CoCl2 induces PC12 cells apoptosis through p53 stability and regulating UNC5B

Highlights • We demonstrate that p53 is upregulated and activated by CoCl2 -induced apoptosis in PC12 cells. • siRNA-mediated knockdown of p53 expression inhibits CoCl2 -induced apoptosis and downregulates UNC5B. • UNC5B is strongly upregulated by p53 in CoCl2 -induced PC12 cells. • Inhibition of UN...

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Bibliographic Details
Published in:Brain research bulletin 2013-07, Vol.96, p.19-27
Main Authors: Lee, Minjae, Kang, Hyereen, Jang, Sung-Wuk
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Caspase 3 - metabolism
Cell Death - drug effects
Cell Line, Tumor
Cobalt - pharmacology
CoCl2
Hypoxia
Nerve Growth Factors - metabolism
Nerve Growth Factors - pharmacology
Netrin-1
Neurology
p53
PC12 Cells
Rats
Receptors, Cell Surface - metabolism
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Tumor Suppressor Proteins - pharmacology
UNC5B
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Summary:Highlights • We demonstrate that p53 is upregulated and activated by CoCl2 -induced apoptosis in PC12 cells. • siRNA-mediated knockdown of p53 expression inhibits CoCl2 -induced apoptosis and downregulates UNC5B. • UNC5B is strongly upregulated by p53 in CoCl2 -induced PC12 cells. • Inhibition of UNC5B signaling significantly blocks hypoxia-induced apoptosis in response to netrin-1.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2013.04.007