Activation of the JNK pathway is essential for transformation by the Met oncogene
about
The role of the c-Jun N-terminal kinase 2-α-isoform in non-small cell lung carcinoma tumorigenesisA selective small-molecule inhibitor of c-Jun N-terminal kinase 1The beta-subunit of the hepatocyte growth factor/scatter factor (HGF/SF) receptor phosphorylates and associates with CrkII: expression of CrkII enhances HGF/SF-induced mitogenesisp38 and extracellular signal-regulated kinases regulate the myogenic program at multiple stepsAn overview of the c-MET signaling pathwayJNK signalling in cancer: in need of new, smarter therapeutic targetsKit signaling through PI 3-kinase and Src kinase pathways: an essential role for Rac1 and JNK activation in mast cell proliferationMet receptor tyrosine kinase: enhanced signaling through adapter proteinsGrb2 interaction with MEK-kinase 1 is involved in regulation of Jun-kinase activities in response to epidermal growth factorMicrotubule dysfunction induced by paclitaxel initiates apoptosis through both c-Jun N-terminal kinase (JNK)-dependent and -independent pathways in ovarian cancer cellsWithdrawal of survival factors results in activation of the JNK pathway in neuronal cells leading to Fas ligand induction and cell deathThe Ras/Rac1/Cdc42/SEK/JNK/c-Jun cascade is a key pathway by which agonists stimulate DNA synthesis in primary cultures of rat hepatocytesDistinct expression patterns and transforming properties of multiple isoforms of Ost, an exchange factor for RhoA and Cdc42.Transcriptional gene expression profiles of HGF/SF-met signaling pathway in colorectal carcinoma.Jnk2 effects on tumor development, genetic instability and replicative stress in an oncogene-driven mouse mammary tumor model.Hepatocyte growth factor, a versatile signal for developing neurons.Sustained c-Jun-NH2-kinase activity promotes epithelial-mesenchymal transition, invasion, and survival of breast cancer cells by regulating extracellular signal-regulated kinase activation.Zoledronic acid effectiveness against breast cancer metastases - a role for estrogen in the microenvironment?The Jun kinase 2 isoform is preferentially required for epidermal growth factor-induced transformation of human A549 lung carcinoma cells.Dependence of Dbl and Dbs transformation on MEK and NF-kappaB activation.Inhibition of c-Jun N-terminal kinase 2 expression suppresses growth and induces apoptosis of human tumor cells in a p53-dependent mannerEnhanced transformation by a plasma membrane-associated met oncoprotein: activation of a phosphoinositide 3'-kinase-dependent autocrine loop involving hyaluronic acid and CD44.Oncogenic mutants of RON and MET receptor tyrosine kinases cause activation of the beta-catenin pathway.The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis.ROS, stress-activated kinases and stress signaling in cancer.Sequential activation of ERK and repression of JNK by scatter factor/hepatocyte growth factor in madin-darby canine kidney epithelial cellsThe Ser/Thr kinase MAP4K4 drives c-Met-induced motility and invasiveness in a cell-based model of SHH medulloblastomaGab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.JNK suppression of chemotherapeutic agents-induced ROS confers chemoresistance on pancreatic cancer stem cells.Gab1 mediates hepatocyte growth factor-stimulated mitogenicity and morphogenesis in multipotent myeloid cells.Integrin-mediated activation of focal adhesion kinase is required for signaling to Jun NH2-terminal kinase and progression through the G1 phase of the cell cycle.c-Jun activation-dependent tumorigenic transformation induced paradoxically by overexpression or block of S-adenosylmethionine decarboxylase.Effects of MAP kinase inhibitors on epidermal growth factor-induced neoplastic transformation of human keratinocytes.SEK1 deficiency reveals mitogen-activated protein kinase cascade crossregulation and leads to abnormal hepatogenesis.The mutationally activated Met receptor mediates motility and metastasis.JNK Signaling in the Control of the Tumor-Initiating Capacity Associated with Cancer Stem Cells.PKC controls HGF-dependent c-Met traffic, signalling and cell migration.Analysis of the chemotherapeutic effects of a propadiene compound on malignant ovarian cancer cells.Targeting MUC1 and JNK by RNA interference and inhibitor inhibit the development of hepatocellular carcinoma.Progress in cancer therapy targeting c-Met signaling pathway.
P2860
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P2860
Activation of the JNK pathway is essential for transformation by the Met oncogene
description
1997 nî lūn-bûn
@nan
1997 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
1997 թվականի մայիսին հրատարակված գիտական հոդված
@hy
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
name
Activation of the JNK pathway is essential for transformation by the Met oncogene
@ast
Activation of the JNK pathway is essential for transformation by the Met oncogene
@en
type
label
Activation of the JNK pathway is essential for transformation by the Met oncogene
@ast
Activation of the JNK pathway is essential for transformation by the Met oncogene
@en
prefLabel
Activation of the JNK pathway is essential for transformation by the Met oncogene
@ast
Activation of the JNK pathway is essential for transformation by the Met oncogene
@en
P2093
P2860
P356
P1433
P1476
Activation of the JNK pathway is essential for transformation by the Met oncogene
@en
P2093
Rodrigues GA
Schlessinger J
P2860
P304
P356
10.1093/EMBOJ/16.10.2634
P407
P577
1997-05-01T00:00:00Z