FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
about
Aberrant regulation of Wnt signaling in hepatocellular carcinomaFocal adhesion kinase depletion reduces human hepatocellular carcinoma growth by repressing enhancer of zeste homolog 2.Identification of miR-101-3p targets and functional features based on bioinformatics, meta-analysis and experimental verification in hepatocellular carcinoma.Sinulariolide Suppresses Human Hepatocellular Carcinoma Cell Migration and Invasion by Inhibiting Matrix Metalloproteinase-2/-9 through MAPKs and PI3K/Akt Signaling Pathways.FAK/PYK2 promotes the Wnt/β-catenin pathway and intestinal tumorigenesis by phosphorylating GSK3β.Focal Adhesion Kinase: Insight into Molecular Roles and Functions in Hepatocellular CarcinomaTargeting protein arginine methyltransferase 5 inhibits human hepatocellular carcinoma growth via the downregulation of beta-catenin.Inhibition of SIRT2 suppresses hepatic fibrosis.The Interaction between Cancer Stem Cell Marker CD133 and Src Protein Promotes Focal Adhesion Kinase (FAK) Phosphorylation and Cell Migration.Force-dependent breaching of the basement membrane.FAK Kinase Activity Is Required for the Progression of c-MET/β-Catenin-Driven Hepataocellular Carcinoma.Modeling a human hepatocellular carcinoma subset in mice through coexpression of met and point-mutant β-catenin.β-Catenin Deficiency in Hepatocytes Aggravates Hepatocarcinogenesis Driven by Oncogenic β-Catenin and MET.Neuropilin-1 regulated by miR-320 contributes to the growth and metastasis of cholangiocarcinoma cells.Prognostic significance of c-Met, β-catenin and FAK in patients with hepatocellular carcinoma following surgery.The in vivo antineoplastic and therapeutic efficacy of troxerutin on rat preneoplastic liver: biochemical, histological and cellular aspects.Shp2 deletion in hepatocytes suppresses hepatocarcinogenesis driven by oncogenic β-Catenin, PIK3CA and MET.Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation.Inhibition of insulin-like growth factor 1 receptor enhances the efficacy of sorafenib in inhibiting hepatocellular carcinoma cell growth and survival.Updates on the hepatocyte growth factor/c-Met axis in hepatocellular carcinoma and its therapeutic implications
P2860
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P2860
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
description
2014 nî lūn-bûn
@nan
2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
name
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@ast
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@en
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@nl
type
label
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@ast
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@en
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@nl
prefLabel
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@ast
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@en
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@nl
P2093
P2860
P356
P1433
P1476
FAK is required for c-Met/β-catenin-driven hepatocarcinogenesis.
@en
P2093
Jimmy Stauffer
Jiwang Zhang
Maribel Arteaga
Nancy J Zeleznik-Le
Scott J Cotler
P2860
P304
P356
10.1002/HEP.27402
P407
P577
2014-11-25T00:00:00Z