Готові списки джерел за темами / KIT tyrosine kinase

Добірка наукової літератури з теми "KIT tyrosine kinase"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "KIT tyrosine kinase"

1

Heinrich, Michael C., Diana J. Griffith, Brian J. Druker, Cecily L. Wait, Kristen A. Ott, and Amy J. Zigler. "Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor." Blood 96, no. 3 (August 1, 2000): 925–32. http://dx.doi.org/10.1182/blood.v96.3.925.

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Abstract STI 571 (formerly known as CGP 57148B) is a known inhibitor of the c-abl, bcr-abl, and platelet-derived growth-factor receptor (PDGFR) tyrosine kinases. This compound is being evaluated in clinical trials for the treatment of chronic myelogenous leukemia. We sought to extend the activity profile of STI 571 by testing its ability to inhibit the tyrosine kinase activity of c-kit, a receptor structurally similar to PDGFR. We treated a c-kit expressing a human myeloid leukemia cell line, M-07e, with STI 571 before stimulation with Steel factor (SLF). STI 571 inhibited c-kit autophosphorylation, activation of mitogen-activated protein (MAP) kinase, and activation of Akt without altering total protein levels of c-kit, MAP kinase, or Akt. The concentration that produced 50% inhibition for these effects was approximately 100 nmol/L. STI 571 also significantly decreased SLF-dependent growth of M-07e cells in a dose-dependent manner and blocked the antiapoptotic activity of SLF. In contrast, the compound had no effect on MAP kinase activation or cellular proliferation in response to granulocyte-macrophage colony-stimulating factor. We also tested the activity of STI 571 in a human mast cell leukemia cell line (HMC-1), which has an activated mutant form of c-kit. STI 571 had a more potent inhibitory effect on the kinase activity of this mutant receptor than it did on ligand-dependent activation of the wild-type receptor. These findings show that STI 571 selectively inhibits c-kit tyrosine kinase activity and downstream activation of target proteins involved in cellular proliferation and survival. This compound may be useful in treating cancers associated with increased c-kit kinase activity.
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2

Heinrich, Michael C., Diana J. Griffith, Brian J. Druker, Cecily L. Wait, Kristen A. Ott, and Amy J. Zigler. "Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor." Blood 96, no. 3 (August 1, 2000): 925–32. http://dx.doi.org/10.1182/blood.v96.3.925.015k50_925_932.

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Анотація:
STI 571 (formerly known as CGP 57148B) is a known inhibitor of the c-abl, bcr-abl, and platelet-derived growth-factor receptor (PDGFR) tyrosine kinases. This compound is being evaluated in clinical trials for the treatment of chronic myelogenous leukemia. We sought to extend the activity profile of STI 571 by testing its ability to inhibit the tyrosine kinase activity of c-kit, a receptor structurally similar to PDGFR. We treated a c-kit expressing a human myeloid leukemia cell line, M-07e, with STI 571 before stimulation with Steel factor (SLF). STI 571 inhibited c-kit autophosphorylation, activation of mitogen-activated protein (MAP) kinase, and activation of Akt without altering total protein levels of c-kit, MAP kinase, or Akt. The concentration that produced 50% inhibition for these effects was approximately 100 nmol/L. STI 571 also significantly decreased SLF-dependent growth of M-07e cells in a dose-dependent manner and blocked the antiapoptotic activity of SLF. In contrast, the compound had no effect on MAP kinase activation or cellular proliferation in response to granulocyte-macrophage colony-stimulating factor. We also tested the activity of STI 571 in a human mast cell leukemia cell line (HMC-1), which has an activated mutant form of c-kit. STI 571 had a more potent inhibitory effect on the kinase activity of this mutant receptor than it did on ligand-dependent activation of the wild-type receptor. These findings show that STI 571 selectively inhibits c-kit tyrosine kinase activity and downstream activation of target proteins involved in cellular proliferation and survival. This compound may be useful in treating cancers associated with increased c-kit kinase activity.
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3

Ledoux, Julie, and Luba Tchertanov. "Does Generic Cyclic Kinase Insert Domain of Receptor Tyrosine Kinase KIT Clone Its Native Homologue?" International Journal of Molecular Sciences 23, no. 21 (October 25, 2022): 12898. http://dx.doi.org/10.3390/ijms232112898.

