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D Owerbach

Publications and source records attributed to D Owerbach.

54 records · Page 3Linked to original sources
PubMed1983

Detection of HLA-D/DR-related DNA polymorphism in HLA-D homozygous typing cells.

Sequences of different sizes are generated when DNA from homozygous HLA-Dw/DR typing cells are digested with restriction endonuclease and analyzed by hybridization with a HLA-D region class II antigen beta-chain cDNA probe. The patterns of hybridization were highly polymorphic but one endonuclease, BamHI, defined sequences unique to all HLA-Dw/DR specificities 1-8 except HLA-Dw/DR 2 and 6; however, these two specificities were resolved with the enzyme EcoRI. Digestion with other endonucleases such as Pst I results in patterns of restriction fragments that differ between homozygous typing cells of the same HLA-Dw/DR specificity. HLA-D region beta-chain probes permit HLA-D region genotyping at the DNA level and may allow detection of genes controlling the association of HLA specificities with a wide variety of diseases.

DNA↗
PubMed1982

Possible association between DNA sequences flanking the insulin gene and atherosclerosis.

The proportion of subjects homozygous for DNA restriction fragments of a large size class (U alleles), in the polymorphic region flanking the 5' end of the insulin gene of chromosome 11, was higher in a group of non-insulin-dependent diabetic (NIDDM) patients than in normal controls. This finding confirms that the U allele is associated with at least one form of NIDDM. The U alleles were also found to be strongly associated with macroangiopathy in diabetic as well as in non-diabetic subjects. Thus, DNA sequences contained in the U alleles might be associated with the development of atherosclerosis in an as yet unknown way.

Alleles↗
PubMed1982

DNA insertion sequences near the insulin gene affect glucose regulation.

There is restriction-fragment length polymorphism in the 5'-flanking region of the insulin gene on the short arm of chromosome 11 in man. The polymorphic DNA sequences in 53 members of a large family were analysed by means of the restriction endonuclease BglI. In this family, the BglI restriction fragments were found in four sizes--2.8 kilobases (kb), 2.9 kb, 4.6 kb, and 4.8 kb. They segregated as alleles. The two larger BglI restriction fragments (U alleles) were associated with high haemoglobin Alc levels in both blood-related and unrelated non-diabetic members of the family.

Adolescent↗
PubMed1982

New approaches to therapy and diagnosis of diabetes.

Recent progress within the field of molecular biology has resulted in the development of a new technology known as 'recombinant DNA'. This technology deals with a number of biochemical techniques for handling DNA which include: (1) cutting DNA at specific sites, (2) inserting DNA into bacteria or mammalian cells so that the cell will replicate the DNA and (3) manipulation of cloned DNA so that the host cell makes the protein for which the DNA codes [1-3]. Already a number of hormones including somatostatin, human growth hormone and human insulin [4] have been produced by these new methods. However, there are certain criteria which should be considered before new sources of hormones are generally accepted for treatment of human diseases. We shall review some of the problems which may arise in the case of insulin, by comparing the chemical and immunological properties of insulin from various sources. Recombinant DNA methods have, in addition, made it possible to study islet cell structure and function at the gene level. These studies include analysis of gene structure and of how they are transcribed and translated. Structural analyses which seem to be significant in the differential diagnosis of diabetes will be reviewed.

Animals↗
PubMed1982

Restriction fragment length polymorphism of the insulin gene in diabetes mellitus.

Variant DNA sequences flanking the human insulin gene were found in the Danish population using restriction endonucleases (restriction fragment length polymorphism). The frequencies of these DNA sequences were determined in 47 non-insulin-dependent diabetics and 93 control individuals. We report an association between a restriction fragment length polymorphism of the insulin gene and NIDDM.

Base Sequence↗
PubMed1981

On the mechanism of variation of pancreatic amylase levels in mouse strains.

The relative levels of pancreatic amylase mRNA closely parallel the 3-fold variation of pancreatic amylase protein levels observed in several mouse strains studied. In contrast pancreatic elastase mRNA levels were similar in these strains. Each of the strains contained the same number of amylase-like genes (about 8). The selective variation in the pancreatic amylase gene expression could be due either to differences in the numbers of active amylase genes or to different rates of synthesis and/or degradation of the amylase mRNA from a constant number of genes.

Amylases↗
PubMed1981

The prolactin gene is located on chromosome 6 in humans.

The gene for prolactin has been located on chromosome 6 in humans. DNA fragments of 4.8 and 4.0 kilobases containing prolactin gene sequences were identified in human genomic DNA, whereas DNA fragments of 7.4, 3.6, and 3.3 kilobases containing prolactin gene sequences were found in mouse cells. In somatic cell hybrids of human and mouse cells the 7.4-, 3.6-, and 3.3-kilobase mouse fragments were always present, whereas the 4.8- and 4.0-kilobase human fragments were only present when human chromosome 6 was also present. We conclude that the prolactin gene resides on chromosome 6, a different location from those of the genes for the related hormones chorionic somatomammotropin and growth hormone.

Animals↗
PubMed1981

The proopiocortin (adrenocorticotropin/beta-lipoprotein) gene is located on chromosome 2 in humans.

