Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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

http://www.ncbi.nlm.nih.gov/pubmed/14657337

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.

Pubmed ID: 14657337 RIS Download

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

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Mouse Genome Informatics (Data, Gene Annotation)

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.