Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective Hck - Wikidata - awgldk - TriplyDB

Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective Hck

Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective Hck

http://www.wikidata.org/entity/Q28138004

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Current concepts in pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia The interaction of the Bcr-Abl tyrosine kinase with the Src kinase Hck is mediated by multiple binding domains Src family kinases phosphorylate the Bcr-Abl SH3-SH2 region and modulate Bcr-Abl transforming activity.The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial.Bosutinib as a fourth-line therapy for a patient with T315I-positive lymphoid blastic phase chronic myeloid leukemia: A case report.Expression of a Src family kinase in chronic myelogenous leukemia cells induces resistance to imatinib in a kinase-dependent manner.Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase.Expression and activity of Fyn mediate proliferation and blastic features of chronic myelogenous leukemia.Development and targeted use of nilotinib in chronic myeloid leukemia.Identification of Hck inhibitors as hits for the development of antileukemia and anti-HIV agents.From Hen House to Bedside: Tracing Hanafusa's Legacy from Avian Leukemia Viruses to SRC to ABL and Beyond Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies.Targeting mutated tyrosine kinases in the therapy of myeloid leukaemias.Src kinase signaling in leukaemia Hematopoietic cell kinase (HCK) as a therapeutic target in immune and cancer cells.Src kinases as targets for B cell acute lymphoblastic leukaemia therapy.Regulation of myeloproliferation and M2 macrophage programming in mice by Lyn/Hck, SHIP, and Stat5 Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells.Dasatinib for the treatment of Philadelphia chromosome-positive leukaemias.Therapeutic options for chronic myeloid leukemia: focus on imatinib (Glivec, Gleevectrade mark).Strategies for overcoming imatinib resistance in chronic myeloid leukemia.Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up.Targeted therapy in chronic myeloid leukemia.Src family kinases and the MEK/ERK pathway in the regulation of myeloid differentiation and myeloid leukemogenesis Src-family kinases in the development and therapy of Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphoblastic leukemia.Dasatinib dosing strategies in Philadelphia chromosome-positive leukemia.An inhibitor-resistant mutant of Hck protects CML cells against the antiproliferative and apoptotic effects of the broad-spectrum Src family kinase inhibitor A-419259.Effects of dasatinib on SRC kinase activity and downstream intracellular signaling in primitive chronic myelogenous leukemia hematopoietic cells Advances in treatment of chronic myelogenous leukemia--new treatment options with tyrosine kinase inhibitors.Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.Natural course and biology of CML.Suppression of programmed cell death 4 (PDCD4) protein expression by BCR-ABL-regulated engagement of the mTOR/p70 S6 kinase pathway.Indirubin derivatives induce apoptosis of chronic myelogenous leukemia cells involving inhibition of Stat5 signaling.Novel virtual lead identification in the discovery of hematopoietic cell kinase (HCK) inhibitors: application of 3D QSAR and molecular dynamics simulation.Identification of protein tyrosine kinases with oncogenic potential using a retroviral insertion mutagenesis screen.The Src tyrosine kinase Hck is required for Tel-Abl- but not for Tel-Jak2-induced cell transformation.Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate.A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2.Src family kinases interfere with dimerization of STAT5A through a phosphotyrosine-SH2 domain interaction.

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P2860

Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective Hck

http://www.wikidata.org/entity/Q28138004

description

2000 nî lūn-bûn

@nan

2000 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի հունիսին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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name

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@ast

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@en

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

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type

label

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

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Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@en

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

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prefLabel

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@ast

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@en

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

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P1433

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P1433

Journal of Biological Chemistry

P1476

Transformation of myeloid leuk ...... ressed by kinase-defective Hck

@en

P2093

J M Lionberger

http://www.w3.org/2001/XMLSchema#string

M B Wilson

http://www.w3.org/2001/XMLSchema#string

T E Smithgall

http://www.w3.org/2001/XMLSchema#string

P2860

The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene

The Src family kinase Hck interacts with Bcr-Abl by a kinase-independent mechanism and phosphorylates the Grb2-binding site of Bcr

Localization of the c-ab1 oncogene adjacent to a translocation break point in chronic myelocytic leukaemia

Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22

The Ras GTPase-activating protein (GAP) is an SH3 domain-binding protein and substrate for the Src-related tyrosine kinase, Hck

Activation of the Src-family tyrosine kinase Hck by SH3 domain displacement

CrkL mediates Ras-dependent activation of the Raf/ERK pathway through the guanine nucleotide exchange factor C3G in hematopoietic cells stimulated with erythropoietin or interleukin-3.

SH2-kinase linker mutations release Hck tyrosine kinase and transforming activities in Rat-2 fibroblasts.

Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis

Structures of Src-family tyrosine kinases.

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18581-5

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scholarly article

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10.1074/JBC.C000126200

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P433

24

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275

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2000-06-16T00:00:00Z

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10849448

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