Gotowe bibliografie tematyczne / Kinases

Gotowa bibliografia na temat „Kinases”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 18 maja 2024

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Artykuły w czasopismach na temat "Kinases"

1

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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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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Songyang, Z., K. P. Lu, Y. T. Kwon, L. H. Tsai, O. Filhol, C. Cochet, D. A. Brickey i in. "A structural basis for substrate specificities of protein Ser/Thr kinases: primary sequence preference of casein kinases I and II, NIMA, phosphorylase kinase, calmodulin-dependent kinase II, CDK5, and Erk1." Molecular and Cellular Biology 16, nr 11 (listopad 1996): 6486–93. http://dx.doi.org/10.1128/mcb.16.11.6486.

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We have developed a method to study the primary sequence specificities of protein kinases by using an oriented degenerate peptide library. We report here the substrate specificities of eight protein Ser/Thr kinases. All of the kinases studied selected distinct optimal substrates. The identified substrate specificities of these kinases, together with known crystal structures of protein kinase A, CDK2, Erk2, twitchin, and casein kinase I, provide a structural basis for the substrate recognition of protein Ser/Thr kinases. In particular, the specific selection of amino acids at the +1 and -3 positions to the substrate serine/threonine can be rationalized on the basis of sequences of protein kinases. The identification of optimal peptide substrates of CDK5, casein kinases I and II, NIMA, calmodulin-dependent kinases, Erk1, and phosphorylase kinase makes it possible to predict the potential in vivo targets of these kinases.
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Moens, Ugo, i Sergiy Kostenko. "Structure and function of MK5/PRAK: the loner among the mitogen-activated protein kinase-activated protein kinases". Biological Chemistry 394, nr 9 (1.09.2013): 1115–32. http://dx.doi.org/10.1515/hsz-2013-0149.

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Abstract Mitogen-activated protein kinase (MAPK) pathways are important signal transduction pathways that control pivotal cellular processes including proliferation, differentiation, survival, apoptosis, gene regulation, and motility. MAPK pathways consist of a relay of consecutive phosphorylation events exerted by MAPK kinase kinases, MAPK kinases, and MAPKs. Conventional MAPKs are characterized by a conserved Thr-X-Tyr motif in the activation loop of the kinase domain, while atypical MAPKs lack this motif and do not seem to be organized into the classical three-tiered kinase cascade. One functional group of conventional and atypical MAPK substrates consists of protein kinases known as MAPK-activated protein kinases. Eleven mammalian MAPK-activated protein kinases have been identified, and they are divided into five subgroups: the ribosomal-S6-kinases RSK1-4, the MAPK-interacting kinases MNK1 and 2, the mitogen- and stress-activated kinases MSK1 and 2, the MAPK-activated protein kinases MK2 and 3, and the MAPK-activated protein kinase MK5 (also referred to as PRAK). MK5/PRAK is the only MAPK-activated protein kinase that is a substrate for both conventional and atypical MAPK, while all other MAPKAPKs are exclusively phosphorylated by conventional MAPKs. This review focuses on the structure, activation, substrates, functions, and possible implications of MK5/PRAK in malignant and nonmalignant diseases.
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LANG, Mark L., Yih-Wen CHEN, Li SHEN, Hong GAO, Gillian A. LANG, Terri K. WADE i William F. WADE. "IgA Fc receptor (FcαR) cross-linking recruits tyrosine kinases, phosphoinositide kinases and serine/threonine kinases to glycolipid rafts". Biochemical Journal 364, nr 2 (1.06.2002): 517–25. http://dx.doi.org/10.1042/bj20011696.

