p38α MAPK Rabbit Monoclonal Antibody (Clone RM245)

p38 MAPK is a serine/threonine protein kinase and member of the MAPK family with roles in the regulation of immune responses and embryonic development, as well as cell differentiation, metabolism, and survival.^1,2 It exists as 4 isoforms, p38α, -β, -γ, and -δ, encoded by MAPK14, MAPK11, MAPK12, and MAPK13, respectively, in humans. p38α MAPK is ubiquitously expressed, with the highest levels of expression in heart, skeletal muscle, and brain.^1,3 It is activated via dual phosphorylation of threonine 180 and tyrosine 182 by the MAP2K kinases MKK3 and MKK6 in response to LPS or the production of inflammatory cytokines.^1,2 Downstream signaling targets of p38α MAPK include protein kinases, transcription factors, and transcriptional regulators, among others.² Knockdown of Mapk14 is embryonic lethal, while macrophage-specific deletion of Mapk14 inhibits inflammatory cytokine production and is protective against cecal ligation and puncture-induced sepsis in mice.^2,3 Mapk14 knockdown also increases lysosomal degradation of β-secretase 1 (BACE1) and decreases amyloid-β (Aβ) production in the APP/PS1 double transgenic mouse model of Alzheimer's disease.⁴ Cayman's p38α MAPK Monoclonal Antibody (Clone RM245) can be used for immunohistochemistry (IHC) and Western blot (WB) applications. The antibody recognizes p38α MAPK at approximately 38 kDa from human samples.

WARNING This product is not for human or veterinary use.

1. Lee, J.K., and Kim, N.-J. Recent advances in the inhibition of p38 MAPK as a potential strategy for the treatment of Alzheimer’s disease. Molecules 22(8), 1287 (2017).

2. Han, J., Wu, J., and Silke, J. An overview of mammalian p38 mitogen-activated protein kinases, central regulators of cell stress and receptor signaling. F1000Res. 9, 653 (2020).

3. Bachstetter, A.D., and Van Eldik, L.J. The p38 MAP kinase family as regulators of proinflammatory cytokine production in degenerative diseases of the CNS. Aging Dis. 1(3), 199-211 (2010).

4. Schnöder, L., Hao, W., Qin, Y., et al. Deficiency of neuronal p38α MAPK attenuates amyloid pathology in Alzheimer disease mouse and cell models through facilitating lysosomal degradation of BACE1. The Journal of Biological Chemisty 291(5), 2067-2079 (2016).