Gotowe bibliografie tematyczne / Kinase

Gotowa bibliografia na temat „Kinase”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 22 czerwca 2024

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Artykuły w czasopismach na temat "Kinase"

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Symons, Antony, Soren Beinke i Steven C. Ley. "MAP kinase kinase kinases and innate immunity". Trends in Immunology 27, nr 1 (styczeń 2006): 40–48. http://dx.doi.org/10.1016/j.it.2005.11.007.

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Buxade, Maria. "The Mnks: MAP kinase-interacting kinases (MAP kinase signal-integrating kinases)". Frontiers in Bioscience Volume, nr 13 (2008): 5359. http://dx.doi.org/10.2741/3086.

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Jouannic, S., A. Hamal, A. S. Leprince, J. W. Tregear, M. Kreis i Y. Henry. "Plant MAP kinase kinase kinases structure, classification and evolution". Gene 233, nr 1-2 (czerwiec 1999): 1–11. http://dx.doi.org/10.1016/s0378-1119(99)00152-3.

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Wang, Qin, Michael Yerukhimovich, William A. Gaarde, Ian J. Popoff i Claire M. Doerschuk. "MKK3 and -6-dependent activation of p38α MAP kinase is required for cytoskeletal changes in pulmonary microvascular endothelial cells induced by ICAM-1 ligation". American Journal of Physiology-Lung Cellular and Molecular Physiology 288, nr 2 (luty 2005): L359—L369. http://dx.doi.org/10.1152/ajplung.00292.2004.

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Previous studies demonstrated that neutrophil adherence induces ICAM-1-dependent cytoskeletal changes in TNF-α-treated pulmonary microvascular endothelial cells that are prevented by a pharmacological inhibitor of p38 MAP kinase. This study determined whether neutrophil adherence induces activation of p38 MAP kinase in endothelial cells, the subcellular localization of phosphorylated p38, which MAP kinase kinases lead to p38 activation, which p38 isoform is activated, and what the downstream targets may be. Confocal microscopy showed that neutrophil adhesion for 2 or 6 min induced an increase in phosphorylated p38 in endothelial cells that was punctate and concentrated in the central region of the endothelial cells. Studies using small interfering RNA (siRNA) to inhibit the protein expression of MAP kinase kinase 3 and 6, either singly or in combination, showed that both MAP kinase kinases were required for p38 phosphorylation. Studies using an antisense oligonucleotide to p38α demonstrated that inhibition of the protein expression of p38α 1) inhibited activation of p38 MAP kinase without affecting the protein expression of p38β; 2) prevented phosphorylation of heat shock protein 27, an actin binding protein that may induce actin polymerization upon phosphorylation; 3) attenuated cytoskeletal changes; and 4) attenuated neutrophil migration to the EC borders. Thus MAP kinase kinase3- and 6-dependent activation of the α-isoform of p38 MAP kinase is required for the cytoskeletal changes induced by neutrophil adherence and influences subsequent neutrophil migration toward endothelial cell junctions.
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Takekawa, Mutsuhiro, Kazuo Tatebayashi i Haruo Saito. "Conserved Docking Site Is Essential for Activation of Mammalian MAP Kinase Kinases by Specific MAP Kinase Kinase Kinases". Molecular Cell 18, nr 3 (kwiecień 2005): 295–306. http://dx.doi.org/10.1016/j.molcel.2005.04.001.

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Nemoto, Shino, Joseph A. DiDonato i Anning Lin. "Coordinate Regulation of IκB Kinases by Mitogen-Activated Protein Kinase Kinase Kinase 1 and NF-κB-Inducing Kinase". Molecular and Cellular Biology 18, nr 12 (1.12.1998): 7336–43. http://dx.doi.org/10.1128/mcb.18.12.7336.

