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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 (show CORO1A Proteins) 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 (show ZBTB7A Proteins) and positively regulated by Pokemon (show ZBTB7A Proteins) in hepatic cells.
Data show that the p38 MAPK (p38 (show MAPK14 Proteins)) isoform (p38beta) mitogen-activated protein kinase 11 (MAPK11) is expressed in breast cancer cell.
Differential roles for p38alpha (show MAPK14 Proteins) and p38beta in the HGF (show HGF Proteins)-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 (show HSPB1 Proteins) as a novel target of ILK (show ILK Proteins)-p38beta signaling complexes, playing a key role in bladder cancer cell migration.
propose that active p38-Mapk14 (show MAPK14 Proteins)/11 act as enablers, and Erk1/2 as drivers, of primitive endoderm differentiation during inner cell mass lineage specification and segregation.
Double deficiency of p38alpha (show MAPK14 Proteins) and p38beta in naive CD4 (show CD4 Proteins)(+) T cells resulted in an attenuation of MAPK (show MAPK1 Proteins)-activated protein kinase (show CDK7 Proteins) (MK)-dependent mTOR (show FRAP1 Proteins) signaling after T cell receptor engagement, and enhanced their differentiation into regulatory T cells under appropriate inducing conditions.
Data indicate that alternatively activated p38alpha (show MAPK14 Proteins) and p38beta up-regulates the transcription factors NFATc1 (show NFATC1 Proteins) and IRF4 (show IRF4 Proteins).
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 (show MAPK14 Proteins)/beta MAPK (show MAPK1 Proteins) activity
work reveals a 'seed and soil' mechanism where TGF-beta2 (show TGFB2 Proteins) and TGF-beta (show TGFB1 Proteins)-RIII signalling through p38alpha (show MAPK14 Proteins)/beta regulates DTC dormancy and defines restrictive (BM) and permissive (lung) microenvironments for HNSCC metastasis
Results suggest that UBR2 (show UBR2 Proteins) up-regulation in cachectic muscle is mediated by the p38beta-C/EBPbeta (show CEBPB Proteins) signaling pathway responsible for the bulk of tumor-induced muscle proteolysis.
inhibition of the SOCE downstream target CaM kinase kinase beta (show CAMKK2 Proteins) (CaMKKbeta) or knockdown of AMPKalpha1 (show PRKAA1 Proteins) suppressed PAR-1 (show MARK2 Proteins)-mediated phosphorylation of p38beta and hence STIM1 (show STIM1 Proteins).
p27 inhibition of COX-2 expression was specifically due to phosphorylation of transcription factor cAMP response element binding (CREB) phosphorylation mediated by p38beta and p38delta.
p38beta MAPK (show MAPK1 Proteins) is dispensable in the brain in regards to proinflammatory cytokine production and neurotoxicity induced by LPS (show TLR4 Proteins) 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