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The human IgA Fc receptor (FcαR, CD89) triggers several important physiological functions, including phagocytosis, NADPH oxidase activation and antigen presentation. Efforts are underway to delineate FcαR signal-transduction pathways that control these functions. In a previous study, we demonstrated that cross-linking of FcαR increased its partitioning into membrane glycolipid rafts and was accompanied by γ-chain-dependent recruitment and phosphorylation of the tyrosine kinases Lck/Yes-related novel protein tyrosine kinase (Lyn) and Bruton's tyrosine kinase (Btk). Here we have performed a more extensive characterization of signalling effectors recruited to rafts on FcαR cross-linking. We demonstrate that in addition to tyrosine kinases Lyn and Btk, FcαR cross-linking also recruits B-lymphocyte kinase (Blk) and spleen tyrosine kinase (Syk) to rafts. We show recruitment of phosphoinositide kinases, including 3-phosphoinositide 3-kinase and phospholipase Cγ2, and serine/threonine kinases such as protein kinase C (PKC) α, PKC∊, and protein kinase B (PKB) α. This suggests that lipid rafts serve as sites for FcαR-triggered recruitment of multiple classes of signalling effectors. We further demonstrate that tyrosine kinases and PKCα have a sustained association with rafts, whereas phosphoinositide 3-kinase and its downstream effectors have a transient association with rafts. This is consistent with temporally regulated divergence of FcαR signalling pathways in rafts. Furthermore, we suggest the spatial separation of signalling effectors by transport of phosphoinositide 3-kinase, phosphoinositide-dependent kinase 1, PKBα and PKC∊ to endocytic compartments containing internalized FcαR.
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Ibrahim, Samar H., Petra Hirsova, Harmeet Malhi i Gregory J. Gores. "Nonalcoholic Steatohepatitis Promoting Kinases". Seminars in Liver Disease 40, nr 04 (11.06.2020): 346–57. http://dx.doi.org/10.1055/s-0040-1713115.

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AbstractNonalcoholic hepatitis (NASH) is the progressive inflammatory form of nonalcoholic fatty liver disease. Although the mechanisms of hepatic inflammation in NASH remain incompletely understood, emerging literature implicates the proinflammatory environment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. Interestingly, numerous NASH-promoting kinases in hepatocytes, immune cells, and adipocytes are activated by the lipotoxic insult associated with obesity. In the current review, we discuss recent advances in NASH-promoting kinases as disease mediators and therapeutic targets. The focus of the review is mainly on the mitogen-activated protein kinases including mixed lineage kinase 3, apoptosis signal-regulating kinase 1, c-Jun N-terminal kinase, and p38 MAPK; the endoplasmic reticulum (ER) stress kinases protein kinase RNA-like ER kinase and inositol-requiring protein-1α; as well as the Rho-associated protein kinase 1. We also discuss various pharmacological agents targeting these stress kinases in NASH that are under different phases of development.
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Atkinson, Eleanor L., Jessica Iegre, Paul D. Brear, Elizabeth A. Zhabina, Marko Hyvönen i David R. Spring. "Downfalls of Chemical Probes Acting at the Kinase ATP-Site: CK2 as a Case Study". Molecules 26, nr 7 (31.03.2021): 1977. http://dx.doi.org/10.3390/molecules26071977.

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Protein kinases are a large class of enzymes with numerous biological roles and many have been implicated in a vast array of diseases, including cancer and the novel coronavirus infection COVID-19. Thus, the development of chemical probes to selectively target each kinase is of great interest. Inhibition of protein kinases with ATP-competitive inhibitors has historically been the most widely used method. However, due to the highly conserved structures of ATP-sites, the identification of truly selective chemical probes is challenging. In this review, we use the Ser/Thr kinase CK2 as an example to highlight the historical challenges in effective and selective chemical probe development, alongside recent advances in the field and alternative strategies aiming to overcome these problems. The methods utilised for CK2 can be applied to an array of protein kinases to aid in the discovery of chemical probes to further understand each kinase’s biology, with wide-reaching implications for drug development.
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Grishin, Andrey, Maia Cherney, Tara Condos, Kathryn Barber, Deborah Anderson, Sadhna Phanse, Mohan Babu, Gary Shaw i Miroslaw Cygler. "Bacterial Effector Kinases". Acta Crystallographica Section A Foundations and Advances 70, a1 (5.08.2014): C428. http://dx.doi.org/10.1107/s2053273314095710.