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ABSTRACT IκB kinases (IKKα and IKKβ) are key components of the IKK complex that mediates activation of the transcription factor NF-κB in response to extracellular stimuli such as inflammatory cytokines, viral and bacterial infection, and UV irradiation. Although NF-κB-inducing kinase (NIK) interacts with and activates the IKKs, the upstream kinases for the IKKs still remain obscure. We identified mitogen-activated protein kinase kinase kinase 1 (MEKK1) as an immediate upstream kinase of the IKK complex. MEKK1 is activated by tumor necrosis factor alpha (TNF-α) and interleukin-1 and can potentiate the stimulatory effect of TNF-α on IKK and NF-κB activation. The dominant negative mutant of MEKK1, on the other hand, partially blocks activation of IKK by TNF-α. MEKK1 interacts with and stimulates the activities of both IKKα and IKKβ in transfected HeLa and COS-1 cells and directly phosphorylates the IKKs in vitro. Furthermore, MEKK1 appears to act in parallel to NIK, leading to synergistic activation of the IKK complex. The formation of the MEKK1-IKK complex versus the NIK-IKK complex may provide a molecular basis for regulation of the IKK complex by various extracellular signals.
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Hurley, Rebecca L., Kristin A. Anderson, Jeanne M. Franzone, Bruce E. Kemp, Anthony R. Means i Lee A. Witters. "The Ca2+/Calmodulin-dependent Protein Kinase Kinases Are AMP-activated Protein Kinase Kinases". Journal of Biological Chemistry 280, nr 32 (24.06.2005): 29060–66. http://dx.doi.org/10.1074/jbc.m503824200.

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Verploegen, Sandra, Jan-Willem J. Lammers, Leo Koenderman i Paul J. Coffer. "Identification and characterization of CKLiK, a novel granulocyte Ca++/calmodulin-dependent kinase". Blood 96, nr 9 (1.11.2000): 3215–23. http://dx.doi.org/10.1182/blood.v96.9.3215.

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Abstract Human granulocytes are characterized by a variety of specific effector functions involved in host defense. Several widely expressed protein kinases have been implicated in the regulation of these effector functions. A polymerase chain reaction–based strategy was used to identify novel granulocyte-specific kinases. A novel protein kinase complementary DNA with an open reading frame of 357 amino acids was identified with homology to calcium-calmodulin–dependent kinase I (CaMKI). This has been termed CaMKI-like kinase (CKLiK). Analysis of CKLiK messenger RNA (mRNA) expression in hematopoietic cells demonstrated an almost exclusive expression in human polymorphonuclear leukocytes (PMN). Up-regulation of CKLiK mRNA occurs during neutrophilic differentiation of CD34+ stem cells. CKLiK kinase activity was dependent on Ca++ and calmodulin as analyzed by in vitro phosphorylation of cyclic adenosine monophosphate responsive element modulator (CREM). Furthermore, CKLiK- transfected cells treated with ionomycin demonstrated an induction of CRE- binding protein (CREB) transcriptional activity compared to control cells. Additionally, CaMK-kinaseα enhanced CKLiK activity. In vivo activation of CKLiK was shown by addition of interleukin (IL)-8 to a myeloid cell line stably expressing CKLiK. Furthermore inducible activation of CKLiK was sufficient to induce extracellular signal-related kinase (ERK) mitogen-activated protein (MAP) kinase activity. These data identify a novel Ca++/calmodulin-dependent PMN- specific kinase that may play a role in Ca++-mediated regulation of human granulocyte functions.
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Verploegen, Sandra, Jan-Willem J. Lammers, Leo Koenderman i Paul J. Coffer. "Identification and characterization of CKLiK, a novel granulocyte Ca++/calmodulin-dependent kinase". Blood 96, nr 9 (1.11.2000): 3215–23. http://dx.doi.org/10.1182/blood.v96.9.3215.h8003215_3215_3223.

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Human granulocytes are characterized by a variety of specific effector functions involved in host defense. Several widely expressed protein kinases have been implicated in the regulation of these effector functions. A polymerase chain reaction–based strategy was used to identify novel granulocyte-specific kinases. A novel protein kinase complementary DNA with an open reading frame of 357 amino acids was identified with homology to calcium-calmodulin–dependent kinase I (CaMKI). This has been termed CaMKI-like kinase (CKLiK). Analysis of CKLiK messenger RNA (mRNA) expression in hematopoietic cells demonstrated an almost exclusive expression in human polymorphonuclear leukocytes (PMN). Up-regulation of CKLiK mRNA occurs during neutrophilic differentiation of CD34+ stem cells. CKLiK kinase activity was dependent on Ca++ and calmodulin as analyzed by in vitro phosphorylation of cyclic adenosine monophosphate responsive element modulator (CREM). Furthermore, CKLiK- transfected cells treated with ionomycin demonstrated an induction of CRE- binding protein (CREB) transcriptional activity compared to control cells. Additionally, CaMK-kinaseα enhanced CKLiK activity. In vivo activation of CKLiK was shown by addition of interleukin (IL)-8 to a myeloid cell line stably expressing CKLiK. Furthermore inducible activation of CKLiK was sufficient to induce extracellular signal-related kinase (ERK) mitogen-activated protein (MAP) kinase activity. These data identify a novel Ca++/calmodulin-dependent PMN- specific kinase that may play a role in Ca++-mediated regulation of human granulocyte functions.
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Pang, Kam-Lee, Wei-Li Thong i Siew-Eng How. "Cinnamomum Iners as Mitogen-Activated Protein Kinase Kinase (MKK1) Inhibitor". International Journal of Engineering and Technology 1, nr 4 (2009): 310–13. http://dx.doi.org/10.7763/ijet.2009.v1.61.

