Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 22, Issue 2, Pages 181-185Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2009.12.001
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Funding
- Ligue Nationale contre le Cancer (Equipe labellisee)
- Agence Nationale pour la Recherche (ANR)
- European Commission
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Cancerpole Ile-de-France
- European Union
- ApopTrain
- EMBO
- Higher Education Commission (HEC) of Pakistan
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Autophagy is an evolutionarily conserved catabolic pathway that is involved in numerous physiological processes and in multiple pathological conditions including cancer. Autophagy is regulated by an intricate network of signaling cascades that have not yet been entirely disentangled. Accumulating evidence indicates that p53, the best-characterized human tumor suppressor protein, can modulate autophagy in a dual fashion, depending on its subcellular localization. On the one hand, p53 functions as a nuclear transcription factor and transactivates proapoptotic, cell cycle-arresting and proautophagic genes. On the other hand, cytoplasmic p53 can operate at mitochondria to promote cell death and can repress autophagy via poorly characterized mechanisms. This review focuses on the recently discovered function of p53 as a master regulator of autophagy.
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