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Protein phosphorylation is one of the main signaling mechanisms in eukaryotic cells. Not surprisingly, pathogenic adopted this mechanism to interfere with signaling processes in the host cell. To this end pathogens evolved kinases that, in addition to other bacterial effector proteins, are injected into the host cell via a syringe-like type 3 (T3SS) or type 4 (T4SS) secretion systems. Kinases NleH1 and NleH2 from pathogenic E. coli, OspG from Shigella, SteC and SboH from Salmonella, LegK1-4 from Legionella and YspK and YpkA from Yersinia represent currently known effector kinases. Some of these kinases were likely derived from eukaryotes via horizontal gene transfer (SteC, LegK1-4, YpkA). Other kinases (NleH, OspG, SboH and YspK) have been so far identified only in the pathogenic bacteria. The structures of NleH and OspG proved that these kinases, which are half the size of an average human kinase, contain only a core kinase fold. These kinases lack the main regulatory element – the activation loop. The structure of NleH suggests that it has no activation mechanism since the apo-kinase domain adopts an active conformation and no change is observed on nucleotide binding. The OspG kinase, which also contains only the core kinase fold, is stimulated by its binding partner, the ubiquitin-conjugating enzyme E2-ubiquitin complex. The structure of OspG:UbcH7-Ub complex shows that OspG binds the E2 and ubiquitin (Ub) at two distinct sites on its surface. In this complex the OspG active site is unobstructed and primed for catalysis. However the mechanism of OspG activation remains presently unknown. Both NleH and OspG were found to inhibit the NF-kB pathway, however the substrates forOspG and NleH kinase activities are not yet known.
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Yamboliev, Ilia A., Kevin M. Wiesmann, Cherie A. Singer, Jason C. Hedges i William T. Gerthoffer. "Phosphatidylinositol 3-kinases regulate ERK and p38 MAP kinases in canine colonic smooth muscle". American Journal of Physiology-Cell Physiology 279, nr 2 (1.08.2000): C352—C360. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c352.

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In canine colon, M2/M3 muscarinic receptors are coupled to extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinases. We tested the hypothesis that this coupling is mediated by enzymes of the phosphatidylinositol (PI) 3-kinase family. RT-PCR and Western blotting demonstrated expression of two isoforms, PI 3-kinase-α and PI 3-kinase-γ. Muscarinic stimulation of intact muscle strips (10 μM ACh) activated PI 3-kinase-γ, ERK and p38 MAP kinases, and MAP kinase-activated protein kinase-2, whereas PI 3-kinase-α activation was not detected. Wortmannin (25 μM) abolished the activation of PI 3-kinase-γ, ERK, and p38 MAP kinases. MAP kinase inhibition was a PI 3-kinase-γ-specific effect, since wortmannin did not inhibit recombinant activated murine ERK2 MAP kinase, protein kinase C, Raf-1, or MAP kinase kinase. In cultured muscle cells, newborn calf serum (3%) activated PI 3-kinase-α and PI 3-kinase-γ isoforms, ERK and p38 MAP kinases, and stimulated chemotactic cell migration. Using wortmannin and LY-294002 to inhibit PI 3-kinase activity and PD-098059 and SB-203580 to inhibit ERK and p38 MAP kinases, we established that these enzymes are functionally important for regulation of chemotactic migration of colonic myocytes.
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Sclafani, Robert A. "Cyclin dependent kinase activating kinases". Current Opinion in Cell Biology 8, nr 6 (grudzień 1996): 788–94. http://dx.doi.org/10.1016/s0955-0674(96)80079-2.

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Rozprawy doktorskie na temat "Kinases"

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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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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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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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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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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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Gravel, Mathieu. "Rôle du gène Mek1 dans la différenciation des trophoblastes souches et lors du développement embryonnaire". Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25697/25697.pdf.

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Waskiewicz, Andrew Jan. "Mitogen-activated protein kinase : evolutionary conservation and activation of downstream kinases /". Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/9216.