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Receptor tyrosine kinases (RTKs) are modular membrane proteins possessing both well-folded and disordered domains acting together in ligand-induced activation and regulation of post-transduction processes that tightly couple extracellular and cytoplasmic events. They ensure the fine-turning control of signal transmission by signal transduction. Deregulation of RTK KIT, including overexpression and gain of function mutations, has been detected in several human cancers. In this paper, we analysed by in silico techniques the Kinase Insert Domain (KID), a key platform of KIT transduction processes, as a generic macrocycle (KIDGC), a cleaved isolated polypeptide (KIDC), and a natively fused TKD domain (KIDD). We assumed that these KID species have similar structural and dynamic characteristics indicating the intrinsically disordered nature of this domain. This finding means that both polypeptides, cyclic KIDGC and linear KIDC, are valid models of KID integrated into the RTK KIT and will be helpful for further computational and empirical studies of post-transduction KIT events.
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4

Marmigère, Frédéric, Frédérique Scamps, and Jean Valmier. "Le récepteur tyrosine kinase c-Kit." médecine/sciences 24, no. 5 (May 2008): 464–66. http://dx.doi.org/10.1051/medsci/2008245464.

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5

Bandi, Srinivasa Rao, Christian Brandts, Marion Rensinghoff, Rebekka Grundler, Lara Tickenbrock, Gabriele Köhler, Justus Duyster, et al. "E3 ligase–defective Cbl mutants lead to a generalized mastocytosis and myeloproliferative disease." Blood 114, no. 19 (November 5, 2009): 4197–208. http://dx.doi.org/10.1182/blood-2008-12-190934.

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Abstract Somatic mutations of Kit have been found in leukemias and gastrointestinal stromal tumors. The proto-oncogene c-Cbl negatively regulates Kit and Flt3 by its E3 ligase activity and acts as a scaffold. We recently identified the first c-Cbl mutation in human disease in an acute myeloid leukemia patient, called Cbl-R420Q. Here we analyzed the role of Cbl mutants on Kit-mediated transformation. Coexpression of Cbl-R420Q or Cbl-70Z with Kit induced cytokine-independent proliferation, survival, and clonogenic growth. Primary murine bone marrow retrovirally transduced with c-Cbl mutants and transplanted into mice led to a generalized mastocytosis, a myeloproliferative disease, and myeloid leukemia. Overexpression of these Cbl mutants inhibited stem cell factor (SCF)–induced ubiquitination and internalization of Kit. Both Cbl mutants enhanced the basal activation of Akt and prolonged the ligand-dependent activation. Importantly, transformation was observed also with kinase-dead forms of Kit and Flt3 in the presence of Cbl-70Z, but not in the absence of Kit or Flt3, suggesting a mechanism dependent on receptor tyrosine kinases, but independent of their kinase activity. Instead, transformation depends on the Src family kinase Fyn, as c-Cbl coimmunoprecipitated with Fyn and inhibition abolished transformation. These findings may explain primary resistance to tyrosine kinase inhibitors targeted at receptor tyrosine kinases.
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6

Kinashi, T., JA Escobedo, LT Williams, K. Takatsu, and TA Springer. "Receptor tyrosine kinase stimulates cell-matrix adhesion by phosphatidylinositol 3 kinase and phospholipase C-gamma 1 pathways." Blood 86, no. 6 (September 15, 1995): 2086–90. http://dx.doi.org/10.1182/blood.v86.6.2086.bloodjournal8662086.

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Анотація:
Receptor tyrosine kinases are known to be important in growth and differentiation. We have recently found that c-kit, the tyrosine kinase receptor for steel factor, also regulates cell-matrix adhesion. Because Steel factor helps regulate cell migration and localization, this may be an important biologic function. Integrin adhesiveness is regulated within minutes by c-kit. The signaling pathways for tyrosine kinase stimulation of integrin adhesiveness and their relation to pathways that regulate growth and differentiation over much longer time periods remain uncharacterized. We have studied the effector pathways by which receptor tyrosine kinases regulate cell-matrix adhesion using wild-type and mutant forms of the platelet-derived growth factor (PDGF) receptor, which is closely related to c-kit. The PDGF receptor expressed in mast cells is as potent as c-kit in stimulating adhesion to fibronectin. We show that induction of adhesion is regulated through two independent pathways of phosphatidylinositol 3 kinase (PI3K) and phospholipase C- gamma 1 (PLC gamma)-protein kinase C by elimination of autophosphorylation sites required for activation of PI3K and PLC gamma or in combination with downregulation of protein kinase C or wortmannin. By contrast, a receptor mutated in both the PI3K and PLC gamma association sites can still stimulate mast cell growth, indicating a crucial role of these effector molecules in regulating adhesion rather than cell growth.
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7

