P38 MAPK

Sun Y, Cheng Z, Ma L, Pei G. Beta-arrestin2 is critically involved in CXCR4-mediated chemotaxis, and this is mediated by its enhancement of p38 MAPK activation. J Biol Chem 2002 277(51) 49212 19219. 

Liu, C., Russell, R.M., and Wang, XD. 2004. Low dose beta-carotene supplementation of ferrets attenuates smoke-induced lung phosphorylation of JNK, p38 MAPK, and p53 proteins. J Nutr 134 2705-2710. 

Roux, P. P., and Blenis, J. (2004). ERK and p38 MAPK-activated protein kinases A family of protein kinases with diverse biological functions. Microbiol. Mol. Biol. Rev. 68, 320-344. 

A third group of MAPKs are p38 kinases, of which there are four subtypes a, [3, y, and 8. P38 MAPKs are activated by many stimuli including hormones, ligands for G-protein-coupled receptors and stresses [13,17]. P38 MAPK has been implicated in the pathological changes accompanying inflammatory and apoptotic processes of various cell types, including neurons [17] (see Ch. 35 for... 

Korcheva, V. et al., Administration of ricin induces a severe inflammatory response via nonredundant stimulation of ERK, JNK, and P38 MAPK and provides a mouse model of hemolytic uremic syndrome, Am. J. Pathol., 166, 323, 2005. 

Yang, G. et al. Apoptosis induction by the satratoxins and other trichothecene mycotoxins Relationship to ERK, p38 MAPK and SAPK/JNK Activation. Toxicol. Appl. Pharmacol. 164, 149-160, 2000. 

Zhou, H. R. and Pestka J.J. Deoxynivalenol-induced apoptosis mediated by p38 MAPK-dependent p53 gene induction in RAW 264.7 macrophages. The Toxicologist 72, 330, 2003. 

Conversely, the SAPK/JNK cascade, which is closely associated with apoptosis, is activated by sphingosine (Pyne et al, 1996). Exogenous sphingosine also activates caspase-7in a Bcl-x(L)-sensitive manner wha-eas caspase-8 was unaffected (Nava et al, 2000 Cuvillier et al, 2001). hi addition, sphingosine stimulates p38 MAPK in osteoblast-like cells (Kozawa et al, 2000) but not in oligodendrocytes where is produces lysis (Hida et al, 1999). p38 MAPK is up-stream of MAPKAP kinase-2 and the... 

Increased p42/p44 MAPK Increased c-jun and c-fos Increased non-receptor tyrosine kinase activity-increased phospholipase C Increased p38 MAPK Reduced cAMP Increased NO and NOS... 

SIP activates p38 MAPK in EDG5-transfected CHO cells (Gonda et al,... 

Kozawa et al, 2000a and b). In both cell types, the p38 MAPK-specific inhibitor, SB203580, blocks SIP hsp27 induction and amplification of inositol phosphates, hi osteoblastic cells, PGE shmulates cyclic AMP formation and inhibits apoptosis. This appears to be mediated by a cyclic AMP-dependent modulation of SPHK and S IP production (Machwate etal., 1998)... 

Holzer TR, Fulford AD, Arkins AM et al (2011) Ischemic time impacts biological integrity of phospho-proteins in PI3K/Akt, Erk/ MAPK, and p38 MAPK signaling networks. Anticancer Res 31 2073-2081... 

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). 

In an in vitro model, exposure of lymphoma cells to rituximab resulted in the activation of the Src-family of protein tyrosine kinases (13), leading to the phosphorylation of PLCy2, which induces calcium influx and activates caspase 3, resulting in promotion of apoptotic cell death (8,14). Another in vitro model showed that exposure to rituximab resulted in the sustained phosphorylation of p38-MAPK, JNK, and ERK kinases... 

Besides ERK1/2, there is experimental evidence that adenosine A3 receptors also activate p38 MAPKs in hCHO-A3 cells (Hammarberg et al. 2004). Furthermore, it has been demonstrated that A3 receptor stimulation is able to increase p38 phosphorylation in human hypoxic melanoma, glioblastoma and colon carcinoma cells (Merighi et al. 2005b, 2006, 2007a). 

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