MAPK9 / JNK2抗体

MAPK9 / JNK2抗体产品信息

免疫原 :
Recombinant human JNK2 proteimn ( Catalog#10745-H08B )
Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
克隆号 :
3C3C12E5
抗体宿主 :
Mouse IgG2b
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 :
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, human cell-derived, recombinant human MAPK9 ( rh MAPK9 ; Catalog#10745-H08B ; NP_002743.3 ; Met 1 - Arg 424 ). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
MAPK9 / JNK2抗体背景综述
Mitogen-activated protein kinase 9 ( MAPK9 ), also well known as c-Jun N-terminal kinase ( JNK2 ), is a member of MAP kinase subfamily belonging to the protein kinase superfamily. As an integration point for multiple biochemical signals, MAPKs are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, such as c-Jun and ATF2. It is most closely related to MAPK8, both of which are involved in UV radiation induced apoptosis. JNK protein kinases includes JNK1 and JNK2, and the activity of JNK2 was approximately 10-fold greater than that of JNK1 in c-Jun phosphorylation. JNK2 is activated by threonine and tyrosine phosphorylation by either of two dual specificity kinases, MAP2K4 and MAP2K7. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells. Inaddition, JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. Several alternatively spliced transcript variants of JNK2 with different binding patterns have been identified: 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.
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