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.

journal_name

Nutr Rev

journal_title

Nutrition reviews

authors

Napoli JL

doi

10.1111/j.1753-4887.2000.tb01870.x

keywords:

subject

Has Abstract

pub_date

2000-08-01 00:00:00

pages

230-6

issue

8

eissn

0029-6643

issn

1753-4887

journal_volume

58

pub_type

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