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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAFMurX5wtHRkoUkoACPonRsTzuwWh0QOHPGIwm7o4YhM#_4 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAFMurX5wtHRkoUkoACPonRsTzuwWh0QOHPGIwm7o4YhM#_3 http://www.w3.org/ns/prov#value The protein encoded by this gene is a regulator of the pancreatic betacell function. It is highly similar to JIP1, a mouse protein known to be a regulator of cJun amino-terminal kinase (Mapk8). This protein has been shown to prevent MAPK8 mediated activation of transcription factors, and decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes. The phenotype of the JIP1 loss-of-function model is very similar to that of JNK1 deficiency in mice, with reduced JNK activity and increased insulin sensitivity (51). Interestingly, the JNK2 isoform plays a significant nonredundant role in atherosclerosis (52), though apparently not in type 2 diabetes. 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