JNK1 Recombinant Rabbit Monoclonal Antibody [JE63-04] (HA721899)

UNIPROT #

P45983

PROTEIN NAME

JNK1

SYNONYMS

AI849689 antibody;c Jun N terminal kinase 1 antibody;C-JUN kinase 1 antibody;c-Jun N-terminal kinase 1 antibody;EC 2.7.11.24 antibody;JNK 1 antibody;JNK antibody;JNK-46 antibody;JNK1A2 antibody;JNK21B1/2 antibody;MAP kinase 8 antibody;MAPK 8 antibody;mapk8 antibody;Mitogen activated protein kinase 8 antibody;Mitogen-activated protein kinase 8 antibody;MK08_HUMAN antibody;p54 gamma antibody;Prkm8 antibody;Protein kinase JNK1 antibody;Protein kinase, mitogen-activated, 8 antibody;SAPK 1 antibody;SAPK gamma antibody;SAPK1 antibody;Stress-activated protein kinase 1 antibody;Stress-activated protein kinase JNK1 antibody

SUBCELLULAR LOCATION

Cytoplasm, Nucleus, Synapse.

FUNCTION

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as pro-inflammatory 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.