For quotations, please use our online quotation form, and you may also contact us by
service@kendallscientific.com
+1-888.733.6849 (Toll-free)
+1-617.299.7367 (Int’l))
+1-888.733.6849
Our customer service representatives are available 24 hours, Monday through Friday to assist you.Reactivity | Human Mouse Rat |
Tested applications | WB IF |
Recommended Dilution | WB 1:500 - 1:2000 IF 1:100 - 1:200 |
Calculated MW | 46/54kDa |
Observed MW | Refer to Figures |
Immunogen | A phospho specific peptide corresponding to residues surrounding T183/Y185of human MAPK8/MAPK9/MAPK10 |
Storage Buffer | Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3. |
Synonym | JNK; JNK1; PRKM8; SAPK1; JNK-46; JNK1A2; SAPK1c/JNK2; SAPK; p54a; JNK2A; JNK2B; PRKM9; JNK-55; SAPK1a; JNK2BETA; p54aSAPK; JNK2ALPHA/JNK3; JNK3A; PRKM10; SAPK1b; p493F12; p54bSAPK |
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
N/A