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Rozprawy doktorskie na temat "Kinase"

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Gopalbhai, Kailesh. "Régulation négative des MAP kinase kinases par phosphorylation /". [Montréal] : Université de Montréal, 2003. http://wwwlib.umi.com/cr/umontreal/fullcit?pNQ92759.

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Thèse (Ph.D.) -- Université de Montréal, 2004.
"Thèse présentée à la Faculté des études supérieures en vue de l'obtention du grade de Philosophiae Doctor en Pharmacologie" Version électronique également disponible sur Internet.
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Sengar, Ameet Singh. "Mkh1, a novel MAP kinase kinase kinase in Schizosaccharomyces pombe". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq20852.pdf.

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Gatesman, Ammer Amanda. "PKCalpha direct cSrc activation and podosome formation through the adaptor protein AFAP-110". Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3762.

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Thesis (Ph. D.)--West Virginia University, 2004
Title from document title page. Document formatted into pages; contains vii, 350 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 322-346).
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Nadeau, Philippe. "Régulation de la MAP3-kinase Ask1 par oxydoréduction". Doctoral thesis, Université Laval, 2009. http://hdl.handle.net/20.500.11794/21223.

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La MAP3-kinase Askl est un point de convergence dans la réponse cellulaire apoptotique induite par le stress oxydant chez les cellules de mammifères. Par contre, le mécanisme par lequel le stress oxydant régule l'activité d'Askl demeure incompris. Plusieurs protéines qui, comme Askl, sont impliquées dans les voies de signalisation induites par le stress oxydant, sont régulées par des mécanismes d'oxydoréduction. La présente étude révèle que le H2O2 induit l'oxydoréduction de plusieurs résidus cysteines d'Askl. Une exposition des cellules au H2O2 induit rapidement la formation d'oligomères covalents d'Askl par l'intermédiaire de ponts disulfures. Sept cysteines sensibles à l'oxydation ayant le potentiel de participer à la formation de ces liens disulfures et de ces oligomères covalents ont été identifiées. Bloquer la formation de ces derniers avec un mutant où toutes les cysteines sensibles à l'oxydation sont mutées permet de bloquer l'apoptose dépendante d'Askl en réponse au H2O2. Parmi les cysteines sensibles à l'oxydation, la cysteine 250 est essentielle pour qu'Askl régule la phosphorylation de JNK en réponse au H2O2. Les résultats montrent aussi que la régulation des résidus cysteines d'Askl implique diverses activités thiol-réductases de la Trxl. Tout d'abord, une activité thiol-réductase rapide et transitoire de la Trxl sur les oligomères covalents d'Askl permet à la Trxl de les réduire et de ramener Askl à son état initial. Dans des cellules non stimulées, une activité thiol-réductase plus lente ou plus stable de la Trxl lui permet de s'associer à la cysteine 250 d'Askl et de réguler négativement la kinase. En effet, à la suite d'une stimulation au H2O2, cette activité de la Trxl est perdue ce qui permet une exposition de la cysteine 250 d'Askl et l'activation de JNK. Les cysteines d'Askl sensibles à l'oxydation ne régulent pas la phosphorylation et l'activation d'Askl, ce qui suggère qu'elles seraient plutôt essentielles à la signalisation régulée par Askl suivant son activation. Enfin, le domaine coil dans le domaine C-terminal d'Askl est aussi essentiel à la régulation de la kinase par le H2O2. Cette thèse propose donc un nouveau mécanisme de régulation d'Askl par le stress oxydant, principalement par l'oxydoréduction de certains de ses résidus cysteines, et enrichie le modèle par lequel la Trxl régule négativement Askl.
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Jean, Steve. "Caractérisation fonctionnelle de nouveaux partenaires protéiques des kinases xPAK1 et xMLK2 chez Xenopus laevis". Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25722/25722.pdf.

