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DESCRIPTION: c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. The JNK-interacting protein (JIP) group of scaffold proteins selectively mediates JNK signaling by aggregating specific components of the MAPK cascade to form a functional JNK signaling module. JIP2 plays a number of roles including IL1 beta-induced apoptosis inhibition in insulin-secreting cells; may function as a regulator of vesicle transport, through interactions with the JNK-signaling components and motor proteins; interacts with components of the JNK signaling pathway namely JNK, MAPKK7 and MLK2, MLK3 and DLK; binds the proline-rich domain-containing splice variant of apolipoprotein E receptor 2 (ApoER2), the cytoplasmic tails of LRP1 and LRP2 (Megalin), the TPR motif-containing C-terminal of kinesin light chain and interacts with the cytoplasmic domain of APP. This protein has been classified as a housekeeping protein based on its essential role in cell physiology. Several splice variants are known with molecular weights (kDa)/pIs of 88.0/4.36 (isoform 1), 84.7/4.40 (isoform 2), 64.9/4.48 (isoform 3), 49.1/4.49 (isoform 4).
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Rabbits were immunized with a synthetic peptide, n-LEYYQEHLAYACPTEDIYLE-c, based on a C-terminal sequence conserved in all isoforms of human JIP2 and differing from mouse, rat and canine JIP2 by a single amino acid substitution.
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