Modulation of intracellular Ca2+ levels in the heart by sorcin and FKBP12, two accessory proteins of ryanodine receptors

Article Abstract:

Researches were conducted to examine the roles of sorcin and the 12kDa immunophilin FK506-binding protein FKBP12 in the modulation of intracellular Ca2+ levels in the heart. Earlier studies have shown that the ryanodine receptor homotetramer was the only physical constituent of Ca2+ release. New studies show that sorcin inhibits the activity of cardiac ryanodine receptors. Thus, new evidence proves that accessory proteins of ryanodine receptors are critical components of the Ca2+-release unit of cardiac and skeletal muscle and as such can regulate Ca2+-induced Ca2+ release.

Calcium ions, Carrier proteins, Transport proteins, Heart muscle, Myocardium

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Alzheimer's disease: the tacrine legacy

Article Abstract:

The Pasteur Institute hosted a two-day meeting of clinical trialists from research centers and pharmaceutical firms that are conducting research on the next generation of drugs being developed for the treatment of Alzheimer's disease. At the Nov 1999 meeting, the results of clinical trials of drugs built from acetylcholinesterase inhibitors were discussed. Tacrine, donepezil, rivastigmine, metrifonate and galantamine were among the drugs whose efficacies were reported on. Research findings on muscarinic receptor agonists and nicotinic receptor agonists were also reported.

Conferences, meetings and seminars, Reports, Physiological aspects, Drug therapy, Alzheimer's disease, Cholinergic mechanisms, Anti-Alzheimer's disease agents, Senile dementia, Pasteur Institute, Pharmaceutical research

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Bcl-2 related proteins, apoptosis and disease

Article Abstract:

Inappropriate modulation of apoptosis, or programmed cell death, can lead to disease. Recent studies have shown that Bcl-2-related proteins are good modulators of apoptosis and therapeutic targets for drug design. Furthermore, there is evidence to support that Bcl-2 members may regulate apoptosis by modulating entry and progression through the cell cycle. These new findings are essential in formulating ways to exploit therapeutically apoptosis-linked molecules.

Therapeutics, Cell death, Nervous system, Proteins, Nerve regeneration

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