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A gene knockout corroborates the integral function of cellular retinol-binding protein in retinoid metabolism.

Abstract
Continually expanding evidence has moved inexorably toward establishing key functions for cellular retinol-binding protein (CRBP) in retinoid metabolism. These experimental data integrate into a model of CRBP as a chaperone that protects retinol from the cellular milieu and interacts with certain retinoid-metabolizing enzymes. Mutant mice with an inactivated CRBP gene show decreased liver retinyl ester storage, a shorter elimination half-life of liver retinoids, and predisposition to vitamin A deficiency. No morphologic phenotype was observed until vitamin A was exhausted. Although the mechanisms underlying diminished vitamin A in the CRBP-null mice have not been elucidated, the observations support the model of CRBP as a chaperone of retinoid metabolism.
AuthorsJ L Napoli
JournalNutrition reviews (Nutr Rev) Vol. 58 Issue 8 Pg. 230-6 (Aug 2000) ISSN: 0029-6643 [Print] UNITED STATES
PMID10946560 (Publication Type: Journal Article, Review)
Chemical References
  • Amino Acids
  • Retinoids
  • Retinol-Binding Proteins
  • Retinol-Binding Proteins, Cellular
  • Vitamin A
Topics
  • Amino Acids (genetics, metabolism)
  • Animals
  • Mice
  • Mice, Knockout
  • Retinoids (metabolism)
  • Retinol-Binding Proteins (genetics, metabolism)
  • Retinol-Binding Proteins, Cellular
  • Vitamin A (metabolism)

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