFv). E06-scFv reversed accelerated NETosis, atherosclerosis, and thrombosis in Lnk –/– mice. We also showed increased NETosis when human induced pluripotent stem cell–derived LNK(TT ) neutrophils were incubated with LNK(TT ) platelet/megakaryocytes, but not in isogenic LNK(CC ) controls, confirming human relevance. Using data from the UK Biobank, we found that individuals with the JAK2 VF mutation only showed increased risk of coronary artery disease when also carrying the LNK R262W allele. Mice with hematopoietic Lnk +/– and Jak2 VF clonal hematopoiesis showed accelerated arterial thrombosis but not atherosclerosis compared with Jak2 VF Lnk +/+ controls. Conclusions: Hematopoietic Lnk deficiency promotes NETosis and arterial thrombosis in an OxPL-dependent fashion. LNK(R262W) reduces LNK function in human platelets and neutrophils, promoting NETosis, and increases coronary artery disease risk in humans carrying Jak2 VF mutations. Therapies targeting OxPL may be beneficial for coronary artery disease in genetically defined human populations.
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Tabayashi, Takayuki, Sigal Gery, Maya Koren-Michowitz, and H. Phillip Koeffler. "Adaptor Protein Lnk Negatively Regulates Bcr-Abl-Induced Cell Proliferation through Inhibition of the Stat5 Signaling Pathway." Blood 116, no. 21 (November 19, 2010): 3406. http://dx.doi.org/10.1182/blood.v116.21.3406.3406.
Повний текст джерелаАнотація:
Abstract Abstract 3406 Adaptor protein Lnk negatively regulates not only several hematopoietic cytokine receptors including MPL, EpoR and c-Kit, but also non-receptor tyrosine kinases such as JAK2 and Src. Our previous studies demonstrated that Lnk, when expressed in hematopoietic cell lines, binds and regulates the mutant proteins, JAK2V617F and MPLW515L. Recent in vivo studies have shown that Lnk has an important role in the development of myeloproliferative neoplasms. These data suggest that Lnk may have the ability to inhibit constitutively activated signaling pathways in hematopoietic malignancies. However, how Lnk can attenuate the activity of Bcr-Abl is unclear. In the present study, we tested the hypothesis that Lnk might play a role in regulating Bcr-Abl function. In order to assess if Lnk can inhibit the proliferation of Bcr-Abl-positive hematopoietic cells, Bcr-Abl-expressing BaF3 cells were stably transfected with either Lnk (BaF3/Bcr-Abl/Lnk) or vector only (BaF3/ Bcr-Abl). Colony-formation assays revealed that Lnk significantly inhibited the proliferation of Bcr-Abl-expressing BaF3 cells. Similarly, overexpression of Lnk inhibited growth in the human CML cell line, K562. To determine the cause of growth inhibition by Lnk, assays for apoptosis were performed. Annexin V staining demonstrated that Lnk overexpression induced apoptosis in Bcr-Abl-expressing BaF3 cells. Western blotting analysis of protein lysates from BaF3/ Bcr-Abl /Lnk cells and BaF3/ Bcr-Abl cells found that Lnk-mediated growth inhibition was associated with downregulation of the Stat5 signaling pathway, but not associated with MAPK and PI3K signaling pathways. In addition, experiments in 293T cells expressing Bcr-Abl and Stat5 with either wild-type Lnk or SH2 mutant Lnk revealed that wild-type Lnk, but not SH2 mutant Lnk, inhibited phosphorylation of Stat5. Interestingly, Lnk inhibited Bcr-Abl-induced Stat5 phosphorylation in a dose-dependent manner. These data suggest that the SH2 domain of Lnk is essential for Lnk–mediated downregulation of the Stat5 signaling pathway in Bcr-Abl-positive cells. Taken together, our data suggest that Lnk inhibits Bcr-Abl-induced cell proliferation by attenuating the Stat5 signal transduction and may become a therapeutic target for Bcr-Abl-positive leukemias such as chronic myeloid leukemia and Philadelphia chromosome positive acute lymphoblastic leukemia. Disclosures: No relevant conflicts of interest to declare.
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Gery, Sigal, Saskia Gueller, Julia Sohn, Shayne Nabavinouri, Amanda Leiter, and H. Phillip Koeffler. "Adaptor Protein Lnk Negatively Regulates Mutant MPL and JAK2 Alleles Associated with Myeloproliferative Disorders." Blood 110, no. 11 (November 16, 2007): 1531. http://dx.doi.org/10.1182/blood.v110.11.1531.1531.
Повний текст джерелаАнотація:
Abstract Activating mutations in the cytokine receptor/JAK2 signaling axis are found at high frequency in myeloproliferative disorders (MPD). Lnk, an SH2-containing adaptor protein, is a negative regulator of several hematopoietic cytokine receptors including MPL and EpoR. Here, we assessed whether Lnk can attenuate the activity of mutant MPLW515L, JAK2V617F and JAK2K539L found in MPD patients. Lnk overexpression in Ba/F3-MPLW515L cells inhibited cytokine-independent growth, while suppression of Lnk in UT7-MPLW515L cells enhanced proliferation. Lnk-mediated growth inhibition was associated with downregulation of JAK/STAT, MAPK and PI3K signaling pathways. Similarly, Lnk inhibited cytokine-independent growth conferred by JAK2V617F and JAK2K539L in Ba/F3-EpoR cells. Following thrombopoietin stimulation, Lnk became tyrosyl-phosphorylated and associated with activated wild-type (WT) MPL and MPLW515L at the plasma membrane of Ba/F3 cells. An SH2 mutant Lnk (R392E) failed to bind and inhibit WT MPL and MPLW515L, demonstrating that the SH2 domain is essential for Lnk down-modulation of the receptors. The Lnk-MPL interaction was also detected with endogenously expressed proteins from cultured bone marrow cells. A series of C-terminally truncated Lnk constructs were used to determine which Lnk regions are required for Lnk inhibition of JAK2. Experiments in 293T cells indicated that Lnk SH2 domain binds to phosphorylated JAK2. In addition, other Lnk regions associated with non-phosphorylated JAK2, and these interactions were critical for Lnk inhibition of JAK2V617F and JAK2K539L constitutive activation. Our data suggest a model wherein Lnk downregulation of the receptor/JAK2 signaling involves two mechanisms; one is inhibition of the cytokine receptor utilizing JAK2, the second is direct suppression of JAK2 kinase activity. Furthermore, while the receptor mediated inhibition requires the SH2 domain, direct inhibition of JAK2 mutants, V617F and K539L, relies on other Lnk domains. Further elucidating the molecular mechanisms underlying Lnk inhibition of signaling pathways abnormally activated by oncogenic alleles, will provide insight into the pathogenesis of MPD and may have therapeutic value.
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Kiladjian, Jean-Jacques, Fanny Baran-Marszak, Christophe Desterke, Bruno Cassinat, Hajer Magdoud, Elisabeth Mazoyer, Pierre Fenaux, et al. "Abnormal Expression and Function of the Lnk Adaptor Protein in Myeloproliferative Neoplasms (MPN)." Blood 114, no. 22 (November 20, 2009): 2897. http://dx.doi.org/10.1182/blood.v114.22.2897.2897.