Sun, Jianmin, Malin Pedersen, and Lars Rönnstrand. "The D816V Mutation of C-Kit Circumvents a Requirement for Src Family Kinases in C-Kit Mediated Signal Tranduction and Transformation." Blood 112, no. 11 (November 16, 2008): 2849. http://dx.doi.org/10.1182/blood.v112.11.2849.2849.

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Анотація:
Abstract The receptor tyrosine kinase c-Kit plays a critical role in hematopoiesis and gain-of-function mutations of the receptor are frequently seen in several malignancies, including acute myeloid leukemia (AML), mastocytoma and sinonasal NK/T cell lymphomas. The most common mutation of c-Kit in these disorders is a substitution of the aspartic acid residue in position 816 to a valine (D816V), leading to constitutive activation of the receptor. In this study we aimed to investigate the role of Src family kinases in c-Kit/D816V signaling. Src family kinases are necessary for the phosphorylation of wild-type c-Kit as well as for activation of downstream signaling pathways including receptor ubiquitination and the Ras/MEK/Erk pathway. Tyrosine 568 of c-Kit, that is important for Src activation by wild-type c-Kit, was mutated to phenylalanine in both wild-type c-Kit and c-Kit/D816V and stably transfected into the hematopoietic cell line Ba/F3. Our data demonstrate that, unlike wild-type c-Kit, the phosphorylation of c-Kit/D816V is not dependent on Src family kinases. In addition we found that neither receptor ubiquitination nor Erk activation by c-Kit/D816V required activation of Src family kinases. In vitro kinase assay using synthetic peptides revealed that c-Kit/D816V had an altered substrate specificity resembling Src and Abl tyrosine kinases. The serine/threonine kinases Akt and Erk play important roles in cell survival and proliferation mediated by receptor tyrosine kinases. We could show constitutive activation of both PI3-kinase pathway and Erk in Ba/F3 cells expressing c-Kit/D816V, although ligand stimulation induced even stronger activation. We further present evidence that, in contrast to wild-type c-Kit, Src family kinases are dispensible for c-Kit/D816V cell survival. Taken together, we demonstrate that the signal transduction pathways mediated by c-Kit/D816V are markedly different from those activated by wild-type c-Kit and that altered substrate substrate specificity of c-Kit circumvents a need for Src family kinases in signaling of growth and survival, thereby contributing to the transforming potential of c-Kit/D816V.
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8

Pan, Jingxuan, Hagop Kantarjian, Jorge Cortes, Francis Giles, and Srdan Verstovsek. "Effect of Tyrosine Kinase Inhibitor INNO-406 on Human Mast Cells Bearing Mutated c-KIT Tyrosine Kinase." Blood 108, no. 11 (November 16, 2006): 4890. http://dx.doi.org/10.1182/blood.v108.11.4890.4890.

