The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and -independent pathways: roles for phosphatidylinositol 3-kinase and Raf.
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8p12 stem cell myeloproliferative disorder: the FOP-fibroblast growth factor receptor 1 fusion protein of the t(6;8) translocation induces cell survival mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt/mTOR pathwaysRoles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistanceChronic myeloid leukemia: reminiscences and dreamsMolecular mechanisms for survival regulation of chronic myeloid leukemia stem cellsKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsPhosphatidylserine and phosphatidylethanolamine in mammalian cells: two metabolically related aminophospholipidsSurvival-factor-induced phosphorylation of Bad results in its dissociation from Bcl-x(L) but not Bcl-2MEK kinase activity is not necessary for Raf-1 function.Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences.Progressive changes in the leukemogenic signaling in BCR/ABL-transformed cells.Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Changes in the proteome associated with the action of Bcr-Abl tyrosine kinase are not related to transcriptional regulation.Disruption of the Shc/Grb2 complex during abelson virus transformation affects proliferation, but not apoptosis.Bcr/Abl interferes with the Fanconi anemia/BRCA pathway: implications in the chromosomal instability of chronic myeloid leukemia cells.SAHA and S116836, a novel tyrosine kinase inhibitor, synergistically induce apoptosis in imatinib-resistant chronic myelogenous leukemia cells.Oncogenic stress induced by acute hyper-activation of Bcr-Abl leads to cell death upon induction of excessive aerobic glycolysis.The follicular microenviroment as a predictor of pregnancy: MALDI-TOF MS lipid profile in cumulus cells.SPARC expression in CML is associated to imatinib treatment and to inhibition of leukemia cell proliferationBCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability.High affinity molecules disrupting GRB2 protein complexes as a therapeutic strategy for chronic myelogenous leukaemia.Cytokines and BCR-ABL mediate suppression of TRAIL-induced apoptosis through inhibition of forkhead FOXO3a transcription factorJAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis.Synergistic interactions between imatinib mesylate and the novel phosphoinositide-dependent kinase-1 inhibitor OSU-03012 in overcoming imatinib mesylate resistance.Conditional expression of oncogenic K-ras from its endogenous promoter induces a myeloproliferative disease.Src kinase signaling in leukaemiaSrc kinases as targets for B cell acute lymphoblastic leukaemia therapy.L5178Y sublines: a look back from 40 years. Part 2: response to ionizing radiation.FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis.Crosstalk between Bcl-2 family and Ras family small GTPases: potential cell fate regulation?Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.Single nucleotide polymorphisms in apoptosis pathway are associated with response to imatinib therapy in chronic myeloid leukemiaBiochemical and biological functions of docosahexaenoic acid in the nervous system: modulation by ethanolBcl-xL anti-apoptotic network is dispensable for development and maintenance of CML but is required for disease progression where it represents a new therapeutic target.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.Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.S-adenosylmethionine limitation induces p38 mitogen-activated protein kinase and triggers cell cycle arrest in G1.Signaling networks associated with BCR-ABL-dependent transformation.The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Induction of apoptosis by directing oncogenic Bcr-Abl into the nucleus.Bcr-Abl-mediated protection from apoptosis downstream of mitochondrial cytochrome c release.
P2860
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P2860
The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and -independent pathways: roles for phosphatidylinositol 3-kinase and Raf.
description
2000 nî lūn-bûn
@nan
2000 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2000 թվականի փետրվարին 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
The survival function of the B ...... idylinositol 3-kinase and Raf.
@ast
The survival function of the B ...... idylinositol 3-kinase and Raf.
@en
type
label
The survival function of the B ...... idylinositol 3-kinase and Raf.
@ast
The survival function of the B ...... idylinositol 3-kinase and Raf.
@en
prefLabel
The survival function of the B ...... idylinositol 3-kinase and Raf.
@ast
The survival function of the B ...... idylinositol 3-kinase and Raf.
@en
P2093
P2860
P1476
The survival function of the B ...... idylinositol 3-kinase and Raf.
@en
P2093
P2860
P304
P356
10.1128/MCB.20.4.1179-1186.2000
P407
P577
2000-02-01T00:00:00Z