58
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene

      , , , ,
      Cell
      Elsevier BV

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The c-abl proto-oncogene, which encodes a cytoplasmic protein-tyrosine kinase, is expressed throughout murine gestation and ubiquitously in adult mouse tissues. However, its levels are highest in thymus, spleen, and testes. To examine the in vivo role of c-abl, the gene was disrupted in embryonic stem cells, and the resulting genetically modified cells were used to establish a mouse strain carrying the mutation. Most mice homozygous for the c-abl mutation became runted and died 1 to 2 weeks after birth. In addition, many showed thymic and splenic atrophy and a T and B cell lymphopenia.

          Related collections

          Most cited references24

          • Record: found
          • Abstract: found
          • Article: not found

          The protein kinase family: conserved features and deduced phylogeny of the catalytic domains.

          In recent years, members of the protein kinase family have been discovered at an accelerated pace. Most were first described, not through the traditional biochemical approach of protein purification and enzyme assay, but as putative protein kinase amino acid sequences deduced from the nucleotide sequences of molecularly cloned genes or complementary DNAs. Phylogenetic mapping of the conserved protein kinase catalytic domains can serve as a useful first step in the functional characterization of these newly identified family members.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Disruption of the proto-oncogene int-2 in mouse embryo-derived stem cells: a general strategy for targeting mutations to non-selectable genes.

            Gene targeting--homologous recombination of DNA sequences residing in the chromosome with newly introduced DNA sequences--in mouse embryo-derived stem cells promises to provide a means to generate mice of any desired genotype. We describe a positive nd negative selection procedure that enriches 2,000-fold for those cells that contain a targeted mutation. The procedure was applied to the isolation of hprt- and int-2- mutants, but it should be applicable to any gene.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Germ-line transmission of genes introduced into cultured pluripotential cells by retroviral vector.

              Embryonic stem cells isolated directly from mouse embryos can be cultured for long periods in vitro and subsequently repopulate the germ line in chimaeric mice. During the culture period these embryonic cells are accessible for experimental genetic manipulation. Here we report the use of retroviral vectors to introduce exogenous DNA sequences into a stem-cell line and show that these modified cells contribute extensively to the somatic and germ-cell lineages in chimaeric mice. Compared with current methods for manipulation of the mouse genome, this approach has the advantage that powerful somatic-cell genetic techniques can be used to modify and to select cells with germ-line potential, allowing the derivation of transgenic strains with pre-determined genetic changes. We have by this means inserted many proviral vector sequences that provide new chromosomal molecular markers for linkage studies in the mouse and that also may cause insertional mutations.
                Bookmark

                Author and article information

                Journal
                Cell
                Cell
                Elsevier BV
                00928674
                June 1991
                June 1991
                : 65
                : 7
                : 1153-1163
                Article
                10.1016/0092-8674(91)90011-M
                2065352
                d7784bba-497b-404e-b654-8d124ab62fcd
                © 1991

                https://www.elsevier.com/tdm/userlicense/1.0/

                History

                Comments

                Comment on this article