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Results provide evidence that p38beta is an unusual enzyme that automodulates its basal, MAPKK-independent activity by several autophosphorylation events, which enhance and suppress its catalytic activity.
p38beta was significantly higher in esophageal squamous cell carcinoma tissues compared with paired normal controls. p38beta expression was observed to be significantly associated with overall prognosis.
Suggest that R-Ras regulates angiogenic activities of endothelial cells in part via inhibition of the p38MAPK-HSP27 axis of VEGF signaling.
These findings suggest that coronin 1A (显示 CORO1A ELISA试剂盒) modulates endothelial cell apoptosis by regulating p38beta expression and activation.
The MAPK11 gene was variably methylated in monozygotic twins discordant for depressive disorder.
p38beta is a novel regulatory target of the transcription factor Pokemon (显示 ZBTB7A ELISA试剂盒) and positively regulated by Pokemon (显示 ZBTB7A ELISA试剂盒) in hepatic cells.
Data show that the p38 MAPK (p38 (显示 MAPK14 ELISA试剂盒)) isoform (p38beta) mitogen-activated protein kinase 11 (MAPK11) is expressed in breast cancer cell.
Differential roles for p38alpha (显示 MAPK14 ELISA试剂盒) and p38beta in the HGF (显示 HGF ELISA试剂盒)-induced expression of key osteogenic markers.
study identified the structural motif responsible for the unique autophosphorylation capability of p38beta and the motif inhibiting this activity in living cells
Study identifies Hsp27 (显示 HSPB1 ELISA试剂盒) as a novel target of ILK (显示 ILK ELISA试剂盒)-p38beta signaling complexes, playing a key role in bladder cancer cell migration.
propose that active p38-Mapk14 (显示 MAPK14 ELISA试剂盒)/11 act as enablers, and Erk1/2 (显示 MAPK1/3 ELISA试剂盒) as drivers, of primitive endoderm differentiation during inner cell mass lineage specification and segregation.
Double deficiency of p38alpha (显示 MAPK14 ELISA试剂盒) and p38beta in naive CD4 (显示 CD4 ELISA试剂盒)(+) T cells resulted in an attenuation of MAPK (显示 MAPK1 ELISA试剂盒)-activated protein kinase (显示 CDK7 ELISA试剂盒) (MK)-dependent mTOR (显示 FRAP1 ELISA试剂盒) signaling after T cell receptor engagement, and enhanced their differentiation into regulatory T cells under appropriate inducing conditions.
Data indicate that alternatively activated p38alpha (显示 MAPK14 ELISA试剂盒) and p38beta up-regulates the transcription factors NFATc1 (显示 NFATC1 ELISA试剂盒) and IRF4 (显示 IRF4 ELISA试剂盒).
the cell autonomous defect in self-renewal in satellite cells from aged mice is due to an impaired response to FGF ligands and elevated p38alpha (显示 MAPK14 ELISA试剂盒)/beta MAPK (显示 MAPK1 ELISA试剂盒) activity
work reveals a 'seed and soil' mechanism where TGF-beta2 (显示 TGFB2 ELISA试剂盒) and TGF-beta (显示 TGFB1 ELISA试剂盒)-RIII signalling through p38alpha (显示 MAPK14 ELISA试剂盒)/beta regulates DTC dormancy and defines restrictive (BM) and permissive (lung) microenvironments for HNSCC metastasis
Results suggest that UBR2 (显示 UBR2 ELISA试剂盒) up-regulation in cachectic muscle is mediated by the p38beta-C/EBPbeta (显示 CEBPB ELISA试剂盒) signaling pathway responsible for the bulk of tumor-induced muscle proteolysis.
inhibition of the SOCE downstream target CaM kinase kinase beta (显示 CAMKK2 ELISA试剂盒) (CaMKKbeta) or knockdown of AMPKalpha1 (显示 PRKAA1 ELISA试剂盒) suppressed PAR-1 (显示 MARK2 ELISA试剂盒)-mediated phosphorylation of p38beta and hence STIM1 (显示 STIM1 ELISA试剂盒).
p27 (显示 CDKN1B ELISA试剂盒) inhibition of COX-2 (显示 COX2 ELISA试剂盒) expression was specifically due to phosphorylation of transcription factor cAMP response element binding (CREB (显示 CREB1 ELISA试剂盒)) phosphorylation mediated by p38beta and p38delta (显示 MAPK1/3 ELISA试剂盒).
p38beta MAPK (显示 MAPK1 ELISA试剂盒) is dispensable in the brain in regards to proinflammatory cytokine production and neurotoxicity induced by LPS (显示 TLR4 ELISA试剂盒) inflammatory insult
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation, and development. This kinase is most closely related to p38 MAP kinase, both of which can be activated by proinflammatory cytokines and environmental stress. This kinase is activated through its phosphorylation by MAP kinase kinases (MKKs), preferably by MKK6. Transcription factor ATF2/CREB2 has been shown to be a substrate of this kinase.
mitogen-activated protein kinase 11
, mitogen-activated protein kinase 11-like
, MAP kinase 11
, MAP kinase p38 beta
, MAPK 11
, mitogen-activated protein kinase p38 beta
, mitogen-activated protein kinase p38-2
, stress-activated protein kinase 2
, stress-activated protein kinase 2b
, stress-activated protein kinase-2
, stress-activated protein kinase-2b
, mitogen activated protein kinase 11
, protein kinase, mitogen activated kinase, 11, p38beta