Повний текст джерелаАнотація:
Abstract Abstract 2897 Poster Board II-873 Introduction: We have shown in a deficient mouse model that the adaptor protein Lnk had an important role as negative regulator of cytokine signaling during hematopoiesis (Velazquez et al., J. Exp Med 2002). Lnk-/- animals display abnormal megakaryopoiesis sharing many features with that found in MPN patients. This phenotype is due to loss of Lnk inhibition of thrombopoietin (TPO)-mediated JAK2 activation (Tong et al., J Exp Med 2004). Recent studies have shown that Lnk, when expressed in hematopoietic cell lines, could bind and regulate two mutant proteins found in MPNs, JAK2V617F and MPLW515L. However, the role of Lnk in MPN pathogenesis is still unclear. In the present study, we studied in detail both Lnk expression and function in MPNs. Patients and methods: The study included a total of 82 MPN patients (pts), including 41 essential thrombocytemia (ET), 29 polycythemia vera (PV) and 12 primary myelofibrosis (PMF). Lnk expression was assessed by quantitative RT-PCR. Biochemical and cellular analyses of Lnk and JAK2 interaction were carried out using co-immunoprecipitation, GST pull-down and proliferation assays on primary hematopoietic cells and cell lines expressing either wild-type (WT) or mutant forms of both Lnk and JAK2. Results: Lnk mRNA was clearly overexpressed in platelets and CD34+ cells of most MPN pts compared to controls (P=0.005 and P=0.03, respectively). Moreover, this increased Lnk expression strongly correlated with JAK2V617F allele burden (P=0.02). In contrast, Lnk mRNA levels were reduced in the 18 pts treated with interferon-α compared to the 34 pts treated with hydroxyurea (P=0.04). TPO specifically upregulated Lnk expression at both mRNA and protein levels in both primary and UT7/Mpl megakaryocytic (MK) cells. Analysis of TPO-stimulated platelets from ET patients revealed the existence of a new interaction site between Lnk and JAK2 located in the N-terminal region of Lnk, in addition to the previously known interaction mediated by Lnk SH2 domain. This interaction resulted in Lnk phosphorylation. In JAK2V617F expressing platelets or cell lines, we observed both increased phosphorylation of Lnk, and stronger binding of JAK2 to the N-terminal region of Lnk compared to WT-JAK2 cells. Overexpression of Lnk in JAK2V617F cells showed a dose dependent growth inhibition, as seen in JAK2 WT cells. In addition, overexpression of various mutant forms of Lnk showed that this inhibition required a fully functional SH2 domain. Finally, expression of either WT or mutant forms of Lnk also demonstrated the crucial role of Lnk SH2 domain in growth inhibition of myeloid and MK progenitors in Lnk-/- hematopoietic cells. Conclusion: This first study of a large cohort of 82 patients allowed us to investigate the role of Lnk in MPN: (1) Lnk mRNA was found to be significantly overexpressed in MPN derived platelets and CD34+ cells, and correlated with JAK2V617F allele burden. (2) Lnk expression is upregulated by TPO, an effect likely mediated by JAK2 activation. (3) The Lnk SH2 domain plays a major role in the down-regulation of both normal and MPN-derived hematopoiesis. (4) We describe here a novel interaction site between the N-terminal region of Lnk and JAK2. Stronger interaction of the JAK2V617F mutant form with this N-terminal binding site may account for the dysregulated hematopoiesis observed in MPN patients despite Lnk overexpression. Disclosures: No relevant conflicts of interest to declare.
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Eto, Koji, Hitoshi Takizawa, Satoshi Takaki, Hidekazu Nishikii, Atsushi Oda та Hiromitsu Nakauchi. "The Cytokine Signal Inhibitor Lnk Promotes αIIbβ3 Integrin Outside-In Signaling through β3 Tyrosine Phosphorylation in Platelets." Blood 110, № 11 (16 листопада 2007): 3651. http://dx.doi.org/10.1182/blood.v110.11.3651.3651.
Повний текст джерелаАнотація:
Abstract Lnk is an SH2 domain-containing adapter protein that inhibits cytokine signaling. Lnk−/− mice exhibit a marked increase in numbers of hematopoietic stem cells, megakaryocytes and platelets, presumably due to the lack of negative regulation in thrombopoietin-mediated signals by Lnk. We previously reported that Lnk might play an unanticipated role in platelet integrin αIIbβ3 outside-in signaling. Lnk−/− platelets exhibited defects in full spreading on fibrinogen, clot retraction and formation of thrombi on collagen under flow conditions while they showed normal inside-out signaling (Blood, 106 (11):115a, 2005). However the mechanism(s) in which Lnk participates in αIIbβ3 outside-in signaling had not been elucidated. Here we report that in normal platelets Lnk forms a complex with c-Src, Syk, Fyn and adhesion and degranulation promoting adaptor protein (ADAP) but not SLP-76 in a manner dependent on αIIbβ3 ligation and Src kinase activation. c-Src-, but not Syk-, mediated tyrosine phosphorylation of C-terminus in Lnk appeared to be indispensable for the complex formation and Lnk-mediated function. Furthermore we have shown that Lnk is required for the association of Fyn to αIIbβ3 and for β3 subunit tyrosine phosphorylation while activation of non-receptor tyrosine kinases (c-Src and Syk) in proximity to αIIbβ3 is independent of Lnk. Thus, these results provide new insights into Lnk function and the mechanism by which Lnk contributes to integrin signaling in the adhesion responses of platelets.
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de Leone, María José, Carlos Esteban Hernando, Andrés Romanowski, Mariano García-Hourquet, Daniel Careno, Joaquín Casal, Matías Rugnone, Santiago Mora-García, and Marcelo Javier Yanovsky. "The LNK Gene Family: At the Crossroad between Light Signaling and the Circadian Clock." Genes 10, no. 1 (December 20, 2018): 2. http://dx.doi.org/10.3390/genes10010002.
Повний текст джерелаАнотація:
Light signaling pathways interact with the circadian clock to help organisms synchronize physiological and developmental processes to periodic environmental cycles. The plant photoreceptors responsible for clock resetting have been characterized, but signaling components that link the photoreceptors to the clock remain to be identified. Members of the family of NIGHT LIGHT–INDUCIBLE AND CLOCK-REGULATED (LNK) genes play key roles linking light regulation of gene expression to the control of daily and seasonal rhythms in Arabidopsis thaliana. Particularly, LNK1 and LNK2 were shown to control circadian rhythms, photomorphogenic responses, and photoperiod-dependent flowering time. Here we analyze the role of the four members of the LNK family in Arabidopsis in these processes. We found that depletion of the closely related LNK3 and LNK4 in a lnk1;lnk2 mutant background affects circadian rhythms, but not other clock-regulated processes such as flowering time and seedling photomorphogenesis. Nevertheless, plants defective in all LNK genes (lnkQ quadruple mutants) display developmental alterations that lead to increased rosette size, biomass, and enhanced phototropic responses. Our work indicates that members of the LNK family have both distinctive and partially overlapping functions, and are an essential link to orchestrate light-regulated developmental processes.
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Tong, Wei, Jing Zhang, and Harvey F. Lodish. "Lnk inhibits erythropoiesis and Epo-dependent JAK2 activation and downstream signaling pathways." Blood 105, no. 12 (June 15, 2005): 4604–12. http://dx.doi.org/10.1182/blood-2004-10-4093.
Повний текст джерелаАнотація:
Abstract Erythropoietin (Epo), along with its receptor EpoR, is the principal regulator of red cell development. Upon Epo addition, the EpoR signaling through the Janus kinase 2 (JAK2) activates multiple pathways including Stat5, phosphoinositide-3 kinase (PI-3K)/Akt, and p42/44 mitogen-activated protein kinase (MAPK). The adaptor protein Lnk is implicated in cytokine receptor signaling. Here, we showed that Lnk-deficient mice have elevated numbers of erythroid progenitors, and that splenic erythroid colony-forming unit (CFU-e) progenitors are hypersensitive to Epo. Lnk-/- mice also exhibit superior recovery after erythropoietic stress. In addition, Lnk deficiency resulted in enhanced Epo-induced signaling pathways in splenic erythroid progenitors. Conversely, Lnk overexpression inhibits Epo-induced cell growth in 32D/EpoR cells. In primary culture of fetal liver cells, Lnk overexpression inhibits Epo-dependent erythroblast differentiation and induces apoptosis. Lnk blocks 3 major signaling pathways, Stat5, Akt, and MAPK, induced by Epo in primary erythroblasts. In addition, the Lnk Src homology 2 (SH2) domain is essential for its inhibitory function, whereas the conserved tyrosine near the C-terminus and the pleckstrin homology (PH) domain of Lnk are not critical. Furthermore, wild-type Lnk, but not the Lnk SH2 mutant, becomes tyrosine-phosphorylated following Epo administration and inhibits EpoR phosphorylation and JAK2 activation. Hence, Lnk, through its SH2 domain, negatively modulates EpoR signaling by attenuating JAK2 activation, and regulates Epo-mediated erythropoiesis. (Blood. 2005; 105:4604-4612)
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Balcerek, Joanna, Jing Jiang, Alexey Bersenev, Yiwen Song, Chao Wu, and Wei Tong. "14-3-3 Regulates the Lnk/JAK2 Pathway In Hematopoietic Stem and Progenitor Cells." Blood 116, no. 21 (November 19, 2010): 86. http://dx.doi.org/10.1182/blood.v116.21.86.86.