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Vaglio, Philippe. "Etude de la relation structure-fonction de la protéine kinase CK2 par mutagenèse dirigée des résidus basiques conservés". Montpellier 1, 1996. http://www.theses.fr/1996MON1T029.

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Wan, Omar Wan Bayani. "Studies into interactions between MAP kinase and MAP kinase kinase proteins of Arabidopsis". Thesis, Heriot-Watt University, 2011. http://hdl.handle.net/10399/2490.

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The Arabidopsis thaliana genome contains genes encoding 10 MAP kinase kinase (MKK) and 20 Map kinase (MAPK) proteins, however the exact relationship between upstream MKK activators and downstream MAPK protein partners has not fully elucidated. In this study, the yeast two -hybrid system was used to identify protein-protein interactions between all Arabidopsis MAPKs and MKKs. In the yeast two- hybrid assay, the result from the qualitative β-galactosidase filter assay showed that 6 MAPK proteins interacted with 6 MKK proteins. Quantitative β-galactosidase liquid assay was used to confirm the interactions between MAPK and MKK in yeast. The BiFC approach was used to test whether MKK1, MKK2 and MKK6 associated with MPK4 and MPK11 in vivo in Arabidopsis. In these assays, GFP fluorescence was observed in the protoplasts suggesting that MKK1, MKK2 and MKK6 interact with MPK4 and MPK11, respectively. However, evidence of reciprocal interaction was only seen with the combination of MKK1 and MPK11, and with MKK2 and MPK11. This contrasts with the findings seen using the yeast two-hybrid system in which reciprocal activity was seen for all combinations of MKK1, MKK2 or MKK6 with MPK4 or MPK11. Furthermore, the negative controls for BiFC (spilt GFP with no fusions partners) gave strong fluorescence, indicative of non-specific interaction between the split GFP. Since MPK4 is known to be an important regulator of plant stress responses, MPK11 (similar in sequence to MPK4) might also be involved in such responses. Therefore, a knock-out allele of MPK11 was obtained and analysed on a molecular and physiological basis. Seed germination experiments showed that no differences between the germination of the wildtype and the mpk11 mutant by increasing levels of salt however seed germination experiments showed that seedling of mpk11 mutant are hypersensitive to ABA during germination. To aid further understanding on the function of MPK11 and the relationship between MPK11 and interacting activators, HA-epitope tagged cDNA for MPK11 was introduced into Arabidopsis Columbia Wildtype, mpk11, mkk1 and mkk2. Results from Western blot analysis indicated that several lines from each transformant produced detectable levels of MPK11-HA, thus generating tools for further analysis
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Mazharian, Alexandra. "Rôle complémentaire des MAP Kinases ERK2, p38 et JNK1 dans l'activation plaquettaire". Paris 7, 2007. http://www.theses.fr/2007PA077217.