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Abstract Systemic mastocytosis (SM) is characterized by a clonal accumulation of mast cells (MC) in bone marrow and other tissues. Malignant MC have abnormal spindle shape, express aberrant surface markers, and carry, in most cases, a mutation involving codon 816 of the c-KIT gene (D816V). This mutation results in a constitutively activated c-kit receptor associated tyrosine kinase and is responsible for disease progression. Agents that affect mutated c-kit may have clinical benefit in SM, but there is none clinically available. INNO-406 is a novel multi-targeted tyrosine kinase inhibitor, previously shown to inhibit the growth of cells expressing c-kit by inhibiting its phosphorylation (Kimura, Blood, 106:3948–54, 2005). We investigated the effects of INNO-406 on mast cells with mutated c-KIT, and compared it to that of imatinib mesylate, tyrosine kinase inhibitor effective against selected c-KIT mutants. HMC-1560 cells carrying juxtamembrane domain c-KIT mutation in codon 560, and HMC-1560, 816 cells carrying both codon 560 mutation and tyrosine kinase domain c-KIT mutation in codon 816, were exposed to increasing concentrations (0.02 to 5 μM) of INNO-406 or imatinib in 72-hour cell proliferation assay. Both INNO-406 and imatinib effectively inhibited the growth of HMC-1560 cells, with IC50 of 45 and 75nM, respectively. Neither drug was effective against HMC-1560, 816 cells at the doses tested. INNO-406 effectively induced apoptosis in HMC-1560, but not in HMC-1560, 816 cells, as judged by the Annexin V flow cytometry test and by PARP specific cleavage seen on western blotting. In addition, INNO-406 was effective in inhibiting phosphorylation of c-kit in HMC-1560 cells in nM range. Our results suggest similar potency of INNO-406 and imatinib in mast cells with mutated codon 560 (found in gastrointestinal stromal tumor), but no activity against cells with mutated codon 816 c-KIT (found in SM).
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9

Kornbluth, S., K. E. Paulson, and H. Hanafusa. "Novel tyrosine kinase identified by phosphotyrosine antibody screening of cDNA libraries." Molecular and Cellular Biology 8, no. 12 (December 1988): 5541–44. http://dx.doi.org/10.1128/mcb.8.12.5541-5544.1988.

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In an attempt to clone protein tyrosine kinases, antiphosphotyrosine antibodies were used to screen lambda gt11 cDNA expression libraries. By this method, a 2.5-kilobase cDNA encoding a novel tyrosine kinase was isolated from a mouse liver cDNA library. This new gene is most closely related to the receptor tyrosine kinases ret, fms, and kit.
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10

Kornbluth, S., K. E. Paulson, and H. Hanafusa. "Novel tyrosine kinase identified by phosphotyrosine antibody screening of cDNA libraries." Molecular and Cellular Biology 8, no. 12 (December 1988): 5541–44. http://dx.doi.org/10.1128/mcb.8.12.5541.

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Анотація:
In an attempt to clone protein tyrosine kinases, antiphosphotyrosine antibodies were used to screen lambda gt11 cDNA expression libraries. By this method, a 2.5-kilobase cDNA encoding a novel tyrosine kinase was isolated from a mouse liver cDNA library. This new gene is most closely related to the receptor tyrosine kinases ret, fms, and kit.
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Дисертації з теми "KIT tyrosine kinase"

1

Edling, Charlotte. "Receptor tyrosine kinase c-Kit signalling in hematopoietic progenitor cells." Doctoral thesis, Umeå : Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-888.

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2

Read, Stuart Hamilton. "Production and function of a soluble c-Kit molecule." Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phr2845.pdf.

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"Research conducted at the Department of Haematology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science."--T.p. Includes bibliographical references (leaves 170-214). Elevated levels of receptor tyrosine kinases have been implicated in carcinogenesis. It is possible that high expression of c-Kit by the leukaemic cell provides them with a growth advantage over their normal counterparts in the bone marrow microenvironment. Thus, a means of inhibiting the interaction of c-Kit on these cells with ligand Steel Factor may remove proliferation and survival signals. Main aim of the study was to produce a biological inhibitor of this interaction and evaluate its ability to prevent ligand Steel Factor from binding to c-Kit on live cells.
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3

Shulman, Johanna. "Biochemical analysis of activating mutations of the kit receptor tyrosine kinase." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0003/MQ40794.pdf.

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4

Rosnet, Olivier. "Caractérisation d'un recepteur à tyrosine kinase apparenté à KIT et FMS." Aix-Marseille 2, 1993. http://www.theses.fr/1993AIX22045.

