Background:  c-Jun NH2-terminal kinases (JNKs) are distant members of the MAP kinase family. JNK1 is activated by dual phosphorylation at a Thr-Pro-Tyr motif in response to ultraviolet (UV) light, and it functions to phosphorylate c-Jun at amino terminal serine regulatory sites, Ser-63 and Ser-73, resulting in transcriptional activation. Two additional JNK family members have been identified as JNK2 and JNK3. JIP-1 (for JNK interacting protein-1) has been identified as a cytoplasmic inhibitor of JNK that retains JNK in the cytoplasm, thereby inhibiting JNK-regulated gene expression. Evidence suggests that JNK1 and JNK2 bind to JIP-1 with greater affinity than to ATF-2 and c-Jun, which are targets of the JNK signaling pathway. JIP-1 contains an amino terminal JNK binding domain and a carboxy terminal SH3 domain. ATF-2 and c-Jun also contain the JNK binding domain and are thought to compete with JIP-1 for JNK binding. Multiple splice variants if JIP-1, including JIP-1b, JIP-1c (also designated islet-brain 1 or IB-1), JIP-2a, JIP-2b and JIP-3, have been identified in brain.

Description: Rabbit polyclonal to JIP2

Immunogen: KLH conjugated synthetic peptide derived from JIP2

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 88 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;

·Immunocytochemistry/Immunofluorescence: 1/100;

·Immunoprecipitation: 1/50;

·ELISA: 1/500;

·Optimal working dilutions must be determined by the end user.