Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012872 (DNA marker)
 929 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genetic basis of various subtypes of the affective disorders has been investigated by family, twin, and adoption studies, as well as by segregation and linkage analysis. Linkage analyses of bipolar disorder with the chromosome 11p15 DNA markers HRAS1 and INS, and the chromosome Xq28 markers for color blindness and G6PD have been reported. We have used restriction fragment length polymorphisms as markers to examine linkage in three extended families with unipolar affective illness, ascertained through probands with either recurrent unipolar or bipolar II illness. Using an inclusive definition of the affected phenotype, linkage could be excluded up to 28cM around the HRAS1-INS linkage group on chromosome 11p15, and up to 5 cM around the DNA marker DXS52 on Xq28. Negative linkage results were also obtained for two more restrictive definitions of affective illness. Thus, we find no evidence for the involvement of the chromosomal regions 11p15 and Xq28 with unipolar affective disorder in these three families.
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PMID:Evidence against close linkage of unipolar affective illness to human chromosome 11p markers HRAS1 and INS and chromosome Xq marker DXS52. 197 4

The etiology of non-insulin-dependent diabetes mellitus (NIDDM) is still unclear, but appears to involve some genetic factors. There have been disputes over the association between DNA sequences flanking the insulin gene and NIDDM. In order to characterize insulin gene polymorphism in the Chinese population and elucidate its association with NIDDM, 100 unrelated Chinese subjects living in Taiwan were observed for polymorphism of this hypervariable region. Most of them were descendants of immigrants from the southern part of mainland China. Among them, 52 were nondiabetic controls, and 48 were subjects with NIDDM. Insulin gene polymorphism was classified into classes 1, 2 and 3 alleles according to Bell et al. Neither the class 2 allele nor the genotype for the homozygous class 3 allele was not observed in this study. The allelic frequencies of class 1 and 3 genes were 97% and 3% in the nondiabetic subjects, and 99% and 1% in the NIDDM group, respectively. The frequencies of genotypes 1/1 and 1/3 were 94% and 6% in nondiabetics and 98% and 2% in the NIDDM group, respectively. No significant association was found between insulin gene polymorphism and NIDDM. It is concluded that DNA marker flanking the insulin gene may not be associated with the development of NIDDM in Chinese subjects.
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PMID:Polymorphic locus in the 5'-flanking region of human insulin gene and non-insulin-dependent diabetes mellitus. 198 27

A low acute insulin response (AIR) is a predictor of non-insulin-dependent diabetes mellitus (NIDDM) in insulin-resistant Pima Indians. We have initiated a search for regions of the genome linked with the AIR using sib-pair linkage analysis as a first step in identifying genes that are determinants of this phenotype. Eighteen short tandem-repeat polymorphisms from chromosome 1 were genotyped in over 900 Pima Indians and tested for linkage with NIDDM and in a subset of Pima Indians for linkage with AIR. The anonymous DNA marker D1S198 on chromosome 1p was linked with AIR (P = 0.000056) in 175 sib pairs from 60 families, all with normal glucose tolerance, but no linkage was observed between D1S198 and NIDDM (P = 0.44, 996 sib pairs). Additional markers genotyped on chromosome 1 did not show linkage with AIR or NIDDM. This study indicates that a locus on chromosome 1p may be a determinant of the phenotypic variation seen in the AIR.
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PMID:Evidence for linkage between a region on chromosome 1p and the acute insulin response in Pima Indians. 769 19