 |
| Search |
|
|
|
|
Hometown:
Tianjin, P.R.
China
Undergraduate/Masters Institution:
Peking
University,
Health Science Center
Master and Bachelor of
Medicine
General Research
Interests:
Neuroscience
|
| |
I am interested in p53-regulated
neural stem cell
apoptosis |
|
Regulation of neural precursor cell
(NPC) death is important for both normal nervous system development and proper
neurological function in the adult. p53 has been shown to be a key regulator of
NPC apoptosis.
Our previous studies showed that p53 deficiency blocked
cerebellar NPC death in response to staurosporine, a broad spectrum protein
kinase inhibitor, and genotoxic agents e.g. cytosine arabinoside (AraC) or
bleomycin. Genotoxic agents, but not staurosporine, increased p53-dependent gene
transcription, and deficiency of PUMA, a p53 transcriptionally regulated
pro-apoptotic molecule, decreased genotoxin-induced, but not
staurosporine-induced NPC death.
In this study, we used C17.2 cells, a
mouse cerebellar NPC line, with high endogenous p53 expression, to further
characterize p53 function in NPC death. C17.2 cells exposed to either
staurosporine or genotoxic agents showed increased caspase-3 activation and
decreased cell viability, which was inhibited by BAF, a broad spectrum caspase
inhibitor. The genotoxin-induced caspase-3 activation was also inhibited by
cycloheximide (CHX), a protein synthesis inhibitor. In contrast, CHX had no
effect on staurosporine-induced caspase-3 activation. Genotoxic agents increased
nuclear p53 immunoreactivity, while staurosporine induced cytoplasmic p53
accumulation.
Combined with our previous findings, these results suggest
that genotoxic agents induce p53 transcription-dependent NPC death, while
staurosporine induces p53 transcription-independent NPC death. |
Previous | Molecular &
Cellular Pathology Graduate Student Profiles | Next
|
© Copyright by the University of Alabama at Birmingham
Site Last Updated: May 10th, 2007 - 10:01:05
Top of Page
|
| |
