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Recombinant Human MAPK9 protein

>90% as determined by SDS-PAGE

Please contact with the lab for this information.

A DNA sequence encoding the human MAPK9 (Tyr26-Ile321) was fused with His tag

P45984

E.coli

Homo sapiens (Human)

33.27 kDa

Supplied as solution form in PBS pH 7.5 or lyophilized from PBS pH 7.5.

In general, proteins are provided as lyophilized powder/frozen liquid. They are shipped out with dry ice/blue ice unless customers require otherwise.

Use a manual defrost freezer and avoid repeated freeze thaw cycles.
Store at 2 to 8 °C for one week .
Store at -20 to -80 °C for twelve months from the date of receipt.

Reconstitute in sterile water for a stock solution.A copy of datasheet will be provided with the products, please refer to it for details.

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. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggest that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally,the JNK2 protein could be a novel therapeutic target in dry eye disease, and may provide a novel target for prevention of vascular disease and atherosclerosis.

Mitogen-activated protein kinase 9,MAP kinase 9,MAPK 9,JNK-55,Stress-activated protein kinase 1a,SAPK1a,Stress-activated protein kinase JNK2,c-Jun N-terminal kinase 2.

For research use only .