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La classe iii des recepteurs a tyrosine kinase (rtks) constitue une famille de cinq molecules apparentees impliquees dans la croissance et la differenciation de nombreux types cellulaires au cours du developpement et chez l'adulte. Nous avons isole un sixieme membre de cette famille sur la base de ses similitudes de sequence avec le recepteur du colony stimulating factor 1 (csf1) code par le gene fms. Nous l'avons nomme flt3 (fms-like tyrosine kinase 3). Les adncs correspondant aux homologues murin et humain de ce recepteur ont ete clones. Ils ont permis les localisations chromosomiques des genes correspondants sur la bande q12 du chromosome 13 humain et la bande g du chromosome 5 de la souris. Dans les deux especes, le gene flt3 est proche du gene flt1 qui code pour un recepteur endothelial appartenant a la classe iv des rtks. Ces donnees, et les localisations d'autres genes codant pour des molecules apparentees, supposent que l'emergence de cette famille multigenique a fait intervenir, au cours de l'evolution, des phenomenes de cis et trans-duplication. Chez la souris adulte, l'arn messager de flt3 et son produit sont presents, dans le placenta, les gonades, le cerveau, le cervelet et les organes lympho-hematopoietiques. Au cours du developpement, l'expression de flt3 n'a pu etre montree que dans le foie et le thymus embryonnaire. Chez l'homme, son expression semble predominante au niveau tissulaire dans les organes lympho-hematopoietiques et au niveau cellulaire dans les progeniteurs lymphoides et myeloides
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5

Lermet, Anne. "Synthèse d'inhibiteurs de la protéine à activité tyrosine kinase c-kit de type sauvage et muté." Lyon 1, 2006. http://www.theses.fr/2006LYO10026.

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6

Cambareri, Antony Charles. "Molecular and cellular studies examining the biological significance of different isoforms of the receptor tyrosine kinase, c-Kit /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phc174.pdf.

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7

Baker, Clare V. H. "XKrk1, a c-kit-related receptor tyrosine kinase expressed in Xenopus embryos." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338070.

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8

André, Catherine. "Les oncogenes c-kit et c-fms : recepteurs a activite tyrosine kinase." Paris 7, 1992. http://www.theses.fr/1992PA077214.

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Les produits des oncogenes c-fms et c-kit, les pdgfra et pdgfrb appartiennent a la sous-classe iii des recepteurs a activite tyrosine kinase (rtk). Leurs genes sont localises par paire chez l'homme et la souris. Nous avons clone et sequence l'oncogene c-kit humain, sa structure genomique est homologue a celle de c-fms; les deux genes: 60 kb pour c-fms, 80 kb pour c-kit, leur structure exons/introns est identique dans le domaine catalytique. L'organisation genomique de c-kit et c-fms, la localisation chromosomique particuliere des genes de la sous-classe iii des rtk, ainsi que leurs fonctions communes, nous ont conduit a emettre l'hypothese selon laquelle ces genes auraient evolue a partir d'un gene ancestral commun, apres cis et trans duplications. Nous nous sommes interesses a l'implication de c-fms et c-kit dans l'hematopoiese. (1) en collaboration avec l'equipe de pierre tambourin (inserm-u. 152, hopital cochin), nous avons mis en evidence, au sein de l'intron 1 de l'oncogene c-fms (m-csfr), un site preferentiel d'integration du retrovirus de friend (f-mulv), implique dans 20% des leucemies myeloblastiques de la souris. (2) nous avons montre l'expression de c-kit dans les progeniteurs myeloides/erythroides et les mastocytes. Actuellement, nous recherchons l'implication de c-kit et de son ligand, kl, dans l'anemie de fanconi et d'autres aplasies, en collaboration avec le pr. Eliane gluckman (service des greffes de moelle osseuse a l'hopital st louis)
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9

An, Ningfei, Bo Cen, Houjian Cai, Jin H. Song, Andrew Kraft, and Yubin Kang. "Pim1 kinase regulates c-Kit gene translation." BIOMED CENTRAL LTD, 2016. http://hdl.handle.net/10150/622957.