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Les MAP Kinases (MAPK) sont des sérine/thréonine kinases regroupées en trois familles: les «Extracellular signal-RegidatedKinases» (ERKs), les p38MAPKs et les «c-jun N-terminal Kinases» (JNKs). L'étude des MAPK dans les plaquettes présente un double intérêt. Elle permet d'identifier de nouvelles cibles et de nouveaux rôles notamment dans l'hémostase et la thrombose. Dans la première étude, nous montrons un rôle complémentaire d'ERK2 et p38 dans l'adhérence des plaquettes sur une matrice de collagène, En effet, ERK2 dépend des taux de cisaillement et de l'interaction vWF/GPIb. En revanche p38, sous le contrôle des récepteurs du collagène (α2β1 et GPVI), est indépendante des taux de cisaillement. La deuxième étude montre un rôle d'ERK2 et p38 dans l'étalement des plaquettes sur une matrice de fibrinogène induit par le récepteur PAR4 de la thrombine. L'activation de la p38 dépend du récepteur P2Y12 de l'ADP alors qu'ERK2 dépend du signal outside-in de l'intégrale αllbβ3. P38 et ERK2 jouent respectivement un rôle sur la polymérisation de l'actine et la phosphorylation de la Myosin Light Chain, toutes deux nécessaires à l'étalement. Enfin, nous montrons un rôle de JNKl dans l'agrégation et la sécrétion plaquettaires induites par le collagène. JNKl contribue à la formation du thrombus in vitro dépendant de l'activation de l'intégrine αllbβ3 et de l'interaction vWF/GPIb, et joue également un rôle dans la thrombose in vivo chez la souris. En conclusions, nos travaux ont permis d'apporter de nouvelles connaissances quant aux rôles complémentaires des MAPK dans les différentes étapes de l'activation plaquettaire
The MAP Kinases belong to a serine/threonine kinase family that include the "Extracellular signal-Regulated Kinases" (ERKs), p38MAPKs and the "c-jun N-terminal Kinases" (JNKs). The study of the MAP Kinase in platelets allows identifying new targets and new rôles in particular in the haemostasis and thrombosis. In the first study, we describe complementary roles of ERK2 and p38MAPK in platelet adhésion and spreading over a collagen matrix. The role of ERK2 is dependent of blood flow and vWF/GPIb interaction. In contrast, the role of the p38MAFK in platelet adhesion is independent of blood flow and involved the α2β1 integrin. In the second study, we show the ERK2 and p38MAPK are involved in platelet spreading on a fibrinogen matrix after PAR4 stimulation. Activation of p38MAPK, required for actin polymerization, is dependent of ADP signalling through its receptor P2Y12, In contrast, ERK2, required for Myosin Light Chain phosphorylation, is dependent on integrin αllbβ3 outside-in signalling and the Rho pathway, Both MAP Kinases act on cytoskeleton rearrangement required for platelet spreading, Lastly, we show for the first time a role of JNKl in platelet aggregation and secretion induced by low concentrations of collagen. In addition, JNKl is required for thrombus growth at high shear involving activation of integrin αllbβ3 and vWF/GPIb interaction. Finally, in vivo, JNKl is involved in a mouse model of arterial thrombosis. In conclusions, our works bring us new knowledge as for the roles of MAP Kinases ERK2, p38MAPK and JNKl in the different stages of platelet activation
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Beggs, James. "The MAP-kinase interacting kinases (Mnks) as targets in cancer". Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/390651/.

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The Mnks appear to play an important role in tumour development, but are not essential for normal cell growth and development. This makes them attractive targets for designing anti-cancer treatments. The Mnks are directly downstream of the RAS-RAF-MEK-ERK pathway, a pathway that is frequently overactive in cancer cells. The Mnks bind to eIF4G, which is part of the translation initiation complex, and are the only kinases known to phosphorylate the 5’ mRNA cap-binding protein eIF4E. Despite numerous studies linking this phosphorylation event to cancer, its precise role in cancer remains unclear. The lack of progress in developing our understanding of the role the Mnks is largely down to the absence of a selective and potent Mnk inhibitor. Presented here are the results of experiments carried out using a novel Mnk inhibitor, Mnk-I1. These results are also backed up with the results of experiments using cells – Mouse Embryonic Fibroblasts (MEFs) - that have had the Mnks genetically knocked out. What the results show, is that Mnk kinase activity appears to play a key role in cancer cell migration. The mechanism appears to involve an important role for Mnk kinase activity in the translation of vimentin mRNA into protein and in preventing the degradation of the vimentin protein: an established marker of cells that have undergone Epithelial-Mesenchymal Transition (EMT) and become motile. The results presented in the last chapter focus on whether the Mnks might be suitable targets for overcoming acquired resistance to the MEK inhibitor AZD6244. In the context of a BRAF600E amplification, Mnk-I1 appeared to have a small antiproliferative effect in one cancer cell line tested; however, there was no effect on the proliferation of a cancer cell line with a KRAS13D amplification. Included in this set of data is an interesting effect of Mnk-I1 on increasing P-Mnk1 levels.
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Chetoui, Nizar. "Caractérisation du rôle de la protéine kinase MEK1 dans les voies de transduction des MAP kinases". Thesis, Université Laval, 2005. http://www.theses.ulaval.ca/2005/22589/22589.pdf.