Повний текст джерелаАнотація:
Abstract Abstract 86 Hematopoietic stem and progenitor cell (HSPC) homeostasis is regulated by intricate signaling networks. The tyrosine kinase JAK2 plays an essential role in cytokine signaling during hematopoiesis and its dysregulation can lead to hematologic malignancies. Recently activating mutations in JAK2 were found in a large fraction of patients with myeloproliferative neoplasms (MPNs). We previously demonstrated that lymphocyte adaptor protein (Lnk) binds JAK2 and attenuates its activity, thereby limiting HSPC expansion (Bersenev et al., JCI, 2008;118:2832-2844). We further showed that loss of Lnk accelerates and exacerbates oncogenic JAK2-induced MPNs in mice (Bersenev et al., JCI, 2010;120:2058-2069). Lnk directly inhibits oncogenic JAK2 as well as acting through JAK2- independent pathways to constrain MPN development. Consistently, aged Lnk–/– mice spontaneously developed a CML-like MPN (Bersenev et al., JCI, 2010;120:2058-2069). More importantly, loss-of-function mutations in Lnk are found in human MPN patients (Oh, et. al., Blood, 2010, in press). This work suggests that Lnk plays a pivotal role in regulating both normal and malignant HSPC expansion. However, it remains to be determined how Lnk attenuates JAK2 activity since Lnk itself does not possess any enzymatic activity. Therefore, we began exploring Lnk regulatory mechanisms by identifying novel Lnk partners through protein purification and mass spectrometric analysis. This resulted in the identification of a number of novel Lnk binding proteins, which include the 14-3-3 proteins as the most robust interactors. 14-3-3s are a group of scaffold proteins that regulate many disease-relevant gene products and play important functions in many aspects of cellular processes. We found that Lnk is phosphorylated at two serine residues, which serve as the critical binding sites for 14-3-3. 14-3-3 abrogates the Lnk-JAK2 interaction thereby alleviating Lnk inhibitory function in both JAK2 signaling and cell growth. Furthermore, 14-3-3 binding is necessary and sufficient to maintain Lnk in an inactive state. We also investigated the signals that regulate Lnk phosphorylation, revealing Lnk as a signaling nodal point that integrates multiple signaling pathways in controlling HSPC homeostasis. The physiological significance of the Lnk-14-3-3 interaction in HSPC development will be discussed. Thus, our data implicate previously unappreciated serine phosphorylation events in Lnk-dependent hematopoietic function and regulation of JAK2. In addition, identification of novel signaling molecules that influence hematopoiesis might facilitate stem cell therapies and provide novel therapeutic targets for the treatment of MPNs. Disclosures: No relevant conflicts of interest to declare.
Дисертації з теми "LNK"
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Magdoud, Hajer. "Implication fonctionnelle de la protéine adaptatrice Lnk dans les cellules normales et pathologiques du lignage mégacaryocytaire." Thesis, Paris 13, 2014. http://www.theses.fr/2014PA132003.
Повний текст джерелаАнотація:
L’adaptateur Lnk est un inhibiteur clé dans le système hématopoïétique. Son invalidation chez la souris entraîne l’hyperprolifération des lignages myéloïdes (mégacaryocytaire et érythoïde). Les cellules Lnk présentent une hypersensibilité à certaines cytokines dont la Trombopoïétine (TPO) et l’Erythropoïétine (EPO) et la dérégulation de leurs voies de signalisation (JAK/STAT et MAPK). D’autre part, le phénotype Lnk s’assimile aux caractéristiques trouvées chez les patients atteints des syndromes myéloprolifératifs (SMPs), suggérant un rôle clé de Lnk dans ces maladies. L’identification récente des mutations de LNK dans ces hémopathies l’a confirmé. Ainsi, l’objectif de mon travail de thèse était de définir les mécanismes moléculaires par lesquels Lnk régule la mégacaryopoïèse en disséquant son interaction avec son partenaire, la kinase JAK2, dans la voie TPO/Mpl. En parallèle, nous avons visé à déterminer le rôle de Lnk dans la pathogénèse de SMPs. Afin d’étudier le rôle de Lnk dans les SMPs, nous avons effectué une analyse transcriptionnelle de Lnk dans les cellules CD34 et les plaquettes de patients exprimant JAK2WT ou JAK2V617F. Nos résultats ont montré uns surexpression de Lnk, dans les témoins sains. Cette surexpression est due à l’induction de l’expression de Lnk par la TPO, montrant une boucle de rétrorégulation par Lnk de la voieTPO/Mpl/JAK2. Par ailleurs l’analyse de l’interaction Lnk/JAK2 dans les plaquettes des patients atteints de SMPs a démontré que Lnk est capable de s’associer à JAK2 (JAK2WT et JAK2V617F) E outre cette liaison est indépendante de la stimulation par la TPO et abouti à une phosphorylation constitutive de Lnk.Notre analyse au niveau moléculaire de l’interaction Lnk/JALK2 a révélé, qu’en plus du domaine SH2 de Lnk, la région N-terminale et le domaine PH de Lnk ont un nouveau rôle important dans l’inhibition de la kinase JAK2. Nous avons également montré une association entre Lnk et les formes mutées dans les SMPs, JAK2V617F ou JAK2K539L avec une infimité plus élevée qu’avec JAK2WT, suggérant ainsi une régulation différentielle de ces formes par Lnk. L’analyse fonctionnelle de ces formes par Lnk. L’analyse fonctionnelle par des essais de prolifération cellulaire, a montré que Lnk, inhibe la croissance de cellules exprimant JAK2V617F et ceci de manière dos-dépendante. Nous avons ensuite entrepris l’étude des effets des mutations de LNK (LNKG152R et LNKE208Q) identifiées dans les SMPs. Nos résultats ont indiqué que seule la mutation LNKE208Q semble affecter la localisation membranaire de l’adaptateur. De plus nous avons montré que cette mutation de LNK altère son effet inhibiteur sur la croissance cellulaire dépendante de JAK2, contrairement à la mutation de LNKG152R ayant elle-même un effet modéré. Ces résultats montrent que ces mutations de LNK affectent différemment les réponses cellulaires dépendantes de JAK2 dans les SMPs. Ainsi, nos données suggèrent que la région N-terminale et le domaine PH de LNK sont importants pour moduler sa fonction inhibitrice sur JAK2. L’ensemble de nos travaux nous a permis une meilleure caractérisation de la régulation de la kinase JAK2, par Lnk dans la voie de le TPO. Ainsi, une déstabilisation du complexe Lnk/JAK2 affecte la fonction inhibitrice de l’adaptateur, ce qui peut contribuer au développement de désordres hématopoïétiques. L’interaction différentielle entre Lnk et les formes JAK2WT ou mutées suggère la possibilité d’utiliser Lnk comme outil thérapeutique innovant dans les SMPs, et éventuellement dans les autres hémopathiesThe Lnk adaptor is a key inhibitor of cytokine signaling during hematopoiesis. Lnk mice show abnormal magakaryopoiesis due to loss of Lnk inhibition of thrombopoietin (TPO)-mediated JAK2/STAT and MAPK activation. The ressemblance between Lnk phenotype and Myeloproliterative Neoplasms (MPNs) features together with the identification of LNK mutations in MPNs patients suggest a role for Lnk in these diseases. We aimed to characterize the functional role of Lnk in regulating magakaryopoiesis and also define its role in MPN pathogenesis. Transcriptional analysis of Lnk in MPN cells (expressing JAK2WT and mutated form JAK2V617F) showed its overexpression, notably in JAK2V617F-positive patients. This increase in Lnk level is partly due to its up-regulation by TPO. Studies on TPO-simulated MPN Platelets revealed the interaction between Lnk and JAK2 and the subsequent Lnk phosphorylation. Our molecular analysis showed that Lnk/JAK2 binding occurs via Lnk SH2 domain and revealed a new role for its N-terminal and PH doamins in the regulation of the kinase. We also showed that Lnk binds more strongly to JAK2V617F and JAK2K539L, mutated in MPNs, that with JAK2WT, suggesting that the adaptor regulates differently the JAK2 forms. Moreover, the overexpression of Lnk in JAK2V617F celles showed a dose dependent growth inhibition.Furthermore, our analysis of the LNK mutations found in MPNs, G152R in N-terminal and E208Q PH domains showed that only the E208Q mutation affect Lnk subcellular localization. Moreover, we demonstrated that these mutations, and mostly E208Q, alter the inhibitory function of Lnk on cell growth in JAK2V617F- expressing cells. Altogether, our results show that Lnk is involved in the regulatory loop TPO/Mpl receptor/JAK2 essential in magakaryopoiesis. Thus, changes in Lnk expression and its JAK2 binding can contribute to the developement of MPNs. The differential binding of Lnk with JAK2WT and mutated forms suggests a potential therapeutic use of the adaptor in the MPNs
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Simon, Clotilde. "Rôle fonctionnel de la protéine adaptatrice Lnk dans le système hématopoïetique." Paris 5, 2008. http://www.theses.fr/2008PA05T018.
