Article Abstract:
The contraction of cardiac and skeletal muscles is regulated by two proteins, troponin and tropomyosin, which interact with actin filaments (molecules involved in the physical contraction and relaxation of the muscle). Troponin contains three subunits, troponin C, troponin I, and troponin T, which have distinct activities. The troponin C molecule has been isolated, purified and examined by X-ray crystallography so that its three-dimensional structure is known. Using site-directed mutagenesis (in which a particular area of the DNA that encodes the gene is altered), the sites and the mechanism of muscle contraction regulation by troponin can be studied. The regulatory sites have been identified as sites where calcium is bound to one end of the troponin molecule. The calcium binding causes a change in the shape of the molecule, and allows the molecule to bind troponin I. The shape of troponin C was stabilized by bridging the molecule through chemical bonding with two molecules of sulphur. The treponin molecule could no longer bind calcium, which affected the ability of troponin C to bind with troponin I. Consequently, it could not regulate the contraction of muscle fibers. These studies will lead to further understanding of how muscle contraction occurs and how it is regulated. (Consumer Summary produced by Reliance Medical Information, Inc.)
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Article Abstract:
The p21 protein, encoded by the p21 gene, is required to arrest the G1 stage of cell cycle following DNA damage by radiations. In mutant mice containing null p21 alleles the ability of cells to suppress their growth, after damage of DNA, is less. Cell death caused by p53 protein and inhibition of CDK2 secretion is unaffected in these mutants. The differentiation of cells in the intestines is not changed by the mutation in the p21 protein. Hence the cell cycle arrest mechanism probably involves several pathways.
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Article Abstract:
A new study investigates the theory that introducing the catalytic subunit of telomerase, TERT, into some cell types can increase their lifespan and immortalizes cells. It is shown that cell proliferation via TERT is is not genoprotective and is associated with the overexpression of c-myc oncogene.
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