Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
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PTPH1 cooperates with vitamin D receptor to stimulate breast cancer growth through their mutual stabilizationp38gamma regulates interaction of nuclear PSF and RNA with the tumour-suppressor hDlg in response to osmotic shockPTPH1 dephosphorylates and cooperates with p38gamma MAPK to increase ras oncogenesis through PDZ-mediated interactionp38alpha and p38gamma mediate oncogenic ras-induced senescence through differential mechanismsReciprocal allosteric regulation of p38γ and PTPN3 involves a PDZ domain-modulated complex formationp38gamma MAPK cooperates with c-Jun in trans-activating matrix metalloproteinase 9.p38alpha antagonizes p38gamma activity through c-Jun-dependent ubiquitin-proteasome pathways in regulating Ras transformation and stress response.p38γ mitogen-activated protein kinase contributes to oncogenic properties maintenance and resistance to poly (ADP-ribose)-polymerase-1 inhibition in breast cancerp38γ promotes breast cancer cell motility and metastasis through regulation of RhoC GTPase, cytoskeletal architecture, and a novel leading edge behavior.Phosphorylation and stabilization of topoisomerase IIα protein by p38γ mitogen-activated protein kinase sensitize breast cancer cells to its poisons.p38γ mitogen-activated protein kinase (MAPK) confers breast cancer hormone sensitivity by switching estrogen receptor (ER) signaling from classical to nonclassical pathway via stimulating ER phosphorylation and c-Jun transcription.Combined deletion of p38γ and p38δ reduces skin inflammation and protects from carcinogenesis.Tyrosine dephosphorylation enhances the therapeutic target activity of epidermal growth factor receptor (EGFR) by disrupting its interaction with estrogen receptor (ER).p38γ Mitogen-activated protein kinase signals through phosphorylating its phosphatase PTPH1 in regulating ras protein oncogenesis and stress response.p38gamma mitogen-activated protein kinase integrates signaling crosstalk between Ras and estrogen receptor to increase breast cancer invasionMK2 Regulates Ras Oncogenesis through Stimulating ROS Production.The p38 MAPK stress pathway as a tumor suppressor or more?p38γ MAPK Is a Therapeutic Target for Triple-Negative Breast Cancer by Stimulation of Cancer Stem-Like Cell Expansion.Loss of p38δ mitogen-activated protein kinase expression promotes oesophageal squamous cell carcinoma proliferation, migration and anchorage-independent growth.Identification of a ternary protein-complex as a therapeutic target for K-Ras-dependent colon cancer.New Insights into the p38γ and p38δ MAPK Pathways.Stress-induced c-Jun-dependent Vitamin D receptor (VDR) activation dissects the non-classical VDR pathway from the classical VDR activity.Quaking and miR-155 interactions in inflammation and leukemogenesis.p38γ overexpression in gliomas and its role in proliferation and apoptosis.The K-Ras effector p38γ MAPK confers intrinsic resistance to tyrosine kinase inhibitors by stimulating EGFR transcription and EGFR dephosphorylation.p38γ MAPK is required for inflammation-associated colon tumorigenesis.MAPKs' status at early stages of renal carcinogenesis and tumors induced by ferric nitrilotriacetate.
P2860
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P2860
Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
@en
type
label
Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
@en
prefLabel
Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
@en
P2093
P2860
P356
P1476
Essential role of p38gamma in K-Ras transformation independent of phosphorylation.
@en
P2093
Dan Mercola
Jiahuai Han
Xiaomei Qi
P2860
P304
23910-23917
P356
10.1074/JBC.M500699200
P407
P577
2005-04-25T00:00:00Z