Повний текст джерелаАнотація:
L'invalidation de Lnk in vivo a mis en évidence le rôle de régulateur négatif de cet adaptateur sur la prolifération des progéniteurs hématopoïétiques. Mon travail a montré que le récepteur Kit est un partenaire physiologique important de Lnk. Leur association implique le domaine SH2 de Lnk et une tyrosine régulatrice de Kit. J'ai également montré que suite à cette association, Lnk régule des voies de signalisation dépendantes de Kit permettant le contrôle de la prolifération, la survie et la migration des mastocytes (voies MAPK, PI3K/Akt et Rac/JNK). Le phénotype des souris Lnk-/- ressemble à celui observé dans certains syndromes myéloprolifératifs. Il est donc probable que Lnk joue un rôle dans ces pathologies. J'ai identifié d'autres partenaires de Lnk essentiels au développement des progéniteurs hématopoïétiques. L'analyse en cours de ces interactions permettra de clarifier le rôle de Lnk dans l'hématopoïèse et son implication dans des pathologies hématologiques.
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Proeschel, Christoph Johann Wolfgang. "The cloning and characterisation of Lnk-1 : a novel LIM-domain containing protein kinase." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294778.
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Jungalee, Anouchka. "Implication physiopathologique de l'adaptateur LNK : mécanismes d'action et perspectives thérapeutiques dans les Néoplasmes Myéloprolifératifs." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD017/document.
Повний текст джерелаАнотація:
L’adaptateur LNK est un régulateur négatif des voies de signalisation, dont la voie JAK/STAT,essentielle au développement du système hématopoïétique. Son implication dans les hémopathies chroniques, notamment les Néoplasmes Myéloprolifératifs (NMP), a été mise en évidence par l’analyse de souris invalidées pour cet adaptateur et l’identification de mutations de LNK chez les patients atteints de ces pathologies. Toutefois, le mécanisme permettant la régulation de ses partenaires, dont la kinase JAK2, et l’implication fonctionnelle des mutations de LNK dans les NMP, restent à définir. Ainsi, mon projet de thèse a porté sur l’analyse structurale et fonctionnelle des complexes de signalisation LNK/JAK2 et sur le développement d’une stratégie moléculaire pour l’utilisation thérapeutique de LNK dans les NMP. Nos résultats ont montré pour la première fois, la fonction inhibitrice de la région N-terminale incluant le domaine d’homologie à la Pleckstrine deLNK sur JAK2 normale et de manière plus importante, sur la forme mutée JAK2-V617F, retrouvée chez les patients atteints de NMP. De plus, nos études sur les mutations de LNK localisées dans cette région régulatrice, ont permis de comprendre leur contribution dans le développement de ces hémopathies et de proposer un mécanisme d’inhibition de l’activation de JAK2 par LNK. Nos résultats permettent d’utiliser le ciblage de la région N-terminale de LNK comme stratégie moléculaire inhibant spécifiquement la forme oncogénique JAK2-V617F à l’aide de peptides pénétrants (CPP). A long terme, cette approche pourrait être utilisée comme outil thérapeutique dans le traitement de patients atteints de NMP positifs pour JAK2-V617FThe LNK adaptor protein is a key negative regulator of signalling pathways, such as JAK/STAT, important in the development of the hematopoietic system. Its implication in chronic blood diseases, such as Myeloproliferative Neoplasms (MPN) has been confirmed by studies on Lnk-deficient mice, as well as the identification of LNK mutations in MPN patients. However, the LNK mechanism of regulation on its partners and the functional implication of LNK mutations in MPN pathogenesis, are still unclear. Therefore, my PhD project covers the structural and functional analysis of theLNK/JAK2 signalling complex and the development of a molecular strategy to use LNK as a therapeutic tool for the treatment of MPN patients. Our study showed, for the first time, the inhibitory function of the N-terminal region and the pleckstrin homology domain of LNK on JAK2 activity, which occurs more importantly on JAK-V617F than JAK2 wild type form. Moreover, our study provided evidence on how LNK mutations located in this LNK region could contribute to these haematological diseases and has allowed us to propose a model for LNK regulatory function on JAK2activity. Furthermore, we developed a cell penetrating peptide-based strategy to deliver this regulatory region of LNK in hematopoietic cells to specifically inhibit JAK2-V617F oncogenic form. The finalaim is to use this region as a therapeutic molecule to treat JAK2-V617F-positive MPN patients
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Devallière, Julie. "Caractérisation des fonctions régulatrices de la protéine adaptatrice Lnk (SH2B3) dans l'endothélium vasculaire et application pour la prévention du rejet en xénotransplantation." Nantes, 2010. https://archive.bu.univ-nantes.fr/pollux/show/show?id=b4116474-b2b4-4b9d-951f-9429014ece87.
Повний текст джерелаАнотація:
Afin de développer de nouvelles stratégies de prévention du rejet de greffe, il est important d'identifier les mécanismes et les effecteurs de l'activation endothéliale. Dans ce but, nous avons cherché à poursuivre la caractérisation des fonctions de la protéine adaptatrice Lnk (SH2B3) dans la signalisation des cellules endothéliales (CE) vasculaires. Nous montrons que l'absence de Lnk inhibe la transduction du signal médié par la β1 intégrine dans les CE. Au contraire, la surexpression de Lnk entraîne une augmentation du nombre des adhésions focales, qui s'accompagne d'une phosphorylation importante des protéines FAK et paxilline. D'un point de vue fonctionnel, l'expression soutenue de Lnk favorise l'adhésion et l'étalement des CE alors que la migration et l'apoptose par anoïkis sont diminuées. Nous avons également identifié l'α-parvine comme étant une cible moléculaire de Lnk et noté que son inhibition est responsable d'une baisse de la motilité des CE. L'ensemble de ces résultats a mis en évidence l'implication de Lnk dans les processus cellulaires associés à la signalisation des intégrines. Par ailleurs, nous avons étudié la possibilité d'une application à la xénotransplantation des fonctions anti-inflammatoires de Lnk. Nous avons montré que la surexpression de la protéine Lnk humaine dans des CE porcines, inhibe l'expression de VCAM-1 induite par le TNFα et protège les cellules de la mort cellulaire par anoïkis et de l'apoptose médiée par le TNFα. Ces résultats révèlent le rôle de Lnk dans la cytoprotection des CE. L'ensemble de ces travaux présente de nouvelles fonctions régulatrices pour Lnk et ouvre des perspectives à la prévention du rejet de xénogreffeIn order to develop new strategies for preventing graft rejection, it is important to identify mechanisms and actors of endothelial activation. To this aim, we have characterized Lnk (SH2B3) protein functions in vascular endothelial cells (EC) signaling. We showed that Lnk suppression inhibits β1 integrin-mediated signal transduction in EC. By contrast, Lnk overexpression increases the number of focal adhesions and induces the phosphorylation of both FAK and paxillin proteins. Functionally, sustained Lnk expression dramatically increases EC adhesion and spreading, whereas EC migration and apoptosis induced by anoïkis are decreased. Lnk reduces the expression of α-parvine protein that we identified as the molecular target impairing EC migration. Collectively, our results demonstrate the involvement of the adaptor Lnk in integrin-mediated signaling and functions. In addition, we have studied the potential application of anti-inflammatory effects of Lnk to xenotranplantation. We showed that Lnk overexpression down-regulated VCAM-1 expression mediated by TNFα and protects cells from death by anoïkis and TNFα-mediated apoptosis. These findings reveal a role for Lnk as a cytoprotective molecule. All together, this study presents new regulatory functions for Lnk and additional insights in the prevention of rejection
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Camargo, Rita Monteiro. "Distribuição espaço-temporal de Olivella minuta (LNK,1807) (Mollusca, Gastropoda, Olividae) na zona entremarés da Baía do Araçá, litoral norte do Estado de São Paulo." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/21/21134/tde-26092013-162941/.