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Simard-Bisson, Carolyne. "Rôles de la "Dual leucine zipper-bearing Kinase" dans la réorganisation des microtubules et la différenciation des kératinocytes humains". Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/28201.

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La fonction barrière de la peau dépend en grande partie d’une différenciation appropriée des kératinocytes épidermiques. Au cours de ce processus, de nombreux changements ont lieu dans ces cellules tels que la diminution de la prolifération, le remodelage du cytosquelette, des changements dans l’expression génique, la dégradation du noyau et des organites de même que la formation d’une structure bien particulière : l’enveloppe cornée. Il est important que de tels évènements soient régulés de façon adéquate puisqu’un débalancement au sein de ces derniers peut mener à l’apparition de conditions pathologiques. La Dual Leucine zipper-bearing Kinase (DLK) est une Mitogen-Activated Protein Kinase Kinase Kinase dont l’expression est très forte au niveau de la couche granuleuse, soit la dernière couche de cellules vivantes avant la couche cornée de l’épiderme. Des études précédentes ont révélé que la surexpression de la DLK dans des kératinocytes en culture avait pour effet d’induire la différenciation terminale. Toutefois, les mécanismes par lesquels la DLK régule ce processus restent encore méconnus faisant en sorte que l’objectif général de cette thèse consiste à mieux les définir. L’hypothèse à la base de ces travaux est que la DLK est requise pour la différenciation des kératinocytes et que celle-ci y participe en favorisant la stabilisation des microtubules de même que l’expression ou l’activité de facteurs de transcription impliqués dans ce processus. Dans un premier temps, un modèle de peau reconstruite in vitro dans lequel l’expression de la DLK a été réduite par interférence à l’ARN a été développé. Il a été noté que la diminution de la DLK avait pour effets d’affecter la distribution de protéines de l’enveloppe cornée telles que la filaggrine et la transglutaminase 1 de même que d’inhiber la formation des couches granuleuse et cornée. Des analyses en immunofluorescence et en microscopie électronique ont permis d’observer des défauts au niveau des jonctions serrées et des desmosomes dans les peaux sous-exprimant la DLK révélant un rôle de cette kinase dans le bon maintien de ces deux types de jonctions cellulaires. L’impact de la DLK sur les microtubules a été étudié dans des kératinocytes en culture transduits à l’aide de vecteurs adénoviraux menant à la surexpression de la DLK de même que dans les peaux reconstruites présentant une expression réduite de cette kinase. Ces études ont permis de conclure que la DLK était non seulement en mesure d’induire la réorganisation et la stabilisation des microtubules en périphérie cellulaire, mais que celle-ci était également requise à la réalisation de ces processus. Afin de mieux décrire les mécanismes par lesquels la DLK assure la réorganisation des microtubules en périphérie cellulaire, les effets de la surexpression ou de la sous-expression de la DLK sur les protéines LIS1 et HSP27 (pour Heat shock protein 27 kDa), des régulateurs de la distribution des microtubules, ont été étudiés. Ces analyses ont permis de définir la DLK en tant qu’élément nécessaire à la bonne distribution en périphérie cellulaire de LIS1 et HSP27. Des études plus poussées ont révélé que l’expression de la DLK dans des kératinocytes en culture était non seulement en mesure d’induire la redistribution en périphérie cellulaire d’HSP27, mais également l’insolubilisation et la phosphorylation de cette protéine de choc thermique. Il a également été démontré que l’ensemble de ces processus dépendaient de l’activité de ERK (pour Extracellular-signal Regulated Kinase). Dans le but de définir l’importance des microtubules dans le processus de différenciation des kératinocytes, des peaux reconstruites ont été traitées avec un agent induisant la dépolymérisation de cette composante cytosquelettique soit plus précisément le nocodazole. Un tel traitement produit un phénotype similaire à celui des peaux reconstruites sous-exprimant la DLK suggérant les microtubules comme d’importants effecteurs de la différenciation induite par la DLK. Dans la perspective de mieux définir les effets de la DLK sur la signalisation cellulaire et l’expression génique globale, nous avons eu recours à l’étude de la phosphorylation d’importants médiateurs de la signalisation moléculaire intracellulaire de même qu’à des analyses en micropuce à ADN d’échantillons provenant de peaux reconstruites sous-exprimant la DLK. Cette démarche a permis de révéler une hausse de la