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  • 1
    Electronic Resource
    Electronic Resource
    Identification of two novel amino acid polymorphisms in beta-cell/liver (GLUT2) glucose transporter in Japanese subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 211-215 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetes ; glucose transporter ; insulin receptor substrate-1 ; insulin ; genetics.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The beta-cell/liver glucose transporter (GLUT2) gene was screened for mutations using single-strand conformation polymorphism analysis (SSCP) in 30 Japanese subjects with non-insulin dependent diabetes mellitus (NIDDM). Analysis of all exons and adjacent intron regions identified six SSCP polymorphisms, three of which resulted in amino acid substitutions: V101I, T110I and G519E. The V101I and G519E substitutions represent new polymorphisms in this gene. The six polymorphisms were observed in both NIDDM and control groups and there were no significant differences in allele frequencies between groups. A portion of the insulin receptor substrate 1 gene in 30 NIDDM subjects and in normal control subjects was also screened for mutations. Two SSCP variants that change the sequence of the protein, ΔS686/687 (deletion of the codons for serine-686 and 687) and G972R, were identified in two different NIDDM subjects, both whom were also heterozygous for the V101I polymorphism in GLUT2. The GLUT2 and IRS1 amino acid polymorphisms did not show a simple pattern of co-inheritance with NIDDM in the families of these subjects suggesting that neither polymorphism is sufficient to cause NIDDM but may increase diabetes-susceptibility through their interaction with other loci and environmental factors. [Diabetologia (1995) 38: 211–215]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400096
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Identification of two novel amino acid polymorphisms in beta-cell/liver (GLUT2) glucose transporter in Japanese subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 211-215 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes ; glucose transporter ; insulin receptor substrate-1 ; insulin ; genetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The beta-cell/liver glucose transporter (GLUT2) gene was screened for mutations using single-strand conformation polymorphism analysis (SSCP) in 30 Japanese subjects with non-insulin dependent diabetes mellitus (NIDDM). Analysis of all exons and adjacent intron regions identified six SSCP polymorphisms, three of which resulted in amino acid substitutions: V101I, T110I and G519E. The V101I and G519E substitutions represent new polymorphisms in this gene. The six polymorphisms were observed in both NIDDM and control groups and there were no significant differences in allele frequencies between groups. A portion of the insulin receptor substrate 1 gene in 30 NIDDM subjects and in normal control subjects was also screened for mutations. Two SSCP variants that change the sequence of the protein, δS686/687 (deletion of the codons for serine-686 and 687) and G972R, were identified in two different NIDDM subjects, both whom were also heterozygous for the V101I polymorphism in GLUT2. The GLUT2 and IRS1 amino acid polymorphisms did not show a simple pattern of co-inheritance with NIDDM in the families of these subjects suggesting that neither polymorphism is sufficient to cause NIDDM but may increase diabetes-susceptibility through their interaction with other loci and environmental factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400096
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Overproduction of Cdc24p (Cls4p), a guanine nucleotide-exchange factor toward Cdc42 GTPase, impairs initiation of budding inSaccharomyces cerevisiae (1995)
    Springer
    Protoplasma 189 (1995), S. 142-148 
    Details
    ISSN: 1615-6102
    Keywords: Cell polarity ; Budding yeast ; Calcium ; CLS4 gene ; CDC24 gene ; Overexpression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary An entire coding region of theCDC24/CLS4 gene and its truncated derivatives were overexpressed in yeast cells under the control of theGAL1 promoter. Western blotting analysis of the yeast cell lysates showed that the CDC24/CLS4 protein (Cdc24p) was induced to reach its maximum level after 9 h incubation of the cells in galactose medium. Overexpression of Cdc24p within the cells caused the morphological change, accumulating large spherical unbudded cells which exhibited actin cytoskeleton disturbed, chitin delocalized on the cell surface, and cell viability decreased. Multiple nuclei were observed in these cells, indicating that only budding cycle but not nuclear division cycle is blocked by the overproduction of Cdc24p. In order to identify the region of Cdc24p responsible for the growth inhibition, several truncatedCDC24 genes were expressed. Surprisingly, overexpression of fragments either containing the C-terminal 76 amino acid residues or deleting the same region inhibited cellular growth. This suggests that Cdc24p contains multiple functional domains for its tasks, likely cooperating signals of bud positioning and bud timing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01280167
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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