Повний текст джерелаАнотація:
O objetivo deste trabalho foi analisar a distribuição espaço-temporal de um representante da macrofauna de praias arenosas protegidas. As abordagens em diferentes escalas (mesoescala, microescala e escala temporal) foram empregadas. O gastrópode Olivella minuta, abundante na região entremarés da Baía do Araçá, foi utilizado para essas análises. Para o estudo em mesoescala, 16 estações foram demarcadas na região entremarés (julho/2009) e, em cada uma, foram coletadas 8 amostras biológicas e 3 de sedimento. Alguns fatores abióticos (carbonato de cálcio, matéria orgânica e coeficiente de seleção) influenciaram negativamente a abundância do gastrópode, enquanto relações entre O. minuta e as demais espécies da macrofauna não foram evidentes. Em microescala, em poças de maré (metros) e em \"ripple marks\" (centímetros) verificou-se que em escala de centímetros, o gastrópode foi mais abundante em locais com maior conteúdo de água no sedimento, enquanto em escala de metros a abundância não diferiu dentro e fora das poças. Em escala temporal, foram observadas flutuações mensais da densidade da população de O. minuta, com diminuição/ausência de indivíduos entre fevereiro e março, o que sugere a ocorrência de migrações e mortalidade. O presente trabalho mostrou que a distribuição desse gastrópode é influenciada por diferentes fatores que atuam em diferentes escalas.The objective of this study was to analyze the temporal and spatial distribution of one of the species representative of the macrofauna of sheltered sandy beaches. Measurements using different scales (mesoscale, microscale and time scale) were utilized. The gastropod Olivella minuta, which is abundant in the intertidal region of Baía do Araçá, was used for these analyses. For the mesoscale study, 16 stations were determined within the intertidal region (July/2009) and, in each station, 8 biological samples and 3 samples of sediment were collected. Some abiotic factors (calcium carbonate, organic matter and selection coefficient) had a negative influence on the abundance of the gastropod, while relationship between the O. minuta and other species of the macrofauna were not evident. In a microscale study of tidal ponds (meters) and ripple marks (centimeters), it was observed that, in a centimeter scale, the gastropod was more abundant in places where there was more water in the sediment, whereas in a meter scale the abundance didn\'t vary in or out of the ponds. In a temporal scale, monthly fluctuations of the O. minuta population\'s density were observed, with reduction/absence of individuals between February and March, which suggests that migration and mortality occurred. This study showed that the distribution of O. minuta is influenced by different factors which act in different scales.
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Johansson, Birgit, Lisbeth Lundén, and Birgitta Nilsson-Schlick. "En länk mellan forskning och skolans praktik, A Link Between Science and School practice." Thesis, Malmö högskola, Lärarutbildningen (LUT), 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-34397.
Повний текст джерелаАнотація:
Arbetet ger en översikt av litteratur kring kunskapsuttnyttjande, forskning och skolutveckling samt kring handledning, profession, tidsbrist och bemötande. Vi har intervjuat blivande specialpedagoger. Med hjälp av svaren har vi fått reda på vilka önskemål om skolutveckling de har, nu och i framtiden och vilka hinder och svårigheter de har sett i sin verksamhet. Vi har inriktat frågorna på forskning och kunskapsuttnyttjande.
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Magnusson, Daniel. "A network based algorithm for aided navigation." Thesis, Linköpings universitet, Institutionen för systemteknik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-75235.
Повний текст джерелаАнотація:
This thesis is concerned with development of a navigation algorithm primarily for the aircraft fighter SAAB JAS 39 Gripen, in swarms of other units. The algorithm uses information from conventional navigation systems and additional information from a radio data link as aiding information, relative range measurements. As the GPS can get jammed, this group tracking solution can provide an increased navigation performance in these conditions. For simplicity, simplified characteristics are used in the simulations where simple generated trajectories and measurements are used. This measurement information can then be fused by using filter theory applied from the sensor fusionarea with statistical approaches. By using the radio data link and the external information sources, i.e. other aircraft and different types of landmarks with often good performance, navigation is aided when the GPS is not usable, at e.g. hostile GPS conditions. A number of scenarios with operative sense of reality were simulated for verifying and studying these conditions, to give results with conclusions.Det här examensarbetet syftar till utveckling av en algoritm för navigering, primärt för stridsflygplanet SAAB JAS 39 Gripen, i svärmar av andra enheter. Algoritmen använder information från konventionella navigeringssystem och ytterligare information från en radiodatalänk som ger understödjande information, relativa avståndsmätningar. Då den förlitade GPS:en kan störas ut, kan denna gruppspårande lösning öka navigeringsprestandan i dessa förhållanden. För enkelhetens skull, används förenklade karaktäristiker i simuleringarna där enkla genererade trajektorier och mätningar används. Denna mätinformation kan sedan ihopviktas genom att använda filterteori från statistisk sensorfusion. Genom att använda radiodatalänkar och den tillförda informationen från externa informationskällor, således andra flygplan och olika typer av landmärken som väldigt ofta har god prestanda, är navigeringen understödd när GPS inte är användbar, t.ex. i GPS-fientliga miljöer. Ett antal scenarion med operativ verklighetsanknytning simulerades för att verifiera och studera dessa förhållanden, för att ge resultat med slutsatser.
© Daniel Magnusson.
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Arja, Pushpak Vasanth Rayudu. "A Reconfigurable SPICE-Based CMOS LNA Design in 90 nm Technology Using ADS RFIC Dynamic Link." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1451852159.
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Zogli, Prince Kudjoe. "Analysis Of Function Of The Son1-Interacting Protein, Lnk2 In Arabidopsis Thaliana." ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/494.
Повний текст джерелаАнотація:
The Arabidopsis SON1 F-box protein was implicated in regulating a pathogen defense pathway, but its exact function in wild-type plants is unknown. As an F-box protein it was predicted that SON1 would assembles into a SON1-SCF ubiquitin ligase complex that recruits specific plant defense-related proteins for proteolysis. The yeast 2-hybrid assay was used to screen for potential substrates for a putative SON1-SCF ligase, leading to the identification of Arabidopsis LNK2 as a SON1-binding factor.
Comprehensive protein-protein interaction analysis has shown that the binding of SON1 to LNK2 protein is specific, because closely related, full-length Arabidopsis F-box proteins do not interact with LNK2. However, when tested in isolation, some fragments derived from the paralog proteins did bind SON1, suggesting that higher order structure or inter-domain interference affects the ability of SON1 to recruit substrate. When analyzed for interaction domains, three regions of SON1 were identified that bind to LNK2 and a LNK2 binding region spans a conserved amino acid region. Phylogenetic analysis revealed that there is a paralogous gene called LNK1 in Arabidopsis, and both LNK1 and LNK2 are restricted to the plant kingdom. LNK2 and LNK1 are seen to be widely distributed in embryophyte seed and spore plants. Genetic analysis and complementation tests showed that LNK1 and LNK2 regulate flowering and photo-morphogenesis redundantly.
Though lnk1 and lnk2 mutants look similar to wild-type plants, lnk1 lnk2 double mutant plants possess a long hypocotyls and flower late compared to wild-type plants. Because SON1 is implicated in plant defense, lnk mutants were assessed for susceptibility to a virulent oomycete pathogen, Hyaloperonospora arabidopsidis (Hpa). Interestingly, lnk mutants supported less disease development, suggesting a role of the wild-type LNK proteins in the enabling of pathogen colonization or in repressing host defenses. To confirm that each of the phenotypes described were a consequence of lnk1 and lnk2 mutations, wild type LNK1 and LNK2 were introduced into lnk1 lnk2 plants and examined. For most phenotypes, genetic complementation and thus restoration of a WT phenotype was observed. However, differences were uncovered in the ability of LNK genes to rescue the phenotypes, indicating specialization of function.
The interaction of LNK2 with SON1 suggests that SON1-dependent ubiquitination and proteasomal degradation may control LNK2 abundance. I show by a cell free protein degradation assays that proteasome-based degradation of LNK2 as well as LNK1 is possible. Data showed that SON1 binds to ASK1 in-planta suggest the existence an SCFSON1 complex that targets LNK2 for polyubiquitination and its subsequent degradation by the proteasome. The data presented in this dissertation indicates a role for LNKs in flowering and plant defense and also suggest that proteasome-base regulation of LNK turnover may be utilized to regulate LNK protein abundance and proper maintenance of the circadian clock.
Книги з теми "LNK"
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Dallimet programore midis LPK & LDK: Vështrim kritik. Prishtinë: Lena, 2021.
