Latest Dyskeratosis congenita Stories
Few molecules are more interesting than DNA—except of course RNA. After two decades of research, that "other macromolecule" is no longer considered a mere messenger between glamorous DNA and protein-synthesizing machines.
Rapidly dividing cancer cells are skilled at patching up damage that would stop normal cells in their tracks, including wear and tear of telomeres, the protective caps at the end of each chromosome.
Telomeres, the complex structures that protect the end of chromosomes, of peripheral blood cells are significantly shorter in patients with familial breast cancer than in the general population.
NEW YORK, June 8, 2011 /PRNewswire/ -- When expressed (turned on), the gene (hTERT) located on Chromosome number 5p15.33 activates the enzyme telomerase. Human cells can keep living and dividing indefinitely when telomerase is continually present; i.e. the cells become immortal.
A rare genetic disease called dyskeratosis congenita, caused by the rapid shortening of telomeres (protective caps on the ends of chromosomes), can be mimicked through the study of undifferentiated induced pluripotent stem cells.
MALAGA, Spain, April 12, 2011 /PRNewswire/ -- Groundbreaking research touting the benefits of telomerase activation has been published in Aging Cell, the # 1 journal in geriatrics and gerontology.
New evidence has emerged from studies in mice that short telomeres or "caps" at the ends of chromosomes may predispose people to age-related diabetes.
It's been nearly 10 years since Beth Israel Deaconess Medical Center (BIDMC) scientists Kun Ping Lu, MD, PhD and Xiao Zhen Zhou, MD, discovered PinX1, the first potent endogenous protein shown to inhibit telomerase in mammals.
RENO, Nev., Nov. 30, 2010 /PRNewswire/ -- On Sunday, a team of scientists at Harvard Medical School led by Dr. Ronald DePinho published research providing strong scientific support for the validity of Sierra Sciences' approach to curing aging.
- A political dynamiter.