|Application ||WB, IHC, IP|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||48296 Da|
|Application & Usage||Western blotting (0.5-4 µg/ml),immunoprecipitation (10-20 µg/ml), and Immunohistochemistry (10-20 µg/ml). Reacts with human and to a lesser extent with mouse and rat. However, the optimal conditions should be determined individually.|
|Other Names||JNK1, JNK 1 , JNK1 antibody , SARP , JNK1A2 , JNK , JAK 1A , JAK1A , Stress activated protein kinase|
|Formulation||100 µg (0.5 mg/ml) affinity purified rabbit anti-JNK polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||JNK Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||JNK1, PRKM8, SAPK1, SAPK1C|
|Function||Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory 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. Phosphorylates STMN2 and hence regulates microtubule dynamics, controlling neurite elongation in cortical neurons. In the developing brain, through its cytoplasmic activity on STMN2, negatively regulates the rate of exit from multipolar stage and of radial migration from the ventricular zone. Phosphorylates several other substrates including heat shock factor protein 4 (HSF4), the deacetylase SIRT1, ELK1, or the E3 ligase ITCH. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the regulation of the circadian clock (PubMed:22441692).|
|Cellular Location||Cytoplasm. Nucleus|
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Provided below are standard protocols that you may find useful for product applications.
The JNK pathway is activated by largely distinct stimuli including inflammatory cytokines (such as TNF-α and IL-1), UV light, inhibitors of protein synthesis and osmotic stress. Activated MEKK1 phosphorylates SEK1 (also known as MKK4), which in turn activates SAPK (also known as JNK). JNK binds tightly to the N-terminal region of c-Jun and ATF-2, and phosphorylates c-Jun at Ser63 and Ser73 and ATF-2 at Thr69 and Thr71.
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