3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Cell-signaling targets for antitumour drug development

      ,
      Cancer Chemotherapy and Pharmacology
      Springer Nature

      Read this article at

      ScienceOpenPublisher
      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.

          Related collections

          Most cited references105

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

          Cancer. p53, guardian of the genome.

          D P Lane (1992)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours.

            Mutations in the p53 tumour-suppressor gene are the most frequently observed genetic lesions in human cancers. To investigate the role of the p53 gene in mammalian development and tumorigenesis, a null mutation was introduced into the gene by homologous recombination in murine embryonic stem cells. Mice homozygous for the null allele appear normal but are prone to the spontaneous development of a variety of neoplasms by 6 months of age. These observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation.

              A cellular phosphoprotein with an apparent molecular mass of 90 kd (p90) that forms a complex with both mutant and wild-type p53 protein has been characterized, purified, and identified. The protein was identified as a product of the murine double minute 2 gene (mdm-2). The mdm-2 gene enhances the tumorigenic potential of cells when it is overexpressed and encodes a putative transcription factor. To determine if mdm-2 could modulate p53 transactivation, a p53-responsive element from the muscle creatine kinase gene was employed. A wild-type p53-expressing plasmid enhanced the expression of the p53-responsive element when cotransfected into cells that contain no endogenous p53. When a cosmid expressing mdm-2 was transfected with this p53-expressing plasmid, the transactivation of the p53-responsive element was inhibited. Thus, a product of the mdm-2 oncogene forms a tight complex with the p53 protein, and the mdm-2 oncogene can inhibit p53-mediated transactivation.
                Bookmark

                Author and article information

                Journal
                Cancer Chemotherapy and Pharmacology
                Cancer Chemother. Pharmacol.
                Springer Nature
                0344-5704
                1432-0843
                1993
                1993
                : 32
                : 1
                : 1-19
                Article
                10.1007/BF00685870
                d51d7c83-7762-451b-ba81-2558aedc3503
                © 1993
                History

                Comments

                Comment on this article