GENE - TERM ANNOTATION REPORT

3 Annotations Found.

An association has been curated linking Glud1 and Hyperinsulinism in Rattus norvegicus.        

  • The association was inferred from sequence or structural similarity (ISS)
  •  
  • The annotation was made from Li C, etal., J Biol Chem. 2010 Oct 8;285(41):31806-18. Epub 2010 Jul 29.
  • The annotation has been inferred from Glud1 (Mus musculus)
  • 2 additional annotations were made from Li C, etal., J Biol Chem. 2010 Oct 8;285(41):31806-18. Epub 2010 Jul 29.
  • 522 RGD objects have been annotated to Hyperinsulinism  (RDO:0004350)
  • 32 papers in RGD have been used to annotate Glud1

  • This annotation was curated on 2012-06-27 10:36:21.0 by RGD curator number 202. For more information contact us

    An association has been curated linking Glud1 and Hyperinsulinism in Rattus norvegicus.        

  • The association was inferred from sequence or structural similarity (ISS)
  •  
  • The annotation was made from Stanley CA, etal., N Engl J Med 1998 May 7;338(19):1352-7.
  • 5 additional annotations were made from Stanley CA, etal., N Engl J Med 1998 May 7;338(19):1352-7.
  • 522 RGD objects have been annotated to Hyperinsulinism  (RDO:0004350)
  • 32 papers in RGD have been used to annotate Glud1


  • An association has been curated linking Glud1 and Hyperinsulinism in Rattus norvegicus.        

  • The association was inferred from sequence or structural similarity (ISS)
  •  
  • The annotation was made from Miki Y, etal., J Pediatr. 2000 Jan;136(1):69-72.
  • The annotation has been inferred from GLUD1 (Homo sapiens)
  • 5 additional annotations were made from Miki Y, etal., J Pediatr. 2000 Jan;136(1):69-72.
  • 522 RGD objects have been annotated to Hyperinsulinism  (RDO:0004350)
  • 32 papers in RGD have been used to annotate Glud1
  • Curation Notes: familial hyperinsulinemic hypoglycemia-6,OMIM:606762;DNA:point mutation:exon:E296A

  • This annotation was curated on 2007-04-17 00:00:00.0 by RGD curator number 14. For more information contact us

    Go Back to source page   Continue to Ontology report