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Obesity, diabetes, and neoplasia in yellow A(vy)/- mice: ectopic expression of the agouti gene.

Abstract
The viable yellow A(vy) mutation results in a mottled yellow mouse that is obese, slightly larger than its nonyellow sibs, and more susceptible to tumor formation in those tissues sensitized by the strain genome. The mutation exhibits variable expressivity resulting in a continuum of coat color phenotypes, from clear yellow to pseudoagouti. The mouse agouti protein is a paracrine signaling molecule that induces hair follicle melanocytes to switch from the synthesis of black pigment to yellow pigment. Molecular cloning studies indicate that the obesity and growth effects of the A(vy) mutation result from ectopic expression of the normal agouti gene product. This review seeks to summarize the current state of knowledge regarding the obesity, stimulation of somatic growth, and enhancement of tumor formation caused by the A(vy) mutation, and to interpret these pleiotropic effects in terms of the normal function of the agouti protein.
AuthorsT T Yen, A M Gill, L G Frigeri, G S Barsh, G L Wolff
JournalFASEB journal : official publication of the Federation of American Societies for Experimental Biology (FASEB J) Vol. 8 Issue 8 Pg. 479-88 (May 1994) ISSN: 0892-6638 [Print] United States
PMID8181666 (Publication Type: Journal Article, Review)
Chemical References
  • Agouti Signaling Protein
  • Intercellular Signaling Peptides and Proteins
  • Proteins
  • a protein, mouse
Topics
  • Agouti Signaling Protein
  • Amino Acid Sequence
  • Animals
  • Diabetes Mellitus (genetics)
  • Gene Expression
  • Intercellular Signaling Peptides and Proteins
  • Mice
  • Mice, Inbred Strains
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • Mutation
  • Neoplasms (genetics)
  • Obesity (genetics)
  • Phenotype
  • Proteins (genetics)

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