产品详情
产品名称JNK1 Rabbit mAb
来源种属Recombinant Rabbit
克隆性Monoclonal antibody
克隆性S05-7A3
亚型Rabbit IgG
纯化Affinity Purified
应用WB
种属反应性Human,Mouse,Rat
免疫原描述Recombinant protein of human JNK1
标记Unconjugated
修饰Unmodification
别名JNK; JNK1; PRKM8; SAPK1; JNK-46; JNK1A2; SAPK1c; JNK21B1/2
数据库入口号Swiss-Prot:Q91Y86
GeneID:26419
UniprotQ91Y86
Gene ID26419
计算分子量Calculated MW: 48 kDa; Observed MW: 46-54 kDa
配方50nM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% Sodium azide and 0.05% BSA
保存Store at 4˚C short term. Aliquot and store at -20˚C long term. Avoid freeze/thaw cycles.
应用详情
WB: 1/1000
背景
Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including p53/TP53 and Yes-associates protein YAP1. In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Contributes to the survival of erythroid cells by phosphorylating the antagonist of cell death BAD upon EPO stimulation. Mediates starvation-induced BCL2 phosphorylation, BCL2 dissociation from BECN1, and thus activation of autophagy. Phosphorylates STMN2 and hence regulates microtubule dynamics, controlling neurite elongation in cortical neurons. In the developing brain, through its cytoplasmic activity on STMN2, negatively regulates the rate of exit from multipolar stage and of radial migration from the ventricular zone (By similarity).