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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Veröffentlicht in:	Brain research bulletin 2013-07, Vol.96, p.19-27
Hauptverfasser:	Lee, Minjae, Kang, Hyereen, Jang, Sung-Wuk
Format:	Artikel
Sprache:	eng
Schlagworte:	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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Zusammenfassung:	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