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Isolation of a cDNA clone encoding a KATP channel-like protein expressed in insulin-secreting cells, localization of the human gene to chromosome band 21q22.1, and linkage studies with NIDDM.
Tsaur, M L; Menzel, S; Lai, F P; Espinosa, R; Concannon, P; Spielman, R S; Hanis, C L; Cox, N J; Le Beau, M M; German, M S.
Afiliação
  • Tsaur ML; Howard Hughes Medical Institute, University of California, San Francisco, USA.
Diabetes ; 44(5): 592-6, 1995 May.
Article em En | MEDLINE | ID: mdl-7729621
ABSTRACT
The metabolism of glucose in insulin-secreting cells leads to closure of ATP-sensitive K+ channels (KATP), an event that initiates the insulin secretory process. Defects in insulin secretion are a common feature of non-insulin-dependent diabetes mellitus (NIDDM), and the beta-cell KATP that couples metabolism and membrane potential is a candidate for contributing to the development of this clinically and genetically heterogeneous disorder. We screened a hamster insulinoma cDNA library by low-stringency hybridization with a probe coding for the G-protein-coupled inwardly rectifying K+ channel GIRK1/KGA and isolated clones encoding a protein, KATP-2, whose sequence is 90% similar to that of the recently described KATP-1, an ATP-sensitive K+ channel expressed in heart and other tissues. RNA blotting showed that KATP mRNA was present in insulin-secreting cells and brain but not in heart. To assess the contribution of KATP-2 to the development of NIDDM, the human KATP-2 gene (symbol KCNJ7) was isolated and mapped to chromosome band 21q22.1 by fluorescence in situ hybridization. A simple tandem repeat DNA polymorphism, D21S1255, was identified in the region of the KATP-2 gene, and linkage studies between this marker and NIDDM were carried out in a group of Mexican-American sib pairs with NIDDM. There was no evidence for linkage between D21S1255 and NIDDM, indicating that KATP-2 is not a major susceptibility gene in this population.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cromossomos Humanos Par 21 / Canais de Potássio / DNA Complementar / Diabetes Mellitus Tipo 2 Limite: Animals / Humans Idioma: En Ano de publicação: 1995 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Cromossomos Humanos Par 21 / Canais de Potássio / DNA Complementar / Diabetes Mellitus Tipo 2 Limite: Animals / Humans Idioma: En Ano de publicação: 1995 Tipo de documento: Article