Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
AvrRpt2 specifically blocks the flagellin-induced activation of MPK11.
findings show that MPK11 activity can be increased through flg22 elicitation
The two kinases HIPK3 and MAPK11 effect on Huntingtin (HTT)levels are mutant HTT protein (mHTT)-dependent, providing a feedback mechanism in which mHTT enhances its own level thus contributing to mHTT accumulation and disease progression.
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 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 and positively regulated by Pokemon in hepatic cells.
Data show that the p38 MAPK (p38) isoform (p38beta) mitogen-activated protein kinase 11 (MAPK11) is expressed in breast cancer cell.
Differential roles for p38alpha and p38beta in the HGF-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 as a novel target of ILK-p38beta signaling complexes, playing a key role in bladder cancer cell migration.
inhibition of the SOCE downstream target CaM kinase kinase beta (CaMKKbeta) or knockdown of AMPKalpha1 suppressed PAR-1-mediated phosphorylation of p38beta and hence STIM1.
Thus, in endothelial cells p38alpha mediates apoptotic signaling, whereas p38beta and p38gamma transduce survival signaling
Overexpression of p38beta or Rac1 significantly enhanced (1.9- and 3.9-fold, respectively), the tRA-stimulated NIS expression in MCF-7 cells.
results demonstrate that IFN-alpha can regulate growth inhibition of Jurkat cells through p38alpha and p38beta
p38alpha/p38beta and phosphoinositide 3-kinase are crucial to Tat-induced IL-10 production
These results demonstrate that activin A induces erythroid differentiation of K562 cells through activation of MKK6-p38alpha/p38beta pathway and follistatin inhibits those effects.
show that p38 MAP kinase directly activates TACE and effects shedding in response to growth factors and Erk MAP kinase activation.
p38 MAP Kinase suppresses the function of Mirk as a transcriptional activator only when cells are proliferating
the p38MAPK activation-Bax expression pathway might be involved in apoptosis induced by oxidative stress
The current study reveals that ActRIIB activation by activin A induces muscle catabolism primarily through the activation of p38beta MAPK-mediated catabolic signalling that activates the ubiquitin-proteasome pathway and the autophagy-lysosome pathway.
in the current study, we used interval mapping to validate a locus on Chr 15, named Ity8, linked to Salmonella resistance in AcB60 mice. Global gene expression analysis during infection identified AcB60-specific expression of genes involved in Ccr7 signaling, including downstream effector Mapk11 (mitogen-activated protein kinase 11), located within the Ity8 interval, and representing a potential positional candidate gene
propose that active p38-Mapk14/11 act as enablers, and Erk1/2 as drivers, of primitive endoderm differentiation during inner cell mass lineage specification and segregation.
Double deficiency of p38alpha and p38beta in naive CD4(+) T cells resulted in an attenuation of MAPK-activated protein kinase (MK)-dependent mTOR signaling after T cell receptor engagement, and enhanced their differentiation into regulatory T cells under appropriate inducing conditions.
Data indicate that alternatively activated p38alpha and p38beta up-regulates the transcription factors NFATc1 and IRF4.
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/beta MAPK activity
work reveals a 'seed and soil' mechanism where TGF-beta2 and TGF-beta-RIII signalling through p38alpha/beta regulates DTC dormancy and defines restrictive (BM) and permissive (lung) microenvironments for HNSCC metastasis
Results suggest that UBR2 up-regulation in cachectic muscle is mediated by the p38beta-C/EBPbeta signaling pathway responsible for the bulk of tumor-induced muscle proteolysis.
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 is dispensable in the brain in regards to proinflammatory cytokine production and neurotoxicity induced by LPS inflammatory insult
The stress kinases p38 and JNK are activated when DNA replication is blocked and their activity allows S/M, but not G 2/M, checkpoint maintenance when Chk1 is inhibited.
suggest a requirement for GADD45gamma in promoting MAP3K4-mediated activation of p38 MAPK signaling in embryonic gonadal somatic cells for testis determination
The neurotransmitter switch is impaired in neurons isolated from p38beta-deficient mice; loss of cells expressing cholinergic properties is observed in the stellate ganglion of mature mice deficient in the p38beta isoform.
Results identify essential roles for p38alpha and p38beta during development and suggest that some specific functions may be explained by differences in expression patterns.
Demonstrate roles of the p38alpha/beta/delta isoforms in the regulation of 12-O-tetradecanoylphorbol 13-acetate-induced skin inflammation.
p38 alpha, and not p38 beta, mitogen-activated protein kinase is required for ischemic preconditioning
Provide direct evidence for p38alpha/beta MAPK in mediating oxidative stress-induced autophagy-related genes, suggesting that p38alpha/beta MAPK regulates both the ubiquitin-proteasome and the autophagy-lysosome systems in muscle wasting.
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