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Biomedical subjects

D Robins

Publications and source records attributed to D Robins.

25 records · Page 2Linked to original sources
PubMed1982

The effect of exogenous DNA insertion at a chromosomal region containing rDNA.

We have previously shown that exogenous DNA may be incorporated into host cell chromosomes following DNA-mediated gene transfer (transformation). Discrete chromosomal changes often accompany the integration event. In this study, the effect of integration of DNA that codes for human growth hormone into a region containing ribosomal DNA in rat chromosomes was investigated. The results show that insertion of exogenous DNA results in the inactivation of the ribosomal DNA and a partial deletion of ribosomal DNA sequences.

Animals↗
PubMed1980

Altering genotype and phenotype by DNA-mediated gene transfer.

Transformation, or DNA-mediated gene transfer, permits the introduction of new genetic information into a cell and frequently results in a change in phenotype. The transforming DNA is ultimately integrated into a recipient cell chromosome. No unique chromosomal locations are apparent, different lines contain the transforming DNA on different chromosomes. Expression of transformed genes frequently results in the synthesis of new polypeptide products which restore appropriate mutant cells to the wild-type phenotype. Thus transformation provides an in vivo assay for the functional role of DNA sequence organization about specific genes. Transforming genes coding for selectable functions, such as adenine phosphoribosyltransferase or thymidine kinase, have now been isolated by utilizing transformation in concert with molecular cloning. Finally, transformation may provide a general approach to the analysis of complex heritable phenotypes by permitting the distinction between phenotypic changes without concomitant changes in DNA and functional genetic rearrangements.

Adenine Phosphoribosyltransferase↗
PubMed1977

Salt-losing syndrome in 2 infants with defective 18-dehydrogenation in aldosterone biosynthesis.

Two infants presented with a salt-losing syndrome, the presenting features of which were subtle. One case appeared to be transient. Deficient production of aldosterone was shown by plasma renin activity and plasma aldosterone profile. Gas chromatography-mass spectrometry of urine indicated a defect in 18-dehydrogenation of 18-hydroxycorticosterone. Treatment with salt supplements and 9alpha-fludrocortisone reversed the salt-losing state and in one case treatment was later stopped. Although the disease may appear transient, the biochemical defect is persistent and for adequate growth a positive salt-balance is necessary.

18-Hydroxycorticosterone↗