In Addition to Telomerase, ATM Kinase Also Shown to Control Telomere Length; New Study from Johns Hopkins; Nobel Laureate Led Work

Since the discovery of the enzyme telomerase in 1984 (recognized by the 2009 Nobel Prize in Physiology or Medicine), identifying other biological molecules that lengthen or shorten the protective caps on the ends of chromosomes has been slow going. Now, researchers at Johns Hopkins, led by one of the three telomerase 2009 Nobel Laureates, report uncovering the role of an enzyme crucial to telomere length and say the new method they used to find this enzyme should speed discovery of other proteins and processes that determine telomere length. Their results were published online on November 12, 2015 in an open-access article in Cell Reports. The article is titled “ATM Kinase Is Required for Telomere Elongation in Mouse and Human Cells.” "We've known for a long time that telomerase doesn't tell the whole story of why chromosomes' telomeres are a given length, but with the tools we had, it was difficult to figure out which proteins were responsible for getting telomerase to do its work," says Carol Greider, Ph.D., the Daniel Nathans Professor and Director of Molecular Biology and Genetics at the Johns Hopkins Institute for Basic Biomedical Sciences. Dr. Greider shared the 2009 Nobel Prize in Physiology or Medicine jointly with Dr. Elizabeth Blackburn and Dr. Jack Szostak, "for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase." ( Figuring out exactly what's needed to lengthen telomeres has broad health implications, Dr. Greider notes, because shortened telomeres have been implicated in aging and in diseases as diverse as lung and bone marrow disorders, while overly long telomeres are linked to cancer.
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