47
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.

      Proceedings of the National Academy of Sciences of the United States of America

      Animals, Apoptosis, Apoptosis Regulatory Proteins, Autophagy, Embryo, Mammalian, cytology, Gene Deletion, Genes, Tumor Suppressor, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, Transgenic, Microscopy, Electron, Models, Genetic, Mutation, Neoplasms, metabolism, Proteins, genetics, physiology, RNA, Messenger, Time Factors, Ultraviolet Rays

      Read this article at

      ScienceOpenPublisherPMC
      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 biochemical properties of beclin 1 suggest a role in two fundamentally important cell biological pathways: autophagy and apoptosis. We show here that beclin 1-/- mutant mice die early in embryogenesis and beclin 1+/- mutant mice suffer from a high incidence of spontaneous tumors. These tumors continue to express wild-type beclin 1 mRNA and protein, establishing that beclin 1 is a haploinsufficient tumor suppressor gene. Beclin 1-/- embryonic stem cells have a severely altered autophagic response, whereas their apoptotic response to serum withdrawal or UV light is normal. These results demonstrate that beclin 1 is a critical component of mammalian autophagy and establish a role for autophagy in tumor suppression. They both provide a biological explanation for recent evidence implicating beclin 1 in human cancer and suggest that mutations in other genes operating in this pathway may contribute to tumor formation through deregulation of autophagy.

          Related collections

          Author and article information

          Journal
          14657337
          299911
          10.1073/pnas.2436255100

          Comments

          Comment on this article