Retinol Binding Protein 4 Knock-out Mice
Lead Inventors: William Blaner, Ph.D.Problem or Unmet Need:There is a need for a useful model to study retinoid (vitamin A and its metabolites) and retinoid-dependent actions, including ones in cancer prevention and normal embryologic development. Reducing the dietary vitamin A intake of retinol-binding protein knockout (RBP-/-) females during pregnancy impairs embryogenesis. With these mice, one can easily modify the amount of vitamin A that reaches the embryo by manipulating diet. Thus, they represent a unique genetic model to be used to evaluate the requirement for maternal vitamins for organogenesis, a study that is relevant to humans. This technology provides a RBP4 KO strain of mice.Mice lacking plasma RBP are phenotypically normal except that they display impaired vision at the time of weaning. This visual defect is associated with greatly diminished eyecup levels of retinaldehyde and is reversible if the mutants are maintained for several months on a vitamin A-sufficient diet. The eye, unlike all other tissues that have been examined, takes up dietary retinol very poorly. Moreover, compared to other tissues, the eye displays a strong preference for retinol uptake when retinol is delivered bound to RBP. Reduction of dietary vitamin A intake in RBP knockout mice (RBP-/-) rapidly reproduces a vitamin A-deficient (VAD) status, making this strain a model to study the role of vitamin A in specific organs and tissues. These mice can be used a model to study the role of vitamin A in specific organs and tissues.
Useful model to study retinoid (vitamin A and its metabolites) and retinoid-dependent actions, including ones in cancer prevention and normal embryologic development Unique genetic model to be used to evaluate the requirement for maternal vitamins for organogenesis
The study of retinoid and retionoid-dependent actions The study the role of vitamin A in specific organs and tissues
Mice lacking plasma RBP are phenotypically normal except that they display impaired vision at the time of weaning. This visual defect is associated with greatly diminished eyecup levels of retinaldehyde and is reversible if the mutants are maintained...
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