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Researchers Map the 3D Structure of the Telomerase Enzyme

Researchers Map the 3D Structure of the Telomerase Enzyme | Longevity science | Scoop.it
Researchers from UCLA and UC Berkeley have, for the first time ever, solved the puzzle of how the various components of an entire telomerase enzyme complex fit together and function in a three-dimensional structure.

 

The telomerase enzyme, which is known to play a significant role in aging and most cancers, represents a breakthrough that could open up a host of new approaches to fighting disease.

 

The creation of the first complete visual map of thetelomerase enzyme, which is known to play a significant role in aging and most cancers, represents a breakthrough that could open up a host of new approaches to fighting disease, the researchers said.

"Everyone in the field wants to know what telomerase looks like, and there it was. I was so excited, I could hardly breathe," said Juli Feigon, a UCLA professor of chemistry and biochemistry and a senior author of the study. "We were the first to see it."


Via Dr. Stefan Gruenwald
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Telomerase Gene Therapy Extends Mouse Lifespan by 24%

Telomerase Gene Therapy Extends Mouse Lifespan by 24% | Longevity science | Scoop.it
Inducing cells to express telomerase, the enzyme which is supposed to slow down the metabolic clock, has enabled researchers boost the lifespan of mouse by 24% with a single treatment.

 

The gene therapy acts on specific genes and is applied in adult life, not from the embryonic stage. Researchers at the Spanish National Cancer Research Center (CNIO) have demonstrated that the mouse lifespan can be extended by the application of one treatment acting directly on the animal’s genes in adult life. The therapy has been found to be safe and effective in mice.

 

Adult and aged mice were treated with the gene therapy, delivering a rejuvenating effect. On average, the mice lived 24% longer. The older mice lived 13% longer. The therapy produces an appreciable improvement on the animal’s health and delayed the onset of age-related diseases.

 

The genes were treated with a DNA-modified virus. The viral genes were replaced by those of the telomerase enzyme, which plays a key role in aging. Telomerase repairs the extreme ends of chromosomes, and slows the cells and therefore the body’s biological clock.

 

There is a potential to develop a telomerase-based anti-aging gene therapy that won’t increase the risk of cancer. Telomeres are the caps that protect the end of chromosomes, but each time the cell divides, the telomeres get shorter until they lose all functionality. The cell then stops dividing or dies. Telomerase prevents telomeres from shortening or even rebuilding them.

 

In most cells, telomerase is only active before birth. The cells of adult organisms contain no telomerase. There are some exceptions such as adult stem cells and cancer cells, which divide limitlessly and could be immortal.

 

The risk of cancer tumor promotion is a risk that has set back telomerase-based anti-aging therapies. The kind of virus employed to carry the telomerase gene to the cells is very important. The viruses used is in this study have been successfully used in gene therapy treatment of hemophilia and eye disease. They are non-replicating viruses derived from others that are non-pathogenic in humans.


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Telomerase Gene Therapy Extends Lives Of Mice By Up To 24 Percent

Telomerase Gene Therapy Extends Lives Of Mice By Up To 24 Percent | Longevity science | Scoop.it

The latest in the fight against ever dying is a gene therapy that gives mice a healthy dose of telomerase, the enzyme that keeps our chromosomes – and thus our cells and bodies – “young.”

 

The therapy extended the lifespans of mice by 24 percent and, at least so far, the therapy appears to be completely safe...

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Sierra Sciences, LLC - Cure Aging or Die Trying

Sierra Sciences, LLC - Cure Aging or Die Trying | Longevity science | Scoop.it

The root cause of aging is very straightforward: we age because our cells age.

In 1961, Leonard Hayflick, a researcher at the Wistar Institute in Philadelphia, discovered that there was a limit to the number of times a human cell could divide.1 After about 70 divisions, a cell derived from embryonic tissue enters a stage where its ability to divide slows and eventually stops. This stage is called cellular senescence. Hayflick also observed that the number of times a cell could divide was governed by the age of the cells: cells from a twenty-year-old could divide more times than cells from a fifty-year-old, which in turn would divide more times than cells from a ninety-year-old.

 

 

Ray and Terry's 's insight:

An interesting discussion on telomerase and aging. We are not yet sure whether attempting to increase telomere length, particularly with current available methods, is the answer to aging. There is some indication that cancer can be triggered by these efforts.

 

The research is promising, but we cannot yet recommend the therapies.

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Blocking Telomerase Kills Cancer Cells but Provokes Resistance, Progression | MD Anderson Cancer Center

Inhibiting telomerase, an enzyme that rescues malignant cells from destruction by extending the protective caps on the ends of chromosomes, kills tumor cells but also triggers resistance pathways that allow cancer to survive and spread, scientists reported.

 

"Telomerase is overexpressed in many advanced cancers, but assessing its potential as a therapeutic target requires us to understand what it does and how it does it," said senior author Ronald DePinho, M.D., president of The University of Texas MD Anderson Cancer Center.

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