phosphorylation de ERK1/2, de JNK1/2/3, de GSK3 (pour Glycogene Synthase Kinase 1) et du récepteur à l’EGF (pour Epidermal Growth Factor). Les analyses en micropuce à ADN ont permis de révéler une réduction dans l’expression de nombreux gènes impliqués dans la formation de l’enveloppe cornée. Finalement, la réduction de c-Jun et de C/EBPα a pu être observée dans les noyaux de peaux reconstruites sous-exprimant la DLK révélant ainsi l’importance de cette kinase dans la régulation de ces facteurs de transcription dans un contexte de différenciation des kératinocytes. Globalement, nos travaux montrent que la DLK est requise pour la différenciation des kératinocytes et que celle-ci y contribue en assurant la réorganisation des microtubules en périphérie cellulaire, la consolidation des desmosomes et des jonctions serrées de même la régulation positive des facteurs c-Jun et C/EBPα.
Skin barrier function greatly depends on proper keratinocyte differentiation in the epidermis. During this process, many changes occur within the cell such as decrease in cell proliferation, cytoskeleton reorganization, changes in gene expression, nucleus and organelles elimination as well as cornified envelope formation. Keratinocyte differentiation must be finely orchestrated since misregulation of this process may lead to pathological conditions. The Dual Leucine zipper-bearing Kinase (DLK) is a Mitogen-Activated Protein Kinase Kinase Kinase showing a strong expression in the granular layer, the last layer composed of living cells before reaching the cornified layer. Previous studies revealed DLK capacity to induce keratinocyte terminal differentiation process. However, how DLK promotes such an event remains unknown. The main objective of this thesis is to identify mechanisms and potential effectors of the DLK-induced keratinocyte differentiation. Our hypothesis is that DLK is required for keratinocyte differentiation by promoting microtubule stabilization as well as the expression or the activity of transcription factors involved in this process. In order to test our hypothesis, a tissue-engineered skin (TES) model with a reduced DLK expression was produced using a RNA interference approach. Impaired distribution of cornified envelope proteins such as filaggrin and transglutaminase 1 as well as reduced granular and cornified layers were observed in TES with reduced DLK expression. In those samples, immunofluorescence and electron microscopy analyses pointed out desmosomal and tight junctional defects suggesting a role for DLK in the maintenance of these types of cell junctions. The impact of DLK expression on microtubules was also studied in TES with reduced DLK expression and in keratinocytes in culture overexpressing DLK following gene transduction using adenoviral vectors. These studies led to the conclusion that DLK not only promotes but is also required for microtubules reorganization and stabilization to cell periphery. To explain DLK capacity to induce such a process, effects of DLK depletion or overexpression on microtubule regulators such as LIS1 and HSP27 were investigated by immunofluorescence staining. These analyses revealed that DLK induces and is required for LIS1 and HSP27 relocalization to cell periphery. In additional studies, our results show that DLK expression in normal human keratinocytes in culture not only promotes HSP27 distribution to cell periphery but also induces HSP27 insolubilization and phosphorylation in an ERK-dependent manner. In order to more precisely define the role of microtubules in keratinocyte differentiation process, TES were treated with nocodazole, a microtubule depolymerizing agent. The effect of such a treatment was to reproduce the phenotype of DLK-depleted TES suggesting that microtubules are important effectors of DLK-induced keratinocyte differentiation. In an attempt to describe the impact of DLK on global gene expression, RNA samples of DLK-depleted TES were studied using microarray analyses. This approach revealed a reduction in the expression of many genes coding for cornified envelope proteins. Reductions of c-Jun and C/EBPα immunofluorescence staining were also noted in TES with a reduced DLK expression suggesting this kinase as a c-Jun and C/EBPα regulator in the context of keratinocyte differentiation. Globally, our works show that DLK is required for keratinocyte differentiation since it promotes microtubule reorganization to cell periphery, desmosomes and tight junction consolidation as well as c-Jun and C/EBPα localization to the nucleus.
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Guillemette, Stéphanie. "La contribution de Mek2 dans le développement du placenta murin". Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24208/24208.pdf.

