Abstract
Several recent studies provided evidence that PUMA, a pro-apoptotic member of the BH3-only protein subgroup of the Bcl-2 family, is critical for restricting survival and recovery of different cell types, including those of the hematopoietic system, after γ-irradiation (IR)-triggered DNA damage. According to its pro-apoptotic function downstream of p53, PUMA is considered to act as a tumor suppressor. While this expectation was met in a model of oncogene-driven lymphomagenesis or carcinogen-driven tumor formation in the gut, studies on IR-driven tumor formation revealed surprising new insights into the role of p53-triggered and PUMA-mediated apoptosis in tumorigenesis and stem cell homeostasis.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis
-
Apoptosis Regulatory Proteins / genetics
-
Apoptosis Regulatory Proteins / metabolism*
-
Apoptosis Regulatory Proteins / physiology
-
Cell Line
-
Cyclin-Dependent Kinase Inhibitor p16 / metabolism
-
DNA Damage
-
Hematopoietic Stem Cells / metabolism
-
Humans
-
Mice
-
Mice, Knockout
-
Proto-Oncogene Proteins / genetics
-
Proto-Oncogene Proteins / metabolism*
-
Proto-Oncogene Proteins / physiology
-
Proto-Oncogene Proteins c-bcl-2 / metabolism
-
Scattering, Radiation
-
Tumor Suppressor Protein p53 / genetics
-
Tumor Suppressor Protein p53 / metabolism
Substances
-
Apoptosis Regulatory Proteins
-
BBC3 protein, human
-
Cyclin-Dependent Kinase Inhibitor p16
-
PMAIP1 protein, human
-
Proto-Oncogene Proteins
-
Proto-Oncogene Proteins c-bcl-2
-
Tumor Suppressor Protein p53