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Download PDF DatasheetCatalogue No : BS1544
| Host | Reactivity | Size | Application | stock | price | cart |
| BS1544 | H,M,R | 200μg | WB IHC IF | ![]() |
218.00 | ![]() |
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Contact information
Email:shdiahds@163.com Click here for qusetions for this product! |
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1 mg/ml in Phosphate buffered saline (PBS) with 15 mM sodium azide, approx. pH 7.2.
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
JNK1/2/3 (T178) antibody detects endogenous levels of JNK1/2/3 protein.
WB: 1:500~1:1000 IP: 1:50~1:200 IF: 1:50~1:200
Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze-thaw cycles.
c-Jun N-terminal kinases (JNKs) phosphorylate and augment transcriptional activity of c-Jun. JNKs originate from three genes that yield 10 isoforms through alternative mRNA splicing, including JNK1α1,JNK1β1, JNK2α1, JNK2β1 and JNK3α1, which represent the p46 isoforms, and JNK1α2, JNK1β2, JNK2α2, JNK2β2 and JNK3β2, which represent the p54 isoforms. JNKs coordinate cell responses to stress and influence regulation of cell growth and transformation. The human JNK1 (PRKM8, SAPK1, MAPK8) gene maps to chromosome 10q11.22 and shares 83% amino acid identity with JNK2. JNK1 is necessary for normal activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. Capsaicin activates JNK1 and p38 in Ras-transformed human breast epithelial cells. Nitrogen oxides (NOx) upregulate JNK1 in addition to c-Fos, c-Jun and other signaling kinases, including MEKK1 and p38. JNK3 (MK10, MAPK10, PRKM10) is activated by pro-inflammatory cytokines and environmental stresss by phosphorylating transcription factors such as c-Jun and ATF2. This is important for AP-1 transcriptional activity regulation. JNK3 is crucial for neuronal apoptosis (stress-induced).