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Background: Receptor tyrosine kinase, c-Kit (CD117) plays a pivotal role in the maintenance and expansion of hematopoietic stem/progenitor cells (HSPCs). Additionally, over-expression and/or mutational activation of c-Kit have been implicated in numerous malignant diseases including acute myeloid leukemia. However, the translational regulation of c-Kit expression remains largely unknown. Methods and results: We demonstrated that loss of Pim1 led to specific down-regulation of c-Kit expression in HSPCs of Pim1(-/-)mice and Pim1(-/-)2(-/-)3(-/-) triple knockout (TKO) mice, and resulted in attenuated ERK and STAT3 signaling in response to stimulation with stem cell factor. Transduction of c-Kit restored the defects in colony forming capacity seen in HSPCs from Pim1 (-/-) and TKO mice. Pharmacologic inhibition and genetic modification studies using human megakaryoblastic leukemia cells confirmed the regulation of c-Kit expression by Pim1 kinase: i.e., Pim1-specific shRNA knockdown down-regulated the expression of c-Kit whereas overexpression of Pim1 up-regulated the expression of c-Kit. Mechanistically, inhibition or knockout of Pim1 kinase did not affect the transcription of c-Kit gene. Pim1 kinase enhanced c-Kit S-35 methionine labeling and increased the incorporation of c-Kit mRNAs into the polysomes and monosomes, demonstrating that Pim1 kinase regulates c-Kit expression at the translational level. Conclusions: Our study provides the first evidence that Pim1 regulates c-Kit gene translation and has important implications in hematopoietic stem cell transplantation and cancer treatment.
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10

Larrue, Clément. "Régulation de l'expression protéique des récepteurs à activité tyrosine kinase FLT3 et KIT dans les leucémies aigües myéloïdes." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30195.

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Les mutations FLT3-ITD et KITD816V sont fréquemment retrouvées dans les leucémies aiguës myéloïdes où elles sont associées à un pronostic défavorable. Ces deux récepteurs à activité tyrosine kinase (RTK) mutés sont des acteurs clés de la leucémogenèse régulant la prolifération, la survie et la différenciation cellulaire. L'objectif de ce travail de thèse a été d'étudier la régulation de l'expression protéique de FLT3 en réponse aux inhibiteurs du protéasome, le rôle de l'autophagie dans les LAM KITD816V et l'impact du 2-deoxy-D-glucose sur la localisation intracellulaire des récepteurs. Les travaux réalisés ont démontré trois manières originales de cibler des cellules portant les oncogènes FLT3-ITD ou KIT en jouant sur leur dégradation, leur localisation intracellulaire et l'autophagie
FLT3-ITD and KITD816V mutations are recurrently found in acute myeloid leukemia, where they are associated with a poor prognosis. These two Tyrosine Kinase Receptors (TKR) are involved in leukemogenesis, regulating proliferation, survival and cell differentiation. The aim of this thesis was to study the regulation of FLT3 protein expression in response to proteasome inhibitors, the role of autophagy in KITD816V-driven AML and the impact of 2-deoxy-D-glucose (2-DG) on the intracellular localization of TKRs. Our studies investigated three original ways to target cells bearing FLT3-ITD or oncogenic KIT mutations playing on their degradation, intracellular localization and autophagy
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Книги з теми "KIT tyrosine kinase"

1

Shulman, Johanna. Biochemical analysis of activating mutations of the Kit receptor tyrosine kinase. Ottawa: National Library of Canada, 1998.

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2

Lam, Lily Po Yee. A transforming mutation induces dimerization and enhances activity of the c-kit soluble tyrosine kinase domain. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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3

Klüppel, Michael. Analysis of regulatory W mutations and the function of the kit receptor tyrosine kinase in the intestine. 1998.

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Частини книг з теми "KIT tyrosine kinase"

1

Salajegheh, Ali. "C-KIT: Tyrosine Kinase Receptors with Potential to Initiate Angiogenesis." In Angiogenesis in Health, Disease and Malignancy, 33–36. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_6.

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2

Ledoux, Julie, and Luba Tchertanov. "Receptor Tyrosine Kinase KIT: A New Look for an Old Receptor." In Bioinformatics and Biomedical Engineering, 133–37. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07802-6_11.

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3

Ray-Coquard, I., T. Bachelot, J. P. Guastalla, and J. Y. Blay. "Les autres inhibiteurs tyrosine kinase de KIT ou de la voie AKT." In Les thérapies ciblées, 117–30. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_8.

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4

Zschäbitz, Stefanie, and Carsten Grüllich. "Lenvantinib: A Tyrosine Kinase Inhibitor of VEGFR 1-3, FGFR 1-4, PDGFRα, KIT and RET." In Recent Results in Cancer Research, 187–98. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91442-8_13.

