Rescue of a human cell line from endogenous Cdk1 depletion by Cdk1 lacking inhibitory phosphorylation sites.

Cells that transiently overexpress cyclin-dependent kinase 1 lacking inhibitory phosphorylation sites (Cdk1-AF) undergo premature and catastrophic mitosis, reflecting the key role for Cdk1 in promoting a timely transit from G(2) into mitosis. Conversely, cells depleted of Cdk1 undergo repeated S phases without intervening mitoses (endoreduplication), reflecting a role for Cdk1 in preventing premature S phases. It is not known how Cdk1 prevents entry into S phase at times in G(2) when it does not promote mitosis.

Heat shock proteins in cardiovascular disease a new therapeutic target.

Cells have the capability of defending themselves from various stressors by activating a genetic program with the production of substances known as heat shock proteins and their regulatory partners, the heat shock transcription factors. In this article, heat shock proteins are discussed, including their roles in pathophysiology and as possible pharmacologic targets to treat disease. Multiple investigations have demonstrated an elevation in heat shock proteins in patients with systemic hypertension, coronary artery disease, carotid atherosclerosis, and myocardial infarction and ischemia.