A Sands

Publications (3)43.59 Total impact

• Article: Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2.

  S K Sharan, M Morimatsu, U Albrecht, D S Lim, E Regel, C Dinh, A Sands, G Eichele, P Hasty, A Bradley
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  ABSTRACT: Inherited mutations in the human BRCA2 gene cause about half of the cases of early-onset breast cancer. The embryonic expression pattern of the mouse Brca2 gene is now defined and an interaction identified of the Brca2 protein with the DNA-repair protein Rad51. Developmental arrest in Brca2-deficient embryos, their radiation sensitivity, and the association of Brca2 with Rad51 indicate that Brca2 may be an essential cofactor in the Rad51-dependent DNA repair of double-strand breaks, thereby explaining the tumour-suppressor function of Brca2.
  Nature 05/1997; 386(6627):804-10. · 36.28 Impact Factor
• Article: Gene-targeting and the p53 tumor-suppressor gene.

  A Sands, L A Donehower, A Bradley
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  ABSTRACT: Gene-targeting techniques are now frequently applied to embryonic stem (ES) cells to introduce mutations of endogenous genes in mice. Modifications introduced into tumor-suppressor genes by this technology have produced mice and cell lines with unique tumorigenic and growth characteristics, respectively. A number of strategies have been developed to enhance the efficiency of homologous recombination between targeting vectors and endogenous genes. This review describes recent advances in the techniques used to construct mice with a variety of genetic alterations. In addition, an application of gene-targeting is illustrated in the study of a class of genes with tumor-suppressor function. Recent findings from experiments using gene targeted mice to study the p53 tumor-suppressor gene are discussed and the potential of gene-targeting for the discovery and study of novel tumor-suppressor genes are explored.
  Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 07/1994; 307(2):557-72. · 2.85 Impact Factor
• Article: A tyrosine aminotransferase glucocorticoid response element also mediates androgen enhancement of gene expression.

  S H Denison, A Sands, D J Tindall
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  ABSTRACT: A glucocorticoid response element of the tyrosine aminotransferase gene was demonstrated to mediate effects of androgen when located upstream of a heterologous promoter linked to the chloramphenicol acetyl transferase gene (CAT).
  Endocrinology 03/1989; 124(2):1091-3. · 4.46 Impact Factor