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Knockouts phenotypes, other

A similar phenotype has not been seen in P450 IB 1-knockout mice" . Other polymorphisms of (human) P450 IBl are known and are predominant in a set of haplotypes involving four variations Arg/Gly 48, Ala/Ser 119, Val/Leu 432, and Asn/Ser 453. Assays involving the metabolism of 17(3-estradiol and polycyclic hydrocarbons by recombinant P450 IBl variants show some variations but have not been particularly dramatic (reviewed by Shimada et a/. ). [Pg.400]

Foster This is critical. It will be important to combine the melanopsin knockout mice with a rodless+coneless mouse model. The rdjrd cl mouse would be the most useful as this phenotype is already well defined, but I understand other rodless+coneless models are also being developed. [Pg.24]

Knockout of the prolactin receptor, rather than knockout of prolactin, is necessary to explore the role of the hormone and its receptor in maternal behavior because several molecules other than prolactin, including growth hormone (GH) and placental lactogens, may stimulate the prolactin receptor. Disruption of the prolactin receptor gene in a mouse model has allowed for assessment of phenotypes associated with partial and complete prolactin receptor deficits (Goffin et ah, 1999). Prolactin receptor knockout mice have severe reproductive deficits. Heterozygous mothers (receptor —/+) were also unable to lactate (Bridges, 1998). [Pg.201]


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See also in sourсe #XX -- [ Pg.230 , Pg.231 ]




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Knockout

Phenotype

Phenotype/phenotyping

Phenotypes other

Phenotypic

Phenotyping

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