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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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Książki na temat "Kinases"

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Francesc, Posas, i Nebreda Angel R, red. Stress-activated protein kinases. New York: Springer, 2008.

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Dissmeyer, Nico, i Arp Schnittger, red. Plant Kinases. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-264-9.

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Xavier, Gabriela Da Silva. Protein kinases. Rijeka: InTech, 2012.

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E, Stefanov Vassili, red. Phosphagen kinases. Boca Raton [Fla.]: CRC Press, 1991.

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1953-, Lester David S., i Epand Richard M. 1937-, red. Protein kinase C: Current concepts and future perspectives. New York: Ellis Horwood, 1992.

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M, Kreis, i Walker J. C, red. Plant protein kinases. San Diego: Academic Press, 2000.

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Fabbro, Doriano, i Frank McCormick, red. Protein Tyrosine Kinases. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1592599621.

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Aalen, Reidunn Birgitta, red. Plant Receptor Kinases. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7063-6.

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Germano, Serena, red. Receptor Tyrosine Kinases. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1789-1.

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Komis, George, i Jozef Šamaj, red. Plant MAP Kinases. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0922-3.

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Części książek na temat "Kinases"

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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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Reboutier, David, i Claude Prigent. "Aurora Kinases". W Encyclopedia of Signaling Molecules, 483–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_81.

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He, Lili, i Jin Q. Cheng. "Aurora Kinases". W Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_465-2.

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Wong, Alice. "Protein Kinases". W Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6621-3.

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Goldberg, Daniel E., Min Zhang i Victor Nussenzweig. "PlasmodiumeIF2α Kinases". W Protein Phosphorylation in Parasites, 123–30. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527675401.ch06.

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Belyi, Yuri F. "Protein Kinases". W Intracellular Parasitism of Microorganisms, 75–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22047-4_8.

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Reboutier, David, i Claude Prigent. "Aurora Kinases". W Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_81-1.

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Malumbres, Marcos. "Mitotic Kinases". W Encyclopedia of Systems Biology, 1382–86. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_11.

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Plevani, Paolo. "Protein Kinases". W Encyclopedia of Systems Biology, 1778. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_722.

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Streszczenia konferencji na temat "Kinases"

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Zorina, A. A. "Protein kinases in cyanobacteria". W IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-182.

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Wu, W. H., V. Geraldine, V. Nadeau, E. Tremblay, V. Toro, J. Omura, M. Orcholski i in. "Checkpoint Kinases Mediate Lung Fibrogenesis". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3653.

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Beljkas, Milan, Jelena Rebić, Milica Radan, Teodora Đikić, Slavica Oljačić i Katarina Nikolic. "3D-Quantitative Structure-Activity Relationship and design of novel Rho-associated protein kinases-1 (ROCK1) inhibitors". W 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.584b.

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Rho-associated coiled-coil kinases (ROCKs) are involved in essential cellular functions such as adhesion, contraction, motility, proliferation, and cell survival/apoptosis. Four ROCK inhibitors have already been approved by the FDA and are used to treat glaucoma (ripasudil and netarsudil), cerebral vasospasm (fasudil), and graft-versus-host disease (belumosudil). Recent studies have focused on exploring the role of ROCK kinase inhibitors in cancer treatment and the development of new ROCK inhibitors. The main objective of this study was to identify critical structural features relevant to the inhibition of ROCK1 using a ligand-based 3D-QSAR (3D quantitative structure-activity relationship) method. The 3D-QSAR model for ROCK1 was created and validated using internal and external validation parameters (R2, Q2, R2pred, rm 2, r/2m, rm̅̅2̅ and ∆r2m). The main structural features that correlate with the inhibition of ROCK1 were identified (e.g., heterocycle with hydrogen donor group like nitrogen atom) and further structural modifications of the ROCK1 inhibitors that contribute to increased activity were proposed (removal of the amino group of the oxadiazole, modification of the substituents of the phenyl ring).
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Bußmann, L., A. Münscher, K. Rothkamm i K. Hoffer. "Kinom profiling of tyrosine kinases identifies Src-family kinases to be highly activated in HNSCC". W Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1639995.

