Polyclonal Antibody to JNK1/JNK2/JNK3 (phospho-Thr183/Tyr185)
Figure 1: Western blot analysis of extracts from C6 cells untreated or treated with anisomycin using JNK1/JNK2/JNK3(phospho-Thr183/Tyr185) Antibody 35-1303 .
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| Format : | Purified |
| Amount : | 100 µl |
| Isotype : | Rabbit IgG |
| Content : | Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. |
| Storage condition : | Store the antibody at 4°C, stable for 6 months. For long-term storage, store at -20°C. Avoid repeated freeze and thaw cycles. |
| Gene : | MAPK8 |
| Gene ID : | 5599 |
| Uniprot ID : | P45983/ P45984 P |
| Alternative Name : | Stress-activated protein kinase JNK1, c-Jun N-terminal kinase 1, JNK-46 |
| Immunogen Information : | Peptide sequence around phosphorylation site of Thr183/Tyr185 (M-M-T(p)-P-Y(p)- V - V ) derived from Human JNK1/JNK2/JNK3. |
Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells By similarity. Phosphorylates heat shock factor protein 4 (HSF4). /Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2 and thus regulates AP-1 transcriptional activity. In T-cells, JNK1 and JNK2 are required for polarized differentiation of T-helper cells into Th1 cells. JNK2 isoforms display different binding patterns: a-1 and a-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. JUNB is not a substrate for JNK2 a-2, and JUND binds only weakly to it. /Responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of transcription factors, primarily components of AP-1 such as c-Jun and ATF2 and thus regulates AP-1 transcriptional activity. Required for stress-induced neuronal apoptosis and the pathogenesis of glutamate excitotoxicity
Davis, R.J. (1999) Biochem Soc Symp 64, 1-12.
Ichijo, H. (1999) Oncogene 18, 6087-93.
Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.
Predicted MW: 46 54 kd, Western blotting: 1:500~1:1000, Immunofluorescence: 1:100~1:200
For Research Use Only. Not for use in diagnostic/therapeutics procedures.
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