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Nāwikkamūn, ʻAnēk. Talāt lek lek. Krung Thēp: Samnakphim Sāithān, 2009.
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General elections in India: Electoral politics, electoral reforms, and political parties. New Delhi: Icon Publishers, 2005.
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Translators, Wycliffe Bible. Luk. [Papua New Guinea]: Wycliffe Bible Translators, 2006.
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MacFarlane, Michael. Link. Beirut: Oxford University Press, 1987.
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LDK. New York: Kodansha America, Incorporated, 2017.
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Mendes, Bob. Link. Amsterdam: Meulenhoff-M, 1994.
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Mit͡skevich, Irena. Lik. [Khaifa]: [s.n.], 2004.
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Sara, Linsley, and Dashiell Christine 1984 translator, eds. LDK. New York: Kodansha America, Incorporated, 2016.
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Ayu, Watanabe. LDK. New York: Kodansha America, Incorporated, 2016.
Знайти повний текст джерелаЧастини книг з теми "LNK"
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Miller, Laura T., Lionel Stange, Charles MacVean, Jorge R. Rey, J. H. Frank, R. F. Mizell, John B. Heppner, et al. "Lek." In Encyclopedia of Entomology, 2197. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_2009.
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Brakmić, Harris. "LND." In Bitcoin and Lightning Network on Raspberry Pi, 323–34. Berkeley, CA: Apress, 2019. http://dx.doi.org/10.1007/978-1-4842-5522-3_11.
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Lewiner, Colette. "LNG." In European Energy Markets Observatory, 40–43. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2753-3_6.
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Weik, Martin H. "link." In Computer Science and Communications Dictionary, 906. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_10353.
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Sherwood, Amanda R., Vikas V. Dukhande, Matthew S. Gentry, Sarah Sullivan, Weiguo Zhang, John H. White, Mario R. Calderon, et al. "Lsk." In Encyclopedia of Signaling Molecules, 1031. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100718.
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Hüls, Ewald, and Hans-Jörg Oestern. "LNA." In Die ICE-Katastrophe von Eschede, 188–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60177-4_28.
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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "LNB." In Encyclopedia of Molecular Mechanisms of Disease, 1206. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7516.
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Welch, Jennifer L., and Jennifer E. Walter. "Scheduling in a Graph." In Link Reversal Algorithms, 67–80. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-031-02006-3_7.
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Welch, Jennifer L., and Jennifer E. Walter. "Resource Allocation in a Distributed System." In Link Reversal Algorithms, 81–86. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-031-02006-3_8.
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Welch, Jennifer L., and Jennifer E. Walter. "Conclusion." In Link Reversal Algorithms, 87. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-031-02006-3_9.
Повний текст джерелаТези доповідей конференцій з теми "LNK"
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Koren-Michowitz, Maya, Sigal Gery, Daniel Nowak, and H. Phillip Koeffler. "Abstract 4010: Adaptor protein Lnk binds to JAK3 and negatively regulates a mutant activating allele associated with megakaryocytic leukemia." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4010.
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Churnside, James H. "Approximate refractive turbulence spectrum." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.wf2.
Повний текст джерелаАнотація:
In calculations of optical propagation through the turbulent atmosphere, one often requires knowledge of the spectrum of the refractivity fluctuations. Several forms of the spectrum are typically used. The Kolmogorov spectrum is a pure −11/3 power law in wavenumber and does not include inner scale effects. The Tatarski spectrum includes a Gaussian taper at high wavenumbers to account for inner scale effects. The Hill spectrum is the result of a rigorous derivation of the spectrum, and includes a bump near the inner scale. Unfortunately, it does not have an analytic form. However, it can be reasonably approximated by multiplying the Kolmogorov spectrum by exp(−70.5K2) + 1.45 exp[−0.97(lnK + 1.55)2], where K is the product of the Kolmogorov microscale (0.135 times the inner scale) and the wavenumber. This formula is within a few percent of the Hill spectrum except at very high wavenumbers where the values are very small.
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Oh, Stephen T., Erin F. Simonds, Carol Jones, Matthew B. Hale, Yury Goltsev, Kenneth D. Gibbs, Jason D. Merker, James L. Zehnder, Garry P. Nolan, and Jason Gotlib. "Abstract 239: Mutation of the inhibitory adaptor protein LNK drives potentiated JAK-STAT signaling in patients with JAK2 V617F-negative myeloproliferative neoplasms." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-239.
Повний текст джерела
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Oh, Stephen T., Jacob M. Zahn, Erin F. Simonds, John Bell, Georges Natsoulis, Jason Buenstro, Carol Jones, et al. "Abstract B6: Identification of novel mutations in the inhibitory adaptor protein LNK in patients with JAK2 V617F-negative and -positive chronic myeloproliferative neoplasms." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-b6.
Повний текст джерела
5
Meyle, Lucy, Emily O'Hara, and Monique Redmond. "El colofón: Donde las partes móviles se unen." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.131.g249.
Повний текст джерелаАнотація:
Esta propuesta considera al colofón como una estructura conceptual para pensar a través de listas y listados dentro de nuestra(s) práctica(s) creativa(s). Convencionalmente, el colofón es un texto breve que detalla información sobre la realización de una publicación o su uso previsto. Muy a menudo, el colofón especifica “cómo, dónde y cuándo”: el tipo de letra y el papel, la ubicación, fecha, número de edición y método de impresión. También puede destacar los aspectos relacionales de la publicación: el “con quién” o el “por qué aquí”. Los colofones aparecen en la apertura o cierre de una publicación, y la información que contienen puede formar una especie de lastre a lo que les precede o les sucede. Es decir, la enumeración del trabajo material, procesual y relacional que se empleó en la realización de las publicaciones se adelanta en el colofón y se reconoce como una necesidad estructural. ¿Cómo es útil esta concepción del colofón para pensar en los otros tipos de listas y listados que se abren paso en nuestras prácticas? Hojas de ruta; Listas de materiales; Contenidos; Listas de títulos; Índices; Subtítulos; Leyendas; Listas; Glosarios; Registros; Manifiestos; Cronologías. Estos modos de “enumerar” comunican contextos relevantes e importantes y, de esa manera, se convierten en una parte conceptual de las obras creativas mismas. Todos estos formatos son también prácticas de citas en las que los materiales, los procesos, la información y las relaciones se comparten libremente, como cualquier texto escrito en la lista de referencias de una publicación. En su libro, “The Hundreds” (2019), las teóricas culturales Lauren Berlant y Kathleen Stewart enumeran los textos de Adorno y Agamben junto a “Una máquina para cocinar huevos” y “Algunos pensamientos atrapados en una jardinera” en la sección de referencia, todos ordenados alfabéticamente bajo el título “Algunas cosas con las que pensamos”. Este tipo de lista (y el concepto de colofón en sí) no es un desglose indiscriminado en partes separadas, sino un resaltado estratégico de las condiciones y abstracciones de la obra de arte. ¿Cómo era la cosa (lista) que tenías antes de reunirte y cómo podrías “hacerlo” también? ¿Cómo podrías tomar diferentes decisiones y cuáles serían esas opciones? El colofón como estructura existe no solo para reconocer lo que contribuye a una publicación, sino también para rastrear posibles puntos de partida de la convención. Como táctica dentro de la práctica creativa, el colofón es como una abstracción conceptual; contiene todas las partes constitutivas que componen un proyecto en un solo lugar. El “-con” que exploran Berlant y Stewart es clave para el “cómo, dónde y cuándo” de las relaciones que une el hecho de enumerar. Este artículo compartirá tres perspectivas sobre el listado, así como una táctica sincrónica con la acción funcional de un colofón, donde las palabras y las imágenes llegan a girar, virar, inclinarse, torcerse y asentir, y la forma conceptual de un proyecto toma forma “con” cosas.
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Chida, Aakifa. "Combater a islamofobia para criar uma mudança global positiva." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.117.g184.
