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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

A polymorphism in New Zealand inbred mouse strains that inactivates phosphatidylcholine transfer protein.

New Zealand obese (NZO/HlLt) male mice develop polygenic diabetes and altered phosphatidylcholine metabolism. The gene encoding phosphatidylcholine transfer protein (PC-TP) is sited within the support interval for Nidd3, a recessive NZO-derived locus on Chromosome 11 identified by prior segregation analysis between NZO/HlLt and NON/Lt. Sequence analysis revealed that the NZO-derived PC-TP contained a non-synonymous point mutation that resulted in an Arg120His substitution, which was shared by the related NZB/BlNJ and NZW/LacJ mouse strains. Consistent with the structure-based predictions, functional studies demonstrated that Arg120His PC-TP was inactive, suggesting that this mutation contributes to the deficiencies in phosphatidylcholine metabolism observed in NZO mice.[1]

References

  1. A polymorphism in New Zealand inbred mouse strains that inactivates phosphatidylcholine transfer protein. Pan, H.J., Agate, D.S., King, B.L., Wu, M.K., Roderick, S.L., Leiter, E.H., Cohen, D.E. FEBS Lett. (2006) [Pubmed]
 
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