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• W2051192888 startingPage "491" @default.
• W2051192888 abstract "OB-R is a high affinity receptor for leptin, an important circulating signal for the regulation of body weight. We identified an alternatively spliced transcript that encodes a form of mouse OB-R with a long intracellular domain. db/db mice also produce this alternatively spliced transcript, but with a 106 nt insertion that prematurely terminates the intracellular domain. We further identified G --> T point mutation in the genomic OB-R sequence in db/db mice. This mutation generates a donor splice site that converts the 106 nt region to a novel exon retained in the OB-R transcript. We predict that the long intracellular domain form of OB-R is crucial for initiating intracellular signal transduction, and as a corollary, the inability to produce this form of OB-R leads to the severe obese phenotype found in db/db mice." @default.
• W2051192888 created "2016-06-24" @default.
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• W2051192888 date "1996-02-01" @default.
• W2051192888 modified "2023-10-14" @default.
• W2051192888 title "Evidence That the Diabetes Gene Encodes the Leptin Receptor: Identification of a Mutation in the Leptin Receptor Gene in db/db Mice" @default.
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• W2051192888 doi "https://doi.org/10.1016/s0092-8674(00)81294-5" @default.
• W2051192888 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8608603" @default.
• W2051192888 hasPublicationYear "1996" @default.
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