Phospho-MAPK8/MAPK9/MAPK10-T183/Y185-Polyclonal Antibodies

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Phospho-MAPK8/MAPK9/MAPK10-T183/Y185

Qty


Total
$300
Catalog #
AP0276
Antibody Type
Polyclonal Antibody
Gene ID
5599/5601/5602
Swiss Prot
P45983/P45984/P53779
Size
Species
Rabbit
Isotype
IgG
Purity
Affinity purification
Additional Information
ReactivityHuman Mouse Rat
Tested applicationsWB IF
Recommended DilutionWB 1:500 - 1:2000 IF 1:100 - 1:200
Calculated MW46/54kDa
Observed MWRefer to Figures
ImmunogenA phospho specific peptide corresponding to residues surrounding T183/Y185of human MAPK8/MAPK9/MAPK10
Storage BufferStore at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
SynonymJNK; 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
Images
  • AP0276: image 1

    Western blot analysis of extracts from C6 cells untreated or treated with anisomycin using Phospho-MAPK8/9/10-T183/Y185 Antibody.

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

Protocol

N/A

MSDS
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