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Le développement tumoral nécessite une dérégulation des contrôles normaux de la prolifération et de la différenciation cellulaires. Il est bien connu que la voie de signalisation ERK/MAP kinase est impliquée dans ces processus de régulation cellulaire. De plus, un rôle essentiel dans la transformation cellulaire est attribué à MEK1 qui est un élément central de cette voie. Une meilleure compréhension de l’implication de MEK1 dans les voies de transduction devrait donc nous permettre de mieux comprendre le developpement cellulaire et la transformation morphologique. Mes travaux de recherche tentent d’élucider les mécanismes de régulation des protéines kinases MEK1 et MEK2 dans le but de mieux comprendre leur divergence fonctionnelle et leur implication dans les différentes réponses cellulaires. Ainsi, l’étude de la voie ERK/MAPK chez les fibroblastes embryonnaires mutants pour le gène Mek1 indique que la transduction du signal amorcée par un neuropeptide, la bombésine, passe spécifiquement par MEK1 et serait indépendant de MEK2. La région C-terminale de MEK1 semble médier la spécificité de la réponse à la bombésine. Le domaine MSS, qui est une insertion d’une séquence riche en proline unique à MEK1 et MEK2 pourrait être la clef de cette réponse spécifique. En outre, nos travaux de délétion et d’interactions protéiques suggèrent qu’une variation de la conformation de la région C-terminale de MEK1 pourrait avoir lieu entre l’état inactif et l’état actif de ces MAPKKs. En absence d’activation, la région en caboxy du domaine kinase semble interagir avec la boucle d’activation se trouvant au cœur du domaine kinase. Cette interaction intramoléculaire serait dépendante de l’état de phosphorylation de MEK1. Par contre, la région en carboxy ne semble pas être un domaine d’autoinhibition ou un pseudo substrat puisque sa délétion ne met pas la protéine dans un état constitutivement actif. Ainsi, il est possible que cette région soit essentielle du point de vue structural pour permettre, en fonction de son activité, la régulation des interactions de MEK1 (ou MEK2) avec ses activateurs, substrats ou protéines d’échafaudage.
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Książki na temat "Kinase"

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Kozlov, Sergei V., red. ATM Kinase. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6955-5.

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Kuster, Bernhard, red. Kinase Inhibitors. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-337-0.

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Reith, Alastair D. Protein Kinase Protocols. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590594.

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Mukai, Hideyuki, red. Protein Kinase Technologies. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5.

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Mellinghoff, Ingo K., i Charles L. Sawyers, red. Therapeutic Kinase Inhibitors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28296-6.

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Ward, Richard A., i Frederick W. Goldberg, red. Kinase Drug Discovery. Cambridge: Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/9781788013093.

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Ward, Richard A., i Frederick Goldberg, red. Kinase Drug Discovery. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733557.

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Pinna, Lorenzo A., red. Protein Kinase CK2. Oxford, UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118482490.

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Li, Rongshi, i Jeffrey A. Stafford, red. Kinase Inhibitor Drugs. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2009. http://dx.doi.org/10.1002/9780470524961.

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Tan, Aik-Choon, i Paul H. Huang, red. Kinase Signaling Networks. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7154-1.

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Części książek na temat "Kinase"

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Cuevas, Bruce D. "Mitogen-Activated Protein Kinase Kinase Kinases". W Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7192-1.

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Cuevas, Bruce D. "Mitogen-Activated Protein Kinase Kinase Kinases". W Encyclopedia of Cancer, 2872–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_7192.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "MKKK (MAP Kinase Kinase Kinase)". W Encyclopedia of Signaling Molecules, 1089. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100826.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "Mitogen-Activated Protein Kinase Kinase Kinase Kinase 1". W Encyclopedia of Signaling Molecules, 1082. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100818.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "Mitogen-Activated Protein Kinase Kinase Kinase 11". W Encyclopedia of Signaling Molecules, 1081. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100814.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "Mitogen-Activated Protein Kinase Kinase Kinase 12". W Encyclopedia of Signaling Molecules, 1081. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100816.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "Mitogen-Activated Protein Kinase Kinase Kinase 8". W Encyclopedia of Signaling Molecules, 1081. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100817.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "MAP Kinase Kinase 3". W Encyclopedia of Signaling Molecules, 1042. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100744.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "MAP Kinase Upstream Kinase". W Encyclopedia of Signaling Molecules, 1042. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100745.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda i in. "MKK (MAP Kinase Kinase)". W Encyclopedia of Signaling Molecules, 1085. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100822.