Повний текст джерелаАнотація:
Os efeitos do preconceito antimuçulmano atingiram uma escala global, com mais de 1,9 bilhão de muçulmanos afetados todos os dias. O design de comunicação pode neutralizar esse preconceito, comunicando mensagens que chamam a atenção e evitam que esses sentimentos se transformem em formas perigosas de ódio. O ódio é incitado por um padrão de ignorância e desinformação. É necessária uma mudança na raiz do problema para quebrar o ciclo e criar uma mudança nas atitudes e no comportamento. Isto pode ser alcançado por meio da educação e da conscientização. Este aumento da islamofobia é um subproduto de experiências históricas, alimentadas contemporaneamente pelos interesses econômicos e políticos de indivíduos e organizações. A comunicação é uma ferramenta frequentemente utilizada no contexto da educação e ativismo. À medida que as mídias digitais e sociais continuam a crescer, o design gráfico e a linguagem que as acompanha frequentemente se tornam verdadeiros motivadores em segundo plano. O design pode ser usado para neutralizar a islamofobia, concentrando-se na mudança de mentalidades e na educação para desmascarar os estereótipos que ocorrem como resultado da deturpação na mídia de massa e na política. Ao focar na mudança dessas mentalidades, uma alteração pode ocorrer em ações consequentes. O design da informação pode ser usado com o propósito de comunicar a seriedade de um problema. Por meio do uso de estatísticas bem elaboradas, infográficos, fatos e histórias vividas, os dados se tornam mais eficazes, pessoais e mais fáceis de assimilar. Ao focar nas diferentes camadas da islamofobia, o design pode lançar luz sobre questões complexas, que vão desde o preconceito até o genocídio aberto. O uso de uma linguagem visual poderosa, junto com sensibilidade estética, pode atingir a empatia dos receptores, fazendo-os pensar sobre suas próprias opiniões. A criação de recursos que abordem uma variedade de formas que a islamofobia pode assumir alcançará os agentes de mudança atuais e futuros da maneira mais relevante para eles. Esse movimento pode ocorrer por meio de produtos projetados que existem no mundo digital, já que a mídia on-line desempenha um papel significativo no ativismo e na conscientização do século 21. A divulgação é crucial para uma campanha de conscientização, pois a islamofobia não se limita a um determinado momento ou lugar. Por meio das mídias sociais, a mensagem pode atingir uma ampla gama de usuários de maneira fácil de acessar e compartilhar. Este projeto de design orientado para a prática usará os métodos de pesquisa, experimentação e resultados de design de comunicação para abordar o pensamento, comportamento, ações e consequências por trás da islamofobia, em um esforço para dar um passo em direção a uma mudança global positiva.
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Sampaio, Valzeli. "Mangueira Desejo: Experimentação e criação híbrida." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.109.g163.
Повний текст джерелаАнотація:
Este ensaio, que apresenta o processo de criação do projeto artístico em realidade aumentada “Wish Mango Tree” configura-se como um site específico/intervenção pública para instalação, nas mangueiras georreferenciadas da cidade de Belém, de um dispositivo tecnológico de etiquetagem eletrônica e criação de um placa de aço oca nestas árvores. Este processo envolve experimentação e criação relacionadas com artes visuais, design e programação, vivenciadas através de uma aplicação móvel, sendo uma intervenção física híbrida. “Wish Mango Tree” é inspirado na obra “Wish Tree”, uma série de instalações de arte em andamento, iniciada em 1981, pela artista japonesa, integrante do grupo Fluxus, Yoko Ono. Ela escolhe uma árvore nativa de um lugar, ou planta sob sua orientação. O público é convidado a amarrar um desejo por escrito e pendurá-lo na árvore. Yoko já instalou essa obra em algumas cidades do mundo. “Wish Mango Tree” propõe uma ação semelhante ao público e aos transeuntes das mangueiras de Belém. O projeto promove a interação entre indivíduos: humanos e mangueiras. O conteúdo digital pode ser visualizado no aplicativo de realidade aumentada do site específico, onde os desejos da folha de manga podem ser acessados por qualquer pessoa. A “Mangueira Desejo” busca preencher uma lacuna ou carência identificada: a invisibilidade das mangueiras, buscando usar a tecnologia para dar visibilidade a um problema social e ecológico. A dimensão política do projeto se revela ao dar visibilidade às mangueiras, ativando a memória coletiva e provocando questionamentos e compromissos dos sujeitos envolvidos: árvores, pessoas e instituições. Este projeto artístico evoca a memória afetiva de seus participantes, buscando valorizar, fortalecer e manter a identidade e a memória cultural do Pará por meio das mídias digitais. O projeto enquadra-se na área artística e cultural: artes visuais, com a criação de propostas em instalação, mecanismos de intervenção, site específico, arte urbana, arte digital, novas mídias e fotografia, sendo um híbrido de proposta entre arte e design digital, além de abordar a experiência das artes visuais em suas reflexões técnicas, formais e conceituais, de criação, difusão, formação e memória. Neste sentido, o projeto promove a criação, experimentação e design associados a um contexto histórico, social, cultural, sustentável e/ou tecnológico, que podem ser traduzidos em ações propositivas que abordem o design gráfico, mídias interativas, web design/aplicativos e design de games. As próprias mangueiras são objetos de interesse público — o aplicativo convida todos a “pendurarem” seus desejos, promovendo a transformação das mangueiras em receptáculo das aspirações das pessoas que as visitam. O aplicativo mobile promoverá, remotamente, uma experiência em rede que desencadeia uma experiência física nas principais mangueiras da praça, o que dará visibilidade à nuvem de anotações nas folhas destas árvores.
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Sabra, Nabil. "Desarrollar un enfoque de aprendizaje de adultos para mejorar el pensamiento crítico de los estudiantes de diseño gráfico en Yemen." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.114.g177.
Повний текст джерелаАнотація:
El pensamiento crítico es una habilidad esencial no solo para el logro educativo sino también para mejorar la calidad de vida (Bakry et al., 2019, págs. 632-633). Sin embargo, Yemen no ha fomentado ni utilizado tradicionalmente el pensamiento crítico en la educación en diseño gráfico, un campo de estudio en el que se requiere el pensamiento crítico para pensar más allá de un problema para crear soluciones a problemas nuevos y existentes. El diseño no presenta la misma solución para cada proyecto, sino que busca nuevas ideas y soluciones que tengan respuestas culturalmente relevantes para resolver un problema (Barbour, 2016). Actualmente, hay una falta de investigación en las áreas de pensamiento crítico en la educación del diseño gráfico en Yemen. Para Nordin y Surajudin (2015), Ijtihad es un representante de la habilidad de pensamiento de orden superior que puede reflejar el Tawhid de Allah (la unificación de Dios) y apoyó su afirmación con un hadiz (las declaraciones del profeta): “Aquellos que se conocen a sí mismos, pueden conoce a su Dios ”(Nordin y Surajudeen, 2015, p. 37). Así, para conocerse a sí mismo, el aprendiz de por vida necesita tener autorregulación para poder utilizar el pensamiento crítico (Szabo, 2019). Al explorar la relación entre el concepto islámico de Ijtihad (razonamiento individual) y la noción occidental de pensamiento crítico, hay varios puntos que requieren consideración. En particular, establecer lo que significa el pensamiento crítico en el contexto de la educación de diseño occidental en relación con el papel de Ijtihad en la educación islámica. El enfoque de esta presentación es explorar la relación entre la noción occidental de pensamiento crítico y el concepto islámico equivalente de Ijtihad. Destaca los cinco elementos de Ijtihad: Tadabbur (aprender y comprender antes de juzgar una idea), Tafkih (analizar usando al-Qalb (corazón) que depende de al-Aqal (mente)), Tafakkur (reflexionar y examinar), Ta’qil (recopilar información antes de saltar a la conclusión), y Tadhakkur (resumir para comprender sabiamente). El pensamiento crítico es culturalmente relativo, por lo que es importante estudiar este fenómeno considerando la cultura yemení proponiendo un marco holístico adecuado de Ijtihad. Esta investigación se basa en un Ph.D. estudio en curso que investiga el pensamiento crítico en la educación en diseño gráfico en Yemen desde una perspectiva islámica. Se llevaron a cabo entrevistas con educadores yemeníes para explorar el concepto de pensamiento crítico e Ijtihad. En última instancia, esta investigación tiene como objetivo identificar las técnicas esenciales de pensamiento que pueden moldearse para reflejar el Ijtihad, junto con la identificación de estrategias de aprendizaje de adultos apropiadas desarrolladas por educadores e investigadores occidentales para mejorar el pensamiento crítico de los estudiantes. El resultado de este estudio distinguirá los marcos dentro de los planes de estudio de diseño gráfico que promueven el pensamiento crítico de los estudiantes y los reflejan desde un contexto occidental a uno yemení considerando Ijtihad.
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Cohen, Lauro Arthur Farias Paiva, and Nubia Suely Silva Santos. "Nuevas demandas en la educación del diseño: De la investigación a la práctica." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.123.g201.