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5

Walker, Christoph, David Rodman, and Trevor T. Hansel. "Therapy directed against c-kit (CD117) and PDGF transmembrane receptor tyrosine kinases." In New Drugs and Targets for Asthma and COPD, 279–82. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320831.

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Hayman, Suzanne R., and Judith E. Karp. "Tyrosine Kinase Inhibitors: Targets Other Than FLT3, BCR-ABL, and c-KIT." In Innovative Leukemia and Lymphoma Therapy, 429–47. CRC Press, 2019. http://dx.doi.org/10.1201/9780429114670-18.

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Choi, Haesun. "Gastrointestinal stromal tumours." In Imaging for Clinical Oncology, 137–47. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198818502.003.0011.

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Gastrointestinal stromal tumour (GIST) is rare, but the most common tumour of non-epithelial origin in the GI tract. It was often misdiagnosed as leiomyomas and leiomyosarcomas, with a dismal prognosis until KIT receptor protein was identified in the tumour cells. GISTs are now thought to derive from a precursor of the interstitial cells of Cajal, which are normally present in the myenteric plexus, and are clearly distinct from other mesenchymal tumours. GISTs typically present with non-specific gastrointestinal symptoms and surgical resection is the only cure, but it most frequently presents with a large, non-resectable or marginally resectable mass. It is one of the solid tumours that took advantage of the early targeted agents, KIT tyrosine kinase receptor inhibitor, such as imatinib, with dramatic improvement of the survival. Prolonged survival with GISTs has been increasingly recognized and the role of imaging has become important not only for diagnosing and staging the tumours, but also for monitoring the tumours during and following treatments. This chapter will review the clinical presentation, diagnosis, current management, and role of imaging in management of GISTs.
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Reiter, Andreas, and Nicholas C. P. Cross. "Eosinophilia-associated myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms, 204–21. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0013.

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Accurate diagnosis of eosinophilia-associated disorders remains problematic. The World Health Organization (WHO) 2008 classification defines a rare subgroup: myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, or FGFR1 (MLN-eo), of which by far the most common is FIP1L1-PDGFRA. It is likely that other tyrosine kinase (TK) fusions will be incorporated into this category in due course. For other cases, the finding of increased numbers of blasts and/or proof of clonality is the basis for chronic eosinophilic leukaemia, not otherwise specified (CEL-NOS); however, in practice this diagnosis is only possible for a small minority of cases. It is also important to recognize cases that do not fulfil the diagnostic criteria for MLN-eo or CEL-NOS but who harbour KIT D816V or JAK2 V617F. As for treatment, disease stage (chronic/blast phase), potential clinical course (indolent/aggressive), potential sensitivity to imatinib, or alternative TK inhibitors and allogeneic stem cell transplantation need to be considered on an individual basis.
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Тези доповідей конференцій з теми "KIT tyrosine kinase"

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Guntur, Vamsi P., Tekla M. Lee-Fowler, John Dodam, Leah A. Cohn, Amy E. DeClue, and Carol R. Reinero. "The Effect Of Masitinib, A C-kit/PDGF Receptor Tyrosine Kinase Inhibitor, On IgE And Ventilator Parameters In Experimental Feline Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4076.

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2

Tetsu, Osamu, Janyaporn Phuchareon, Annie Chou, Darren P. Cox, David W. Eisele, and Richard CK Jordan. "Abstract 351: Mutations of genes in the c-Kit receptor tyrosine kinase signaling pathway are inactive in adenoid cystic carcinoma of the salivary glands: Implications for c-Kit targeted therapy." 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.am10-351.

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Agarwal, Shruti, Julhash U. Kazi, Sofie Mohlin, Sven Påhlman, and Lars Rönnstrand. "Abstract 128: Tyrosine 823 in the activation loop of c-Kit regulates the transforming capacity of the oncogenic mutant D816V and its sensitivity to kinase inhibitors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-128.

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Jeffers, Michael, Henrik Seidel, Susanne Schwenke, Joachim Reischl, Mark Rutstein, Christian Kappeler, Iris Kuss, and Michael Teufel. "Abstract 929: Tumor genotyping in the phase III GRID study of regorafenib vs placebo in tyrosine kinase inhibitor (TKI)-refractory GIST: Detection of KIT mutations in circulating tumor DNA comparing digital PCR and massive parallel sequencing." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-929.

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