Sentences with phrase «which telomerase»

The method by which telomerase and associated regulatory factors physically interact and function with each other to maintain appropriate telomere length is poorly understood.

When Lin engineered the telomerase - expressing hepatocytes to die in response to a chemical signal and gave the mice with a liver - damaging chemical, he found that those animals in which the telomerase cells had been killed exhibited much more severe liver scarring than those in which the cells were functional.

The researchers used mice in which the telomerase gene was eliminated; specifically in bone marrow cells.

Not exact matches

TERT is a subunit of the enzyme telomerase, which is a widely known enzyme because it has been touted as an anti-aging enzyme.

To find out, the researchers injected a cloned telomerase gene into cultured cells from retina, skin, and blood vessels, all of which are associated with degenerative, aging - related diseases.

For instance, one small study found that people who ate healthier diets, did yoga or meditation, and exercised daily increased the activity of telomerase, which could lead to longer telomeres.

Telomerase is a «ribonucleoprotein complex» composed of a protein component and an RNA primer sequence which acts to protect the terminal ends of chromosomes.

Several biotech companies — most prominently Geron, which first made a name for itself in telomere research — are working to develop anticancer drugs that would work by deactivating telomerase.

The key to immortalization is an enzyme called telomerase, which keeps chromosomes healthy in cells that divide frequently.

New experiments by UC Berkeley and UCSF researchers suggest that immortalization of skin cells, which is essential to turning them cancerous, is a two - step process: a mutation in nevus cells slightly raises levels of telomerase, which keep the cells alive long enough for a second change, still unknown, that up - regulates telomerase to make the cells immortal and malignant.

Yet, Hockemeyer says, telomerase levels are marginal, resulting is some unprotected chromosome ends in the surviving mutant cells, which could cause mutations and further fuel tumor formation.

The new research, which studied the immortalization process using genome - engineered cells in culture and also tracked skin cells as they progressed from a mole into a malignant melanoma, suggests that telomerase plays a more complex role in cancer.

Sometimes telomerase is a good guy because it helps produce immune cells and stops telomeres from shortening, but it can also make cells immortal, which prompts them to turn malignant.

We used liposomes — which are almost like tiny soap bubbles in the bloodstream — to deliver a gene that knocks the telomerase RNA down.

Researchers chased the gene down and found it was a mutant telomerase RNA gene component, and patients had about half the normal amount of telomerase, which meant their telomeres shorten prematurely.

Experiments confirmed that there was an enzyme, which we called telomerase, and that it is actually doing something inside cells that matters.

The second animal model attempts to reproduce hereditary aplastic anemia, which is produced by mutations associated with the telomeres and telomerase.

Stem cells, which have to divide regularly to regenerate tissues with new cells, can produce telomerase, but not the amount required to counteract the shortening of telomeres that accumulates with aging: over time, the tissues have fewer fresh cells and they lose their regenerative capacity.

The treatment is based on making bone marrow cells express the telomerase enzyme, which is responsible for repairing telomeres.

One strategy, which occurs in about 90 percent of cancers, requires increase production of a telomere - elongating enzyme called telomerase.

The studies on autophagy by Yoshinori Ohsumi, which earned him the Nobel Prize in Medicine in 2016, and the discovery of cell cycle regulatory genes for which Leland Hartwell, Timothy Hunt and Paul Nurse received the same award in 2001, including the research of Elizabeth Blackburn, Carol Greider and Jack Szostak on telomeres, telomerase and its protective effect on the chromosomes, were all made possible thanks to yeast.

Telomerase is an enzyme responsible for the production of telomeres, which play an important role in the regulation of normal cell division.

Dang's team traced the clumping back to malfunctions in the enzyme telomerase, which maintains the caps at the ends of the chromosomes and keeps the chromosomes apart from one another.

The limitation may be that normal cells do not produce active telomerase, which can rebuild the telomeres and keep cells from becoming senescent.

In tomorrow's Cell, researchers describe how older mice lacking the enzyme telomerase — which helps protect dividing chromosomes — go prematurely grey and begin to lose their fur.

The findings come on the heels of a March study in the New England Journal of Medicine, which similarly discovered telomerase mutations in fibrosis patients.

The telomerase ribonucleoprotein has a phylogenetically divergent RNA subunit, which contains a short template for telomeric DNA synthesis.

In 2001 researchers at the biotech giant Geron Corporation isolated a molecule called TA - 65 from the herb astragalus, which they said boosted telomerase activity (its effect has not yet been evaluated in published, peer - reviewed studies).

Scientists think that normal cells, which apparently lack the telomerase enzyme, stop dividing and die off appropriately after 50 to 100 divisions when their telomeres are worn to the nub.

«The lack of telomerase results in the telomeres shrinking, which provides a way for the cells to mark time and age every time they divide.»

Her lab also discovered a hidden regulatory landscape on the surfaces of cellular proteins, which act as traffic cops for telomerase.

While most chemotherapy drugs kill all rapidly dividing cells in the body, causing serious side effects which limit their use, a drug that inhibits telomerase would only affect those cells that are immortal and malignant.

Telomeres don't shrink significantly in healthy humans for decades due to an enzyme called telomerase, which partially repairs and lengthens them after each shortening.

The enzyme telomerase extends telomere length thus prolonging the life of individual cells - which usually leads to cancer rather than extended life.

Additionally, the allogeneic platform has the flexibility to leverage alternative antigens beyond telomerase, which could extend AST - VAC2 applications even further.

The second animal model attempts to reproduce hereditary aplastic anaemia, which is produced by mutations associated with the telomeres and telomerase.

Stem cells, which have to divide regularly to regenerate tissues with new cells, can produce telomerase, but not the amount required to counteract the shortening of telomeres that accumulates with ageing: over time, the tissues have fewer fresh cells and they lose their regenerative capacity.

Dr. Elizabeth Blackburn received the Nobel Prize in medicine in 2009 for discovering how chromosomes are protected by telomeres and the enzyme telomerase, which repairs and rebuilds them.

Telomerase renews (elongates) the telomeres, which are responsible for the protection of human DNA from damage and cancer causing errors.

Healthy cells saw their telomerase rise and p16 decrease, which would explain the boost in healthy cell growth, the researchers explained.