IMMORTAL Cell Sciences

Extending telomeres is our business

The shortening of our Telomeres is indicated to have direct correlation with aging and age-related conditions. For the same reason color coping requires borders, Every chromosome of our DNA requires an end because all the DNA can not be completely copied.  These "borders" shorten with every cell division.  "When the Telomeres get too short they are unable to support the DNA and all sorts of mutations begin to occur, leading to disease and eventually death. By putting a halt to Telomere shortening, even better, re-lengthening them, the prevention of signs of premature aging may become achievable" -Dr. Bill Andrews PhD

2009 Nobel Prize in Medicine

As cells divide, their chromosomes get shorter. This is because the DNA sequences at both ends of a chromosome, called telomeres, shrink in length every time the DNA is copied. James Watson, who had resolved the structure of the DNA molecule along with Francis Crick, pointed out a perplexing circumstance. The established theory of how DNA was copied before cell division could not be reconciled with the fact that DNA strands have ends. Try as they might, the researchers could not figure out how the DNA strands could be copied without losing bits off their ends. After repeated replication and shortening, the genes and cells would be damaged.

This quandary, known as the end-replication problem, was elegantly resolved by the discoveries of Elizabeth H. Blackburn, Carol W. Greider, and Jack W Szostak who were awarded the 2009 Nobel Prize in medicine. Their team discovered the enzyme Telomerase which stops shortening by adding base pairs that grow short telomeres.

All human DNA contains the instructions for making telomerase, but in most cells these instructions are turned off. So-called Telomerase Activators, as the name implies, turns on these enzymes in cells

For more information about the 2009 Nobel Prize in Medicine, click here:

Five Reasons Henrietta Lacks is the Most Important Woman in Medical History

It was discovered that Lacks's cancerous cells used an enzyme called telomerase to repair their DNA, allowing them, and other types of cancer cells, to function when normal cells would have died. Anti-cancer drugs that work against this enzyme are currently in early clinical trials.