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Biomedical subjects

T B Shows

Publications and source records attributed to T B Shows.

At least 379 records · Page 21Linked to original sources
PubMed1974

Human beta-D-N-acetylhexosaminidases A and B: expression and linkage relationships in somatic cell hybrids.

Knowledge of the genetic relationships between beta-D-N-acetylhexosaminidases A and B (EC 3.2.1.30) may help in understanding the hexosaminidase deficiency associated with GM(2) gangliosidosis, a fatal lipid storage disease in man. Through the use of man-mouse somatic cell hybrids we have found that a gene involved in hexosaminidase A expression was linked to the genes coding for mannosephosphate isomerase and pyruvate kinase-3. The gene coding for hexosaminidase B was not linked to any of the genes coding for 25 enzyme markers tested. A combination of immunological and electrophoretic techniques was employed to identify human hexosaminidases A and B with certainty in cell hybrids. Discordant segregation of hexosaminidase A and hexosaminidase B in 60 clones indicated that the genes coding for their expression were not linked. However, hexosaminidase A was never expressed in cell hybrids in the absence of hexosaminidase B. This suggests that the gene responsible for the hexosaminidase A phenotype, linked to mannosephosphate isomerase and pyruvate kinase-3, requires the presence of the gene coding for hexosaminidase B for the expression of hexosaminidase A. These observations offer a genetic explanation for the biochemical and immunological relationships between hexosaminidases A and B and provide the framework for identifying the basic genetic defects responsible for GM(2) gangliosidosis.

Animals↗
PubMed1972

Human-mouse cell hybrids: a suggestion of structural mutation for dipeptidase-2 deficiency in mouse cells.

The dipeptidase-2 enzyme is inactive in certain cultured cell lines from the mouse. In somatic cell hybrids between such deficient cells and diploid human fibroblasts, the mouse deficiency was complemented when the homologous human peptidase-A was retained. The results suggested that the murine peptidase deficiency was the result of a structural mutation, rather than a regulatory one.

Animals↗
PubMed1972

Genetics of human-mouse somatic cell hybrids: linkage of human genes for lactate dehydrogenase-A and esterase-A 4 .

By use of human-mouse somatic cell hybrids, an autosomal gene linkage has been determined for the human loci controlling the phenotypes of lactate dehydrogenase-A (EC 1.1.1.27) and esterase-A(4) (EC 3.1.1.2). These structural loci were not linked to the lactate dehydrogenase-B, peptidase-B linkage, the X chromosome, the E(17) chromosome, or to nine other enzyme phenotypes examined.

Animals↗
PubMed1968

Malate dehydrogenase: evidence for tetrameric structure in Mus musculus.

Two electrophoretically distinct variants of supernatant nicotinamideadenine dinucleotide phosphate-dependent malate dehydrogenase exist in mice (Mus musculus). They are controlled by codominant alleles segregating at an autosomal locus. The two forms exist in a polymorphic condition in wild populations of Mus musculus and are fixed in a homozygous condition in inbred lines. These genetic electrophoretic variants are used here to study the subunit structure of this enzyme. Evidence indicating a tetrameric structure for mouse nicotinamideadenine dinucleotide phosphate-dependent malate dehydrogenase is presented. This interpretation is based on the occurrence in heterozygote tissue extracts of five electrophoretically distinct enzymes. This is the predicted phenotype for tetramers composed of two types of subunits which associate randomly in heterozygotes forming three hybrid enzymes having mobilities intermediate between the parental forms.

Alleles↗