Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl.
about
A gain-of-function mutation in STAT6Mechanisms of STAT protein activation by oncogenic KIT mutants in neoplastic mast cellsDirect interaction of Jak1 and v-Abl is required for v-Abl-induced activation of STATs and proliferationCharacterization of a novel member of the DOK family that binds and modulates Abl signalingMast cell homeostasis and the JAK-STAT pathwayDepletion of Pleckstrin homology domain leucine-rich repeat protein phosphatases 1 and 2 by Bcr-Abl promotes chronic myelogenous leukemia cell proliferation through continuous phosphorylation of Akt isoformsUbp43 regulates BCR-ABL leukemogenesis via the type 1 interferon receptor signalingKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsCurrent concepts in pediatric Philadelphia chromosome-positive acute lymphoblastic leukemiaNovel targeted therapies for Bcr-Abl positive acute leukemias: beyond STI571.Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective HckAssociation of Bcr-Abl with the proto-oncogene Vav is implicated in activation of the Rac-1 pathwayPAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesisUrsolic acid-mediated apoptosis of K562 cells involves Stat5/Akt pathway inhibition through the induction of Gfi-1Src 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.Progressive changes in the leukemogenic signaling in BCR/ABL-transformed cells.Bcr-Abl with an SH3 deletion retains the ability To induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancySignal 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 leukemogenesisAbrogation of interleukin-3 dependence of myeloid cells by the v-src oncogene requires SH2 and SH3 domains which specify activation of STATsNovel mechanism of tumor suppression by polarity gene discs large 1 (DLG1) revealed in a murine model of pediatric B-ALL.Chromium(VI) stimulates Fyn to initiate innate immune gene induction in human airway epithelial cells.Signaling pathways activated by oncogenic forms of Abl tyrosine kinase.Adult B-cell acute lymphoblastic leukemia cells display decreased PTEN activity and constitutive hyperactivation of PI3K/Akt pathway despite high PTEN protein levels.STAT signaling in the pathogenesis and treatment of cancerSelecting the best frontline treatment in chronic myeloid leukemiaErythropoietin and Friend virus gp55 activate different JAK/STAT pathways through the erythropoietin receptor in erythroid cellsHuman and simian T-cell leukemia viruses type 2 (HTLV-2 and STLV-2(pan-p)) transform T cells independently of Jak/STAT activation.Constitutive activation of signal transducer and activator of transcription 3 regulates expression of vascular endothelial growth factor in human meningioma differentiation.Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation.Transformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transduced TEL/JAK2 fusion genes.Targeted therapies in hematology and their impact on patient care: chronic and acute myeloid leukemia.Challenges in small screening laboratories: implementing an on-demand laboratory information management system.Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581STAT signaling in the pathogenesis and treatment of leukemias.The role of STATs in myeloid differentiation and leukemia.JAK-STAT signaling activated by Abl oncogenes.IL-3 signaling and the role of Src kinases, JAKs and STATs: a covert liaison unveiled.The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and -independent pathways: roles for phosphatidylinositol 3-kinase and Raf.The NH(2)-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-Abl
P2860
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P2860
Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@ast
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@en
type
label
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@ast
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@en
prefLabel
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@ast
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@en
P2093
P2860
P356
P1476
Tyrosyl phosphorylation and DN ...... lines transformed by Bcr/Abl.
@en
P2093
J D Griffin
N Carlesso
P2860
P304
P356
10.1084/JEM.183.3.811
P407
P577
1996-03-01T00:00:00Z