Activation of STAT3 by the c-Fes protein-tyrosine kinase.
about
A point mutation in the N-terminal coiled-coil domain releases c-Fes tyrosine kinase activity and survival signaling in myeloid leukemia cellsClosing in on the biological functions of Fps/Fes and FerFER kinase activation of Stat3 is determined by the N-terminal sequenceCell volume-dependent phosphorylation of proteins of the cortical cytoskeleton and cell-cell contact sites. The role of Fyn and FER kinasesConstitutive activation of STAT transcription factors in acute myelogenous leukemiaInhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decreased Mcl-1 expressionThe Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.Activation of STAT3 by the Src family kinase Hck requires a functional SH3 domain.Genetic complementation of cytokine signaling identifies central role of kinases in hematopoietic cell proliferation.Lymphokine dependence of STAT3 activation produced by surface immunoglobulin cross-linking and by phorbol ester plus calcium ionophore treatment in B cells.The KRAB-associated co-repressor KAP-1 is a coiled-coil binding partner, substrate and activator of the c-Fes protein tyrosine kinase.STAT3 is a substrate of SYK tyrosine kinase in B-lineage leukemia/lymphoma cells exposed to oxidative stress.A single amino acid substitution in the v-Eyk intracellular domain results in activation of Stat3 and enhances cellular transformation.Control of myeloid differentiation and survival by Stats.Targeted disruption of the murine fps/fes proto-oncogene reveals that Fps/Fes kinase activity is dispensable for hematopoiesis.Signal transducer and activator of transcription-3, inflammation, and cancer: how intimate is the relationship?.Integration of HIV-1 caused STAT3-associated B cell lymphoma in an AIDS patientSTAT3 and importins are novel mediators of early molecular and cellular responses in experimental duodenal ulceration.Activation of Stat3 in v-Src-transformed fibroblasts requires cooperation of Jak1 kinase activity.Activation of the Notch1/STAT3/Twist signaling axis promotes gastric cancer progression.Suppressor of cytokine signaling 3 expression in anaplastic large cell lymphoma.Src kinases mediate STAT growth pathways in squamous cell carcinoma of the head and neck.Butein suppresses constitutive and inducible signal transducer and activator of transcription (STAT) 3 activation and STAT3-regulated gene products through the induction of a protein tyrosine phosphatase SHP-1.A growth-suppressive function for the c-fes protein-tyrosine kinase in colorectal cancer.Fes tyrosine kinase promotes survival and terminal granulocyte differentiation of factor-dependent myeloid progenitors (32D) and activates lineage-specific transcription factors.The nonreceptor protein-tyrosine kinase c-Fes is involved in fibroblast growth factor-2-induced chemotaxis of murine brain capillary endothelial cells.
P2860
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P2860
Activation of STAT3 by the c-Fes protein-tyrosine kinase.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Activation of STAT3 by the c-Fes protein-tyrosine kinase.
@en
type
label
Activation of STAT3 by the c-Fes protein-tyrosine kinase.
@en
prefLabel
Activation of STAT3 by the c-Fes protein-tyrosine kinase.
@en
P2093
P2860
P356
P1476
Activation of STAT3 by the c-Fes protein-tyrosine kinase.
@en
P2093
P2860
P304
P356
10.1074/JBC.273.12.7072
P407
P577
1998-03-01T00:00:00Z