The proopiocortin gene is located on chromosome 2 in humans. A 13-kb DNA fragment containing proopiocortin gene sequences was identified in human cells while proopiocortin-related genes sequences of 9.8 and 6.2 kb were present in mouse cells. In human-mouse cell hybrids which contained reduced numbers of human chromosomes and a complete set of mouse chromosomes, the 9.8- and 6.2-kb fragments were always present while the 13-kb fragment segregated with human chromosome 2 and the chromosome 2 enzyme markers acid phosphatase-1 (ACP1), malate dehydrogenase-1 (MDHI), and isocitrate dehydrogenase-1 (IDH1). Analysis of a single cell hybrid with a broken chromosome 2 indicates that the proopiocortin and ACP1 genes are closely linked and in the distal region of the short arm of chromosome 2.

Animals↗
PubMed1981

Leukocyte and fibroblast interferon genes are located on human chromosome 9.

At least eight leukocyte interferon genes (IFL) and the single fibroblast interferon gene (IFF) have been located on chromosome 9 in humans. In somatic cell hybrids of human and mouse cells containing a normal complement of mouse parental cell chromosomes but reduced numbers of human chromosomes, the human leukocyte and fibroblast interferon DNA sequences were present only when human chromosome 9 was also present.

Animals↗
PubMed1981

The insulin gene is located on the short arm of chromosome 11 in humans.

The human insulin gene has been previously localized to chromosome 11. We have analyzed the human DNA sequences present in a human-mouse somatic cell hybrid line possessing a translocation involving human chromosomes 11 and X. These data indicate that the human insulin gene is located on the short arm of chromosome 11 in the region p13 leads to pter.

Animals↗
PubMed1980

Genes for growth hormone, chorionic somatommammotropin, and growth hormones-like gene on chromosome 17 in humans.

The human genes for growth hormone (GH), chorionic somatomammotropin (CSH), and a third growth hormone-like gene (GHL) have been located on chromosome 17 in humans. DNA fragments of 2.6, 2.8, and 9.5 kilobase pairs containing GH, CSH, and GHL, respectively, were identified in human genomic DNA, and a 7.5-kilobase DNA fragment related to growth hormone DNA sequences was found in mouse cells. In somatic hybrids of human and mouse cells containing reduced numbers of human chromosomes, but a normal complement of mouse chromosomes, the mouse, 7.5-kolobase DNA fragment was always present, whereas the 2.6-, 2.8-, and 9.5-kilobase human fragments were present only when human chromosome 17 was also present.

Animals↗
PubMed1980

Inheritance of a parotid secretory protein in mice and its use in determining salivary amylase quantitative variants.

Among inbred strains of mice, a major protein, PSP, produced and secreted by the parotid glands, shows variation in electrophoretic mobility and in the peptides produced by cyanogen bromide treatment. This variation is inherited as a single Mendelian factor with two alleles showing co-dominant expression. In genetic crosses, it segregates independently from the amylase complex and is closely linked to the agouti locus on chromosome 2. The protein ratios between amylase and PSP in saliva, obtained by scanning of electrophoretic gel separations, were found to reflect genetic differences in salivary amylase production in strains YBR/Cv and C3H/As.

Alleles↗
PubMed1978

Genetics of the large, external, transformation-sensitive (LETS) protein: assignment of a gene coding for expression of LETS to human chromosome 8.

Techniques have been developed to analyze the genetics of the large, external, transformation-sensitive (LETS) protein (fibronectin). External membrane proteins of human-mouse somatic cell hybrids with reduced numbers of human but not mouse chromosomes were labeled by lactoperoxidase-catalyzed iodination. Cell surface proteins were identified after sodium dodecyl sulfate/polyacrylamide gel electrophoresis by autoradiography of the dried gel. The LETS protein was identified in parental human cells, and LETS segregated in human-mouse cell hybrids formed from human WI-38 fibroblasts and a mouse L-cell line not expressing LETS. The LETS protein segregated concordantly with the chromosome 8 enzyme marker glutathione reductase (EC 1.6.4.2) and human chromosome 8. These findings demonstrate that a gene, LETS, encoded on chromosome 8, is responsible for the LETS protein expression in humans. Because LETS has been implicated in tumorigenicity and cellular transformation, it is of interest that rearrangement or modifications in the number of chromosome 8 have been associated with certain forms of cancer.

Animals↗
PubMedDate not supplied

Linkage analyses in type I diabetes mellitus using CASPAR, a software and statistical program for conditional analysis of polygenic diseases.

We have developed software and statistical tools for linkage analysis of polygenic diseases. We use type I diabetes mellitus (insulin-dependent diabetes mellitus, IDDM) as our model system. Two susceptibility loci (IDDM1 on 6p21 and IDDM2 on 11p15) are well established, and recent genome searches suggest the existence of other susceptibility loci. We have implemented CASPAR, a software tool that makes it possible to test for linkage quickly and efficiently using multiple polymorphic DNA markers simultaneously in nuclear families consisting of two unaffected parents and a pair of affected siblings (ASP). We use a simulation-based method to determine whether lod scores from a collection of ASP tests are significant. We test our new software and statistical tools to assess linkage of IDDM5 and IDDM7 conditioned on analyses with 1 or 2 other unlinked type I diabetes susceptibility loci. The results from the CASPAR analysis suggest that conditioning of IDDM5 on IDDM1 and IDDM4, and of IDDM7 on IDDM1 and IDDM2 provides significant benefits for the genetic analysis of polygenic loci.

Alleles↗