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A sampling of Telomerase Antibodies:
anti-Telomerase Rb x Mo
anti-Telomerase Rb x Hu
USBio's 2009 catalog is ready for shipping.
2009 Nobel Prize in Medicine:
How Chromosomes are Protected by Telomeres and Telomerase
The 2009 Nobel Prize in physiology or medicine is shared by Elizabeth H. Blackburn, Ph.D, of University of California, San Francisco; Carol W. Greider, Ph.D, of Johns Hopkins University School of Medicine; and Jack W. Szostak, Ph.D, of Massachusetts General Hospital, Harvard Medical School and Howard Hughes Medical Institute. The three researchers are honored for discovering how telomeres, through the enzyme telomerase, protect chromosomes against degradation.
Drs. Elizabeth Blackburn and Jack Szostak discovered that a unique DNA sequence in the telomeres protects chromosomes from degradation (1). Drs. Carol Greider and Elizabeth Blackburn further identified telomerase, the enzyme that makes telomere DNA (2,3). These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are extended by telomerase.
Telomeres are protein-DNA complexes that cap the ends of chromosomes, the structures that contain our DNA. Telomeres prevent chromosomes from unraveling and keep the ends of chromosomes from attaching to each other, which can contribute to cancer. Human telomeres consist of tandem repetitive arrays of the hexameric sequence TTAGGG, with overall telomere sizes ranging from 15 kb at birth to sometimes <5 kb in chronic disease states. These telomere repeats help maintain chromosomal integrity and provide a buffer of potentially expendable DNA.
Telomeres also act to limit the number of times a cell can divide. Before cells divide, they must copy all their DNA so the resulting cells have the same amount of genetic material. However, the genetic machinery of the cell can't copy the DNA all the way to the end tips, so telomeres gradually shorten with each cell division. When the telomeres become too short, the cell stops dividing or dies.
Telomerase, a reverse transcriptase enzyme, is responsible for elongating telomeres. It is usually not produced in normal adult cells, rather, it is expressed in cells such as embryonic cells, adult stem cells and immune cells, which are all responsible for producing other more specialized cells. In 80-90% of cancers, telomerase is reactivated—a hallmark of malignant cell transformation—enabling the cells to maintain long telomeres and divide indefinitely. This feature makes telomerase an attractive target for new cancer-fighting therapies. In addition, some inherited diseases are now known to be caused by telomerase defects, including certain forms of congenital aplastic anemia, and some inherited skin and lung diseases.
Telomerase is a ribonucleoprotein enzyme responsible for adding telomeric repeats onto the 3' ends of chromosomes. It has two major components (protein and RNA): an enzymatic human telomerase reverse transcriptase catalytic subunit, hTERT, and an RNA component (hTR or hTERC). Telomerase uses its integral RNA component as a template in order to synthesize telomeric DNA (TTAGGG)n, directly onto the ends of chromosomes. After adding six bases, the enzyme pauses while it repositions the template RNA for the synthesis of the next 6 bp repeat.
During cell division, the ends of the chromosomes are not completely copied, so telomeres become progressively shorter. Over time telomeres become so short that their function is disrupted, and this, in turn, leads the cell to stop proliferating. Average telomere length, gives some indication of how many divisions the cell has already undergone and how many remain before it can no longer replicate.
In more recent work, Elissa Epel, Ph.D and Elizabeth Blackburn found evidence to support the long suspected association between stress and cellular aging. In this work, Epel and her colleagues demonstrated that both prolonged psychological stress and the perception of stress had a dramatic impact on three specific biological factors: oxidative stress, lower telomerase activity, and shorter telomere length -all of which are related to cell longevity and disease.
In comparing 39 healthy women caring for a chronically ill child with 19 healthy women raising a healthy child, Epel and her colleagues made the stunning discovery that the cells of the high stress women appeared to be about 13 years older, on average, than the cells of the low stress women (4). These findings have implications for understanding how, at the cellular level, stress may promote earlier onset of age-related diseases.