sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_4 ;
    pav:version "1.4" .
  sub:_3 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. Recent studies in mice demonstrate that JNK inhibition in established diabetes or atherosclerosis might be a viable therapeutic avenue for these diseases in humans" ;
    prov:wasQuotedFrom pubmed:15864338 .
  sub:_4 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15864338 ;
    prov:wasDerivedFrom beldoc: , sub:_3 .
}