|IP||1-2 μL/mg of lysate|
**********Please Note: Optimal concentrations/dilutions should be determined by the end user.**********
MAPK9 was immunoprecipitated using:
Lane A:0.5 mg HepG2 Whole Cell Lysate
Lane B:0.5 mg Hela Whole Cell Lysate
Lane C:0.5 mg Jurkat Whole Cell Lysate
Lane D:0.5 mg MCF-7 Whole Cell Lysate0.5 µL anti-MAPK9 mouse monoclonal antibody and 15 μl of 50 % Protein G agarose.Primary antibody:
Anti-MAPK9 mouse monoclonal antibody,at 1:500 dilutionSecondary antibody:
Dylight 800-labeled antibody to Mouse IgG (H+L), at 1:7500 dilutionDeveloped using the odssey technique.
Performed under reducing conditions.Predicted band size: 44 kDa
Observed band size: 44 kDa
Anti-MAPK9 mouse monoclonal antibody at 1:500 dilution
Lane A: HEPG2 Whole Cell Lysate
Lane B: A549 Whole Cell Lysate
Lane C: Jurkat Whole Cell LysateLysates/proteins at 30 μg per lane.
Rabbit Anti-Mouse IgG F(ab)2/HRP at 1/10000 dilution.Developed using the ECL technique.
Performed under reducing conditions.Predicted band size:48 kDa
Observed band size:52 kDa
(We are unsure as to the identity of these extra bands.)
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.
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