Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Apoptosis is a mode of cell death characterized by chromatin condensation and disassembly of the nuclear lamina, processes that are also characteristic of mitosis. The apparent similarity between the two events, together with observations that apoptosis can occur following G2 arrest, has led to the suggestion that apoptosis could be a defective form of mitosis. Further support for this idea comes from the recent description of activation of the p34cdc2 protein kinase (Cdc2), the universal M-phase promoter, during death induced by a lymphocyte granule protease. We have monitored the protein kinase activity of Cdc2 during apoptosis of primary rat thymocytes, which die from a quiescent (G0) state. We demonstrate unequivocally that activation of Cdc2 is not involved in the induction of apoptosis in thymocytes, indicating that chromatin condensation and lamina disassembly occur in this system by processes different from those that operate in mitosis.

Original publication

DOI

10.1006/bbrc.1994.2086

Type

Journal article

Journal

Biochem Biophys Res Commun

Publication Date

15/08/1994

Volume

202

Pages

1400 - 1406

Keywords

Animals, Apoptosis, CDC2 Protein Kinase, Cells, Cultured, Dexamethasone, Enzyme Activation, Etoposide, Lymphocytes, Male, Rats, Rats, Inbred F344, Resting Phase, Cell Cycle, Thymus Gland, Tosyllysine Chloromethyl Ketone