MAPK8/MAPK9/MAPK1 (pThr183), (pTyr185) antibody
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- Target
- MAPK8/MAPK9/MAPK1
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Binding Specificity
- pThr183, pTyr185
- Reactivity
- Human
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Host
- Rabbit
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Clonality
- Polyclonal
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Conjugate
- Un-conjugated
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Application
- ELISA, Western Blotting (WB), Immunofluorescence (IF)
- Cross-Reactivity
- Human, Mouse, Rat
- Purification
- Antibodies were produced by immunizing rabbits with synthetic phosphopeptide and KLH conjugates. Antibodies were purified by affinity-chromatography using epitope-specific phosphopeptide. Non-phospho specific antibodies were removed by chromatogramphy usi
- Immunogen
- Peptide sequence around phosphorylation site of Thr183/Tyr185 (M-M-T(p)-P-Y(p)- V - V ) derived from Human JNK1/JNK2/JNK3.
- Isotype
- IgG
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- Application Notes
- WB:1:500-1:1000, IF:1:100-1:200,
- Restrictions
- For Research Use only
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- Format
- Liquid
- Buffer
- Supplied at 1.0 mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02 % sodium azide and 50 % glycerol.
- Preservative
- Sodium azide
- Precaution of Use
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- Storage
- -20 °C,-80 °C
- Storage Comment
- Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
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- Target
- MAPK8/MAPK9/MAPK1
- Background
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Background:
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.Aliases: Stress-activated protein kinase JNK1, c-Jun N-terminal kinase 1, JNK-46
- UniProt
- P45983, P45984, P53779
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