TY - JOUR
T1 - Autophagy regulation by p53
AU - Maiuri, Maria Chiara
AU - Galluzzi, Lorenzo
AU - Morselli, Eugenia
AU - Kepp, Oliver
AU - Malik, Shoaib Ahmad
AU - Kroemer, Guido
N1 - Funding Information:
GK is supported by the Ligue Nationale contre le Cancer (Equipe labellisée), Agence Nationale pour la Recherche (ANR), European Commission (Apo-Sys, ChemoRes, ApopTrain, Active p53), Fondation pour la Recherche Médicale (FRM), Institut National du Cancer (INCa), and Cancéropôle Ile-de-France. LG is supported by the Apo-Sys consortium of the European Union. EM is funded by a PhD student grant from ApopTrain. OK receives a postdoctoral fellowship from EMBO. SAM receives a grant from the Higher Education Commission (HEC) of Pakistan.
PY - 2010/4
Y1 - 2010/4
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=77951243028&partnerID=8YFLogxK
U2 - 10.1016/j.ceb.2009.12.001
DO - 10.1016/j.ceb.2009.12.001
M3 - Review article
C2 - 20044243
AN - SCOPUS:77951243028
SN - 0955-0674
VL - 22
SP - 181
EP - 185
JO - Current Opinion in Cell Biology
JF - Current Opinion in Cell Biology
IS - 2
ER -