Повний текст джерелаАнотація:
Uno de los desafíos contemporáneos para la investigación y la práctica en diseño y los materiales es la capacidad de asociar información técnica sobre propiedades y procesamiento de materiales con actividades y aplicaciones creativas. Actualmente, hay un retorno a las prácticas y procesos artesanales, en los que hay un diálogo continuo entre el creador, el material y el proceso de creación (Bak-Andersen, 2021). El acto de diseñar implica comprender las cualidades sensoriales y las limitaciones técnicas de un material, proceso que se puede lograr mediante la manipulación manual y exploratoria (Karana et al., 2015). Este estudio demuestra la relevancia de los procesos de diseño orientados a la práctica en la construcción del conocimiento. A lo largo de una experiencia facilitada a través de talleres de reciclaje de papel postconsumo con estudiantes de la carrera de Diseño de la Universidad del Estado de Pará (Brasil), se investigaron formas de producir baldosas de papel reciclado. El contexto de la actividad se basa en estudios teóricos en materiales y diseño, con un enfoque metodológico centrado en la experimentación práctica en un escenario de investigación y docencia. Dentro del procedimiento metodológico adoptado, la actividad brindó una red de contactos y encuentros en los que los estudiantes tuvieron la oportunidad de reflexionar sobre la eliminación de residuos. Uno de los aportes estuvo en la posibilidad de abordar la conciencia y los conceptos críticos a través de la experiencia en el reciclaje de papel. Los participantes compartieron sus experiencias e historias relacionadas con los temas presentados, además de perspectivas sobre sostenibilidad. Se discutieron las formas de construcción colectiva y el impacto e identidad que tiene un azulejo, ya sea individualmente o en conjunto. Luego de la exhibición se inició la práctica, que consistía en preparar desperdicios de papel postconsumo, producir pulpa de celulosa y confeccionar piezas de azulejos de papel para su posterior pintado. Al reciclar el material y hacer las piezas, los estudiantes tuvieron la oportunidad de explorar mediante un contacto cercano con el proceso de producción. El taller permitió la construcción de nuevos significados y experiencias con la elaboración de productos a través de los aspectos lúdicos de la elaboración manual. Durante la creación de los azulejos, los participantes expresaron sus sentimientos, referencias e intereses a través de la pintura. Los distintos colores y texturas trabajados durante la actividad le dan al artefacto la característica de quienes lo manipulan. Cada mosaico presentaba su particularidad, ya que cada alumno elegía su paleta de colores y estilo de pintura, capaz de transmitir un mensaje de forma individual o colectiva. Como resultado, se obtuvieron piezas con potencial para ambientes interiores y se diseñó una instalación de arte. La aplicación de las piezas en una habitación transforma y provoca. A través de la contemplación, el público de la instalación utilizó el tacto para interactuar con las piezas, apreciar la estética e investigar la individualidad de las baldosas de papel. El espacio se transformó en un punto de referencia, un lugar de encuentro e interacción. Para el educador y los estudiantes en formación, los resultados de los talleres representan una oportunidad para compartir información, ideas y procesos experimentales intermedios, orientados a las demandas contemporáneas del área.
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Eickel, Bianca, and Richard Perassi. "A evolução do posicionamento da comunicação gráfico-simbólica da marca tecnológica Multilaser." In LINK 2021. Tuwhera Open Access, 2021. http://dx.doi.org/10.24135/link2021.v2i1.97.g133.
Повний текст джерелаАнотація:
Com o processo de globalização, o conceito de tecnologia é amplamente difundido na construção de uma sociedade mais simplificada. A tecnologia torna-se um fenômeno global no século 21, com o uso de computadores capazes de mudar o dia a dia das pessoas. Com o tempo, a tecnologia evolui e se transforma, nesse processo a comunicação e a cultura acompanham as mudanças. As empresas inseridas na sociedade e cultura atuais buscam se comunicar com os consumidores em todos os momentos; por isso, o posicionamento é irrefutável neste processo de marketing. Se a tecnologia, a comunicação e a cultura mudam com o tempo, o posicionamento da marca também deve acompanhar esse movimento. A partir deste contexto, o tema desta proposta irá descrever o processo de evolução do posicionamento da comunicação gráfico-simbólica da marca tecnológica Multilaser e, assim, analisar as mudanças de posicionamento sob a perspectiva do design. A marca escolhida traz relevância ao estudo, pois passou por diversos marcos históricos que contribuirão para a análise descritiva da evolução. A empresa foi fundada por Israel Ostrowiecki no Brasil, em 1987. Começou a atuar no segmento de impressoras e fotocopiadoras, reciclando cartuchos para impressoras até 2003. Após vários fatos históricos em sua trajetória, atualmente possui 44 mil pontos de venda no Brasil, com um portfólio de 15 departamentos, incluindo smartphones, celulares, gamers, drones, automotivo, entre outros. A problemática da proposta leva em consideração o grande volume de importação de produtos tecnológicos pelo Brasil e, assim, o estudo se justifica pela necessidade de avaliar a percepção de uma hipertrofia da função estética na comunicação do segmento tecnológico brasileiro. Para alcançar este resultado, será utilizada uma abordagem metodológica qualitativa, voltada para a percepção de significados intrínsecos às crenças, valores e atitudes nas relações humanas. Portanto, para atingir os objetivos da pesquisa, o estudo será dividido em três etapas de desenvolvimento, sendo a primeira a etapa exploratória, com a busca de artigos e livros que contribuam para a pesquisa bibliográfica e a análise descritiva de produtos de comunicação, impressos ou digitais, selecionados dentre a marca Multilaser. Para a segunda etapa, será realizada uma pesquisa bibliográfica, visando elaborar a construção do referencial teórico a partir dos materiais identificados na etapa anterior. A terceira etapa é a documental, para analisar e descrever as mudanças no posicionamento da marca sob a óptica da concepção dos documentos selecionados na primeira etapa. As discussões nesta proposta trazem a comunicação visual, aspectos históricos do termo tecnologia e sobre a empresa Multilaser; depois, a relação entre comunicação e cultura, que irá elucidar a trajetória da comunicação visual como forma de posicionamento da marca, bem como a representação gráfica publicidade na comunicação na perspectiva do design. O estudo se limitará a produtos gráficos de comunicação publicitária, onde se pretende compreender um olhar sobre o avanço do conhecimento na visualidade das marcas tecnológicas brasileiras, a atuação dos profissionais da área de design, e ainda pretende-se promover novas pesquisas que estabeleçam um posicionamento gráfico-simbólico para a tecnologia brasileira.
Звіти організацій з теми "LNK"
1
ZHAO, D., and P. OCONNOR. DESIGN OF 2.4 GHZ CMOS DIRECT CONVERSION LNA AND MIXER COMBINATION FOR WIRLESS DATA LINK TRANSCEIVER. Office of Scientific and Technical Information (OSTI), April 2002. http://dx.doi.org/10.2172/794023.
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2
mann, Douglas. LNG measurement :. Gaithersburg, MD: National Bureau of Standards, 1986. http://dx.doi.org/10.6028/nbs.ir.85-3028.
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3
Henderson, James, and Vitaly Yermakov. Russian LNG. Oxford Institute for Energy Studies, November 2019. http://dx.doi.org/10.26889/9781784671501.
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4
Taylor, R., and S. Ratliff. Dynamic Link Exchange Protocol (DLEP) Link Identifier Extension. RFC Editor, February 2020. http://dx.doi.org/10.17487/rfc8703.
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5
Luu, Brian B. Secure Link Middleware. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada485508.
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6
Berry, Pauline M., Ian Harrison, John D. Lowrance, Andres C. Rodriguez, and Enrique H. Ruspini. Link Analysis Workbench. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada426802.
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7
Skone, Timothy J. LNG Liquefaction, Operation. Office of Scientific and Technical Information (OSTI), October 2010. http://dx.doi.org/10.2172/1509078.
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8
Skone, Timothy J. LNG Liquefaction, Construction. Office of Scientific and Technical Information (OSTI), June 2013. http://dx.doi.org/10.2172/1509282.
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9
Skone, Timothy J. LNG Regasification, Construction. Office of Scientific and Technical Information (OSTI), June 2013. http://dx.doi.org/10.2172/1509284.
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10
Fruhauf, Anne. Mozambique's LNG revolution. Oxford Institute for Energy Studies, March 2014. http://dx.doi.org/10.26889/9781784670016.
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