High impact information on Mapk11

• Next, transgenic mice with cardiac-specific expression of dominant negative forms of p38alpha (DN-p38alpha) and p38beta (DN-p38beta) MAPK were examined [1].
• As p38 is activated by tumor necrosis factor, the p38beta-/- mice were crossed onto a TNFDeltaARE mouse line [2].
• The p38beta-/- mice also showed normal T-cell development [2].
• Lipopolysaccharide-induced cytokine production was also normal in the p38beta-/- mice [2].
• The transcription of p38-dependent immediate-early genes was also not affected by the knockout of p38beta, suggesting that p38alpha is the predominant isoform involved in these processes [2].

Biological context of Mapk11

• The p38beta MAPK mediated the effects of CO on cytoprotection and Hsp70 regulation [3].
• JNK and p38alpha activation have been associated with apoptosis; p38beta with cell survival; and ERK with proliferation [4].
• We also demonstrate that E2F1 downregulation by novel PKC isozymes requires activation of p38beta mitogen-activated protein kinase (MAPK) [5].
• Among them, p38 alpha is the best characterized isoform and many biological phenomena, especially in the inflammatory responses, were attributed to the specific inhibitor-sensitive isoforms, namely p38 alpha and p38 beta [6].
• Consistent with early activation of p38beta kinase, the phosphorylation of ATF-2 was also detected in early stage of adipocyte differentiation [7].

Anatomical context of Mapk11

• Our results indicate that p38beta is not required for insulin-stimulated glucose uptake in adipocytes or muscle [8].
• Glucose uptake in adipocytes and soleus muscle was stimulated by insulin by up to fourfold irrespective of whether tissues were isolated from wild-type or p38beta-null mice [8].
• E2F1 stability is regulated by a novel-PKC/p38beta MAP kinase signaling pathway during keratinocyte differentiation [5].
• Both p38alpha and p38beta were highly expressed in brain areas including cerebral cortex, hippocampus, cerebellum, and few nuclei of the brainstem [9].
• At the subcellular level, p38alpha was distributed in dendrites and in cytoplasmic and nuclear regions of cell body of neurons, which is in contrast to p38beta, since p38beta was preferentially expressed in nucleus of neurons [9].

Associations of Mapk11 with chemical compounds

• Heat shock protein-70 mediates the cytoprotective effect of carbon monoxide: involvement of p38 beta MAPK and heat shock factor-1 [3].
• Intraperitoneal injection of SB202190, an inhibitor of p38alpha and p38beta MAPK activity, markedly increased the ability of DN-14-3-3 mice to compensate for pressure overload, with decreased mortality [10].
• Consistent with this finding, mice lacking p38beta exhibited normal glucose tolerance, insulinemia, and glycemia compared with their wild-type counterparts [8].
• Although insulin also failed to induce any detectable activation of p38 MAPK in muscle, insulin-dependent glucose uptake was reduced by SB 203580 (approximately 44%) in muscle of both wild-type and p38beta-null mice [8].
• The induction of p38beta was sustained for more than 10 days after KA-treatment [11].

Enzymatic interactions of Mapk11

• Activating transcription factor-2 (ATF-2) is efficiently phosphorylated and activated by p38beta kinase [7].

Other interactions of Mapk11

• 17beta-E significantly down-regulated JNK and p38alpha activities, whereas I/R-I promoted p38beta and ERK activation [4].
• The immunoreactivities of p38alpha and p38beta MAPKs were markedly increased in the brain 4 days after KA administration, especially in the areas undergoing selective neuronal loss [11].
• By using dominant negative mutants and mice deficient in the genes for the various MAP kinases, we demonstrate that the cytoprotective effects of CO are mediated by selective activation of the MKK3/p38 beta protein MAP kinase pathway [12].

Analytical, diagnostic and therapeutic context of Mapk11

• RT-PCR analysis identified p38alpha and p38beta2 MAPK mRNA in rat cardiac myocytes [13].

References