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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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Nickkholgh, Bita, Sivanandane Sittadjody, Michael B. Rothberg i KC Balaji. "Abstract LB-243: Protein kinase D1 induces cell cycle arrest independent from check point kinases". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-243.

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Henzler, Tanja, Stefanie Pohl, Nicole Schneiderhan-Mara, Stefanie Rimmele, April Livengood, Robert Kovelman i Thomas Herget. "Abstract LB-227: Receptor tyrosine kinase phosphorylation: Simultaneous detection of 10 kinases upon inhibitor treatment". 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-lb-227.

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Nomanbhoy, Tyzoon K., Heidi E. Brown, Jiangyue Wu, Subha Vogeti, Arwin Aban, Wendy Grant, Alemayehu Senait, Shuzhen Wu, Christa Dias i Geeta Sharma. "Abstract B23: Chemoproteomic profiling of native kinases during the treatment of cells with kinase inhibitors". W Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-b23.

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Mueller, Daniel, Frank Totzke, Thomas Weber, Marcel Pathe, Christoph Schaechtele i Michael H. Kubbutat. "Abstract 2388: IC50 profiling against 320 protein kinases: Improving the accuracy of kinase inhibitor selectivity testing". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2388.

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LeDuc, Philip R. "Dynamic Formation for the Mechanical Connection of Focal Adhesion Complexes to Study Localized Mechanisms of Angiogenesis Through Modeling With Cellular Automata". W ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23159.

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Abstract The mechanical connection through the formation of focal adhesion complexes (FACs) is critical in cell growth and apoptosis. The FACs act between the cells and the extracellular matrix (ECM), which in turn influences angiogenesis, the growth of new capillary blood vessels [1]. These complexes form direct connections from ECM into the cell cytoskeleton through a series of protein binding events. This linkage is critical for mechanical force sensing and mechanotransduction signaling [2]. Here, the probabilistic modeling of this complex formation is undertaken to begin to uncover the effect of the spatial distribution and temporal effects on this dynamic process. In this, the rich dynamic process of the FACs formation through the binding events of integrin, paxillin, talin, and vinculin are examined. The FACs are mediated through the clustering of transmembrane integrins, which initiate the binding cascade. This interaction has been shown to be a critical event in the activation of the mechanochemical cascade and further mediates downstream signaling of protein tyrosine kinases including focal adhesion kinase [3].
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Raporty organizacyjne na temat "Kinases"

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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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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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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 2011. http://dx.doi.org/10.21236/ada550805.

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Chernoff, Jonathan. Identification of Protein Kinases Required for NF2 Signaling. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2007. http://dx.doi.org/10.21236/ada494392.

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Kyriakis, John M. The Role of HAP Kinases in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1995. http://dx.doi.org/10.21236/ada300037.

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Chernoff, Jonathan. Identification of Protein Kinases Required for NF2 Signaling. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2006. http://dx.doi.org/10.21236/ada465844.

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Edwards, David. Molecular Recognition of Endocytic Codes in Receptor Tyrosine Kinases. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1999. http://dx.doi.org/10.21236/ada375148.

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Beumr, Paul. The Role of KSR-Associated Kinases in Breast Cancer Signaling. Fort Belvoir, VA: Defense Technical Information Center, luty 2002. http://dx.doi.org/10.21236/ada401105.

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Schreiner, Steven J., i Robert E. Lewis. The Role of KSR-Associated Kinases in Breast Cancer Signaling. Fort Belvoir, VA: Defense Technical Information Center, luty 2003. http://dx.doi.org/10.21236/ada413743.

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