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Streszczenia konferencji na temat "Kinase"

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Brown, R. D., S. K. Ambler, Timothy P. Garrington, Carlin S. Long i Kurt R. Stenmark. "MAP Kinase Kinase Kinase-2 (MEKK2) Regulates Hypertrophic Remodeling Of Right Ventricle In Hypoxia-Induced Pulmonary Hypertension". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6590.

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Shelton, Abby, Erin Smithberger, Madison Butler, Alex Flores, Ryan Bash, Steve Angus, Noah Sciaky i in. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-331.

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Shelton, Abby, Erin Smithberger, Madison Butler, Alex Flores, Ryan Bash, Steve Angus, Noah Sciaky i in. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-331.

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Huber-Keener, Kathryn J., Brad R. Evans i Jin-Ming Yang. "Abstract 2071: Regulation of EF-2 kinase stability by the mTOR/S6 kinase- and AMP kinase-mediated phosphorylation in human glioma cells". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2071.

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Coppé, Jean-Philippe F., Zhongzhong Chen, Aaron Boudreau, Neil Park, Zidar Xu, Joe Gray, Logan Liu i Laura van ‘t Veer. "Abstract 4790: Mapping the oncogenic kinome using a kinase activity screening array". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4790.

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Ayati, Marzieh, Serhan Yilmaz, Filipa Blasco Tavares Pereira Lopes, Mark Chance i Mehmet Koyuturk. "Prediction of Kinase-Substrate Associations Using The Functional Landscape of Kinases and Phosphorylation Sites". W Pacific Symposium on Biocomputing 2023. WORLD SCIENTIFIC, 2022. http://dx.doi.org/10.1142/9789811270611_0008.

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Van Calenbergh, Serge, Ineke Van Daele, Sara Van Poecke, Matheus Froeyen, Hélene Munier Lehmann i Jan Balzarini. "From M. tuberculosis thymidine monophosphate kinase (TMPKmt) inhibitors towards mitochondrial thymidine kinase (TK-2) inhibitors". W XIVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2008. http://dx.doi.org/10.1135/css200810087.

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Riddle, Steven, Connie Lebakken, Jason Ellefson, Laurie Reichling i Jill Wolken. "Abstract 3688: A flexible kinase inhibitor assay for active, non-activated, and impure kinase preparations". W 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.am10-3688.

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Lebakken, Connie S., Laurie Reichling, Jason Ellefson, Kun Bi i Steven M. Riddle. "Abstract C95: A flexible kinase inhibitor assay platform for active, nonactivated, and impure kinase preparations." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c95.

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Luo, Ming, Max S. Wicha i Jun-Lin Guan. "Abstract 1627: Kinase-independent function of focal adhesion kinase in lung metastasis of breast cancer". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1627.

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Raporty organizacyjne na temat "Kinase"

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Balajee, A. S., J. A. Meador i Y. Su. Cellular response to low dose radiation: Role of phosphatidylinositol-3 kinase like kinases. Office of Scientific and Technical Information (OSTI), marzec 2011. http://dx.doi.org/10.2172/1009811.

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Parker, Amanda P., Barbara S. Beckman i Matthew Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2002. http://dx.doi.org/10.21236/ada409382.

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Parker, Amanda, Barbara Beckman i Matthew E. Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada431891.

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Weier, Heinz-Ulrich. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada423672.

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Weier, Heinz U. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2000. http://dx.doi.org/10.21236/ada391061.

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Konisky, J. Structural Studies of Archaealthermophilic Adenylate Kinase. Office of Scientific and Technical Information (OSTI), lipiec 2002. http://dx.doi.org/10.2172/761906.

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Kraft, Andrew S. Overcoming Resistance to Inhibitors of the AKT Protein Kinase by Modulation of the Pim Kinase Pathway. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada597882.

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Kraft, Andrew S. Overcoming Resistance to Inhibitors of the Akt Protein Kinase by Modulation of the Pim Kinase Pathway. Fort Belvoir, VA: Defense Technical Information Center, październik 2014. http://dx.doi.org/10.21236/ada615425.

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Balk, Steven P. Identification and Targeting of Upstream Tyrosine Kinases Mediating PI3 Kinase Activation in PTEN Deficient Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2010. http://dx.doi.org/10.21236/ada535588.

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Balk, Steven P. Identification and Targeting of Upstream Tyrosine Kinases Mediating PI3 Kinase Activation in PTEN-Deficient Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2009. http://dx.doi.org/10.21236/ada510490.

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