p38 alpha (K53A), Unactive(M39-16H)
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Description :Recombinant human full-length mutant p38 alpha (K53A) was expressed in E. coli using an N-terminal His tag. This kinase-dead protein is designed for up-stream kinase assay.
Species :Human
Tag :His tag
Expression System:E.coli
Sequence :Full Length
Genbank Number :NM_139012
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Kinase Assay, Western Blot
Molecular Weight :~42 kDa
Gene Aliases :RK, p38, EXIP, Mxi2, CSBP1, CSBP2, CSPB1, PRKM14, PRKM15, SAPK2A, p38ALPH
Scientific Background :p38α (SAPK2A) is a member of the p38 MAPK family which are activated by various environmental stresses and proinflammatory cytokines (1). The activation of p38 requires its phosphorylation by MAP kinase kinases (MKKs), or its autophosphorylation triggered by the interaction of MAP3K7IP1/TAB1 protein with this kinase (2). The substrates of p38 include transcription regulator ATF2, MEF2C, and MAX, cell cycle regulator CDC25B, and tumor suppressor p53, which suggest the roles of this kinase in stress related transcription and cell cycle regulation, as well as in genotoxic stress response.
References :
1. Han, J. et al: A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. Science 265: 808-811, 1994.
2. Ge, B. et al: MAPKK-independent activation of p38-alpha mediated by TAB1-dependent autophosphorylation of p38-alpha. Science 295: 1291-1294, 2002.
Product Sheets (By Lot #) :
Research Areas :Angiogenesis, Apoptosis/Autophagy, Cardiovascular Disease, Cellular Stress, Inflammation, Metabolic Disorder, Neurobiology, NfkB Pathway, p38 Pathway, Ser/Thr Kinases, Neurobiology, Inflammation, Metabolic Disorder, Cardiovascular Disease, p38 Pathway, NfkB Pathway, Apoptosis/Autophagy, Cellular Stress, Angiogenesis, Ser/Thr Kinases