Genetic inactivation of Par4 results in hyperactivation of NF-kappaB and impairment of JNK and p38.
about
The signaling adapter p62 is an important mediator of T helper 2 cell function and allergic airway inflammationPar-4 inhibits Akt and suppresses Ras-induced lung tumorigenesisMitogen Activated Protein kinase signal transduction pathways in the prostateThe atypical PKCs in inflammation: NF-κB and beyondAn aPKC-exocyst complex controls paxillin phosphorylation and migration through localised JNK1 activationDirect binding to ceramide activates protein kinase Czeta before the formation of a pro-apoptotic complex with PAR-4 in differentiating stem cellsRegulation of mature T lymphocyte proliferation and differentiation by Par-4Unraveling the molecular targets pertinent to junction restructuring events during spermatogenesis using the Adjudin-induced germ cell depletion modelThe Ras effector RASSF2 controls the PAR-4 tumor suppressor.Role of protease-activated receptor-2 on cell death and DNA fragmentation in Helicobacter pylori-infected gastric epithelial cells.Tumour-suppression activity of the proapoptotic regulator Par4.Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiationProstate apoptosis response 4 (Par-4), a novel substrate of caspase-3 during apoptosis activation.Th1/Th2 Differentiation and B Cell Function by the Atypical PKCs and Their Regulators.PKCzeta at the crossroad of NF-kappaB and Jak1/Stat6 signaling pathways.Protein kinase Czeta represses the interleukin-6 promoter and impairs tumorigenesis in vivo.Simultaneous inactivation of Par-4 and PTEN in vivo leads to synergistic NF-kappaB activation and invasive prostate carcinoma.Nephrin deficiency activates NF-kappaB and promotes glomerular injury.Post-translational regulation of the cleaved fragment of Par-4 in ovarian and endometrial cancer cells.The Par-4/PTEN connection in tumor suppression.Of the atypical PKCs, Par-4 and p62: recent understandings of the biology and pathology of a PB1-dominated complex.Prostate apoptosis response-4 mediates TGF-β-induced epithelial-to-mesenchymal transition.Polarity protein alterations in carcinoma: a focus on emerging roles for polarity regulators.Par-4 as a potential target for cancer therapy.Involvement of protease-activated receptor 4 in over-expression of matrix metalloproteinase 9 induced by Porphyromonas gingivalis.Fbxo45-mediated degradation of the tumor-suppressor Par-4 regulates cancer cell survivalExpression Pattern of the Pro-apoptotic Gene PAR-4 During the Morphogenesis of MCF-10A Human Mammary Epithelial Cells.Crosstalk between PKCzeta and the IL4/Stat6 pathway during T-cell-mediated hepatitis.Loss of RASSF2 Enhances Tumorigencity of Lung Cancer Cells and Confers Resistance to Chemotherapy.Molecular heterogeneity in chronic lymphocytic leukemia is dependent on BCR signaling: clinical correlation.Novel role of prostate apoptosis response-4 tumor suppressor in B-cell chronic lymphocytic leukemia.Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling.
P2860
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P2860
Genetic inactivation of Par4 results in hyperactivation of NF-kappaB and impairment of JNK and p38.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
Genetic inactivation of Par4 r ...... and impairment of JNK and p38.
@en
type
label
Genetic inactivation of Par4 r ...... and impairment of JNK and p38.
@en
prefLabel
Genetic inactivation of Par4 r ...... and impairment of JNK and p38.
@en
P2093
P2860
P1433
P1476
Genetic inactivation of Par4 r ...... and impairment of JNK and p38
@en
P2093
Isabel Garcia-Cao
Jorge Moscat
Luis M Criado
María José Lafuente
María Teresa Diaz-Meco
P2860
P304
P356
10.1038/SJ.EMBOR.EMBOR769
P577
2003-03-01T00:00:00Z