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- W272742017 abstract "A locus contributing to IDD susceptibility has previously been mapped to a region on human chromosome 11p near the INS gene. To fine map the position of this susceptibility locus, polymorphisms in and flanking INS were analyzed in normal and IDD populations by PCR and restriction enzyme digestion. Regions flanking INS were not associated with IDD (p=NS). In contrast, homozygosity for the {open_quotes}+{close_quotes} INS allele was significantly increased in the IDD population (n=197) compared to 159 controls (RR=2.0, p<0.005), indicating an INS association with IDD. Transmission of the IDD-associated INS {open_quotes}+{close_quotes} alleles from parents to children in unaffected families was random (p=NS). However, in 107 multiplex and 15 simplex IDD families, transmission of the INS {open_quotes}+{close_quotes} allele from heterozygous parents to diabetic children revealed linkage of the INS gene to IDD (p<0.003). This linkage was limited to male meioses (p=0.01), suggest the potential for maternal imprinting of INS. The expression of the {open_quotes}+{close_quotes} and {open_quotes}-{close_quotes} INS allele was analyzed by RT-PCR in two normal heterozygous human fetal pancreases. Both transcripts were detected, indicating a lack of INS maternal imprinting in the human pancreas. Our results suggest that the IDD susceptibility locus on 11p is the INS gene, and that malemore » transmission bias of the INS gene in IDD can not be explained by maternal imprinting.« less" @default.
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- W272742017 modified "2023-09-23" @default.
- W272742017 title "The male transmission bias of the insulin (INS) gene in insulin-dependent diabetes (IDD) can not be explained by maternal imprinting" @default.
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