Novel targeting strategy for generating mouse models with defects in the retinoid cycle.
In addition to RDH5, other enzymes capable of oxidizing 11-cis-retinol are present within the retinal pigment epithelium, Müller cells and/or photoreceptors. Candidate proteins have meanwhile been identified. To study the physiological and pathological aspects of these enzymes, mice in which these genes are no longer functional are being generated. A fast-targeting strategy for the disruption of genes was developed. Generation of double and triple knockouts will aid in determining if these retinol dehydrogenases are responsible for the remaining 11-cis-retinol oxidation observed in RDH5 knockout animals.
Driessen
Carola
C
Department of Biochemistry (160), University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. c.driessen@ncmls.kun.nl
Winkens
Huub
H
Haeseleer
Françoise
F
Palczewski
Krzysztof
K
Janssen
Jacques
J
D000429:Alcohol Oxidoreductases / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D010084:Oxidation-Reduction; D010857:Pigment Epithelium of Eye / Q000378:metabolism*; D012168:Retinal Pigments / Q000235:genetics / Q000378:metabolism*; D014162:Transfection; D014801:Vitamin A / Q000378:metabolism
D012168:Retinal Pigments; D014801:Vitamin A; D000429:Alcohol Oxidoreductases; C022520:retinol dehydrogenase