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Product Description
JNK1 / JNK2 (phospho Thr183 / Tyr185) Antibody | 79-504 | ProSci
Host: Rabbit
Reactivity: Human, Mouse, Rat
Homology: N/A
Immunogen: JNK1/JNK2 (phospho-Thr183/Tyr185) antibody was raised against a peptide sequence around phosphorylation site of Thr183/Tyr185 (M-M-T (p) -P-Y (p) - V - V ) derived from Human JNK1/JNK2.
Research Area: Phospho-Specific
Tested Application: WB, IF
Application: Western Blot: 1:500~1:1000, Immunofluorescence: 1:100~1:200
Specificiy: This antibody detects endogenous level of JNK1/JNK2 only when phosphorylated at Thr183/Tyr185.
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 46, 54 kDa
Validation: N/A
Isoform: N/A
Purification: Antibodies were purified by affinity-chromatography using epitope-specific phosphopeptide. Non-phospho specific antibodies were removed by chromatogramphy using non-phosphopeptide.
Clonality: Polyclonal
Clone: N/A
Isotype: N/A
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Antibody supplied in phosphate buffered saline (without Mg2+ and Ca2+) , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Concentration: 1 mg/mL
Storage Condition: Store antibody at -20˚C for up to one year.
Alternate Name: JNK, JNK1, PRKM8, SAPK1, JNK-46, JNK1A2, SAPK1c, JNK21B1/2, FLT, FRT, VEGFR1, Stress-activated protein kinase JNK1, c-Jun N-terminal kinase 1
User Note: N/A
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: alpha-1 and alpha-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 alpha-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
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