Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein.
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Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathwaysThe alpha subunits of Gz and Gi interact with the eyes absent transcription cofactor Eya2, preventing its interaction with the six class of homeodomain-containing proteinsCannabinoid 1 receptor and interleukin-6 receptor together induce integration of protein kinase and transcription factor signaling to trigger neurite outgrowthReceptor heterodimerization leads to a switch in signaling: beta-arrestin2-mediated ERK activation by mu-delta opioid receptor heterodimersMost central nervous system D2 dopamine receptors are coupled to their effectors by GoMolecular mechanisms of go signalingSimultaneous tyrosine and serine phosphorylation of STAT3 transcription factor is involved in Rho A GTPase oncogenic transformationThe cleaved cytoplasmic tail of polycystin-1 regulates Src-dependent STAT3 activation.Activation of STAT proteins and growth control.Calpain as an effector of the Gq signaling pathway for inhibition of Wnt/beta -catenin-regulated cell proliferationG protein coupled receptor signaling through the Src and Stat3 pathway: role in proliferation and transformation.G(z) signaling: emerging divergence from G(i) signaling.The alpha subunit of Go modulates cell proliferation and differentiation through interactions with Necdin.Regulation of neurite outgrowth by G(i/o) signaling pathways.STAT3-induced S1PR1 expression is crucial for persistent STAT3 activation in tumors.Transcriptional regulation of the major HIV-1 coreceptor, CXCR4, by the kappa opioid receptorMolecular basis of opioid dependence: role of signal regulation by G-proteins.Compartmentalization of protein kinase A signaling by the heterotrimeric G protein Go.Dihydroxypentamethoxyflavone down-regulates constitutive and inducible signal transducers and activators of transcription-3 through the induction of tyrosine phosphatase SHP-1Drosophila C-terminal Src kinase negatively regulates organ growth and cell proliferation through inhibition of the Src, Jun N-terminal kinase, and STAT pathways.Stat3 orchestrates interaction between endothelial and tumor cells and inhibition of Stat3 suppresses brain metastasis of breast cancer cells.Inhibition of JAK1, 2/STAT3 signaling induces apoptosis, cell cycle arrest, and reduces tumor cell invasion in colorectal cancer cells.Role of the Go/i signaling network in the regulation of neurite outgrowth.Gαo potentiates estrogen receptor α activity via the ERK signaling pathwaySTAT3 signaling in pulmonary arterial hypertension.STAT3 signaling in immunity.δ-opioid receptor activation leads to neurite outgrowth and neuronal differentiation via a STAT5B-Gαi/o pathway.Molecular basis of a novel oncogenic mutation in GNAO1.Activation of STAT3 by G alpha(s) distinctively requires protein kinase A, JNK, and phosphatidylinositol 3-kinase.Pyk2 amplifies epidermal growth factor and c-Src-induced Stat3 activation.Constitutively active Galpha16 stimulates STAT3 via a c-Src/JAK- and ERK-dependent mechanism.Small-Molecule Inhibition of Rho/MKL/SRF Transcription in Prostate Cancer Cells: Modulation of Cell Cycle, ER Stress, and Metastasis Gene Networks.The C-terminal activation domain of the STAT-1 transcription factor is necessary and sufficient for stress-induced apoptosis.Signal transducer and activator of transcription 3 activates CCAAT enhancer-binding protein delta gene transcription in G0 growth-arrested mouse mammary epithelial cells and in involuting mouse mammary gland.Sperm factor induces intracellular free calcium oscillations by stimulating the phosphoinositide pathway.Autocrine-mediated activation of STAT3 correlates with cell proliferation in breast carcinoma lines.RGS7 is recurrently mutated in melanoma and promotes migration and invasion of human cancer cells.Correlation analysis of JAK-STAT pathway components on prognosis of patients with prostate cancer.
P2860
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P2860
Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein.
description
2000 nî lūn-bûn
@nan
2000 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2000 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2000年の論文
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2000年学术文章
@wuu
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
@zh-sg
2000年學術文章
@yue
name
Stat3-mediated transformation ...... active Q205L Galphao protein.
@ast
Stat3-mediated transformation ...... active Q205L Galphao protein.
@en
type
label
Stat3-mediated transformation ...... active Q205L Galphao protein.
@ast
Stat3-mediated transformation ...... active Q205L Galphao protein.
@en
prefLabel
Stat3-mediated transformation ...... active Q205L Galphao protein.
@ast
Stat3-mediated transformation ...... active Q205L Galphao protein.
@en
P1433
P1476
Stat3-mediated transformation ...... y active Q205L Galphao protein
@en
P2093
C M Horvath
P304
P356
10.1126/SCIENCE.287.5450.142
P407
P577
2000-01-01T00:00:00Z