The Role Of Antibodies In Cobalt Chloride Induced Apoptosis In PC12 Cells

Mon, 12/07/2009 - 10:00

Various studies have been performed tracking the involvement of p38 mitogen-activated protein kinase (MAPK) and caspase-3 antibodies in cobalt chloride (CoCl2) induced apoptosis in PC12 cells.

Studies have proven the usefulness of CoCl2 treatment to induce apoptosis in PC12 rat tumor cells. Treating these cells with CoCl2 leads to programmed cell death (apoptosis). Such cells provide a simple and useful model for the study of hypoxia-related neuronal disorders, as hypoxia involves a lack of oxygen.

The mechanism of action is known to involve caspase cleavage. Antibody suppliers, such as Novus Biologicals, supply caspase and p38 antibody preparations, which are then used to study caspase cleavage in PC12 cells. p38 MAP Kinase (MAPK), also known as RK and CSBP, is known to be a pro-apoptotic factor, which when activated leads to the cleavage of caspase-3; thus, MAPK antibodies and caspase-3 antibodies are often used in tandem.

Much of this ground-breaking research was carried out in 2001, when researchers at the Shanghai Institute generated the viral caspase inhibitor gene p35 from PC12 cells. The effect of p35 on CoCl2 induced apoptosis was then studied. From these experiments, it was shown that caspase-3 proteases may be involved in CoCl2 induced apoptosis of PC12 tumor cells. The apoptotic marker p38 MAPK was also activated by the process. When blocked, cell death was inhibited. This study had huge implications for future research into disorders induced by hypoxia.

Recently, we at Novus Biologicals have used suspension culture techniques to produce CoCl2 treated lysates, specific for use as positive controls for the hypoxia antibodies on our antibody database. These are proving invaluable to neuronal research.

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