Reactive species
Human; Mouse;Rat
Antibody type
Monoclonal antibodies
Gene Name
MAPK9 JNK2 PRKM9 SAPK1A
Immunogen
Synthesized peptide derived from human JNK2
Specificity
This antibody detects endogenous levels of JNK2 at Human, Mouse,Rat
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.59% sodium azide.
Dilution rate
IHC 1:50-200
Purification process
The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
Other name
Mitogen-activated protein kinase 9 (MAP kinase 9) (MAPK 9) (EC 2.7.11.24) (JNK-55) (Stress-activated protein kinase 1a) (SAPK1a) (Stress-activated protein kinase JNK2) (c-Jun N-terminal kinase 2)
Background
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase targets specific transcription factors, and thus mediates immediate-early gene expression in response to various cell stimuli. It is most closely related to MAPK8, both of which are involved in UV radiation induced apoptosis, thought to be related to the cytochrome c-mediated cell death pathway. This gene and MAPK8 are also known as c-Jun N-terminal kinases. This kinase blocks the ubiquitination of tumor suppressor p53, and thus it increases the stability of p53 in nonstressed cells. Studies of this gene's mouse counterpart suggest a key role in T-cell differentiation. Several alternative
Function
catalytic activity:ATP + a protein = ADP + a phosphoprotein.,cofactor:Magnesium.,domain:The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.,enzyme regulation:Activated by threonine and tyrosine phosphorylation by either of two dual specificity kinases, MAP2K4 and MAP2K7. Inhibited by dual specificity phosphatases, such as DUSP1.,function:JNK2 isoforms display different binding patterns: alpha-1 and alpha-2 preferentially bind to c-Jun, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 alpha-2, and JUND binds only weakly to it.,function:Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily com
