Sentences with phrase «telomerase in»

Before and after the experiment the researchers measured the concentration of the enzyme telomerase in the participants» blood.

Meditation delays molecular aging Meditation boosts the activity of the enzyme telomerase in the cells.

Telomeres and Telomerase in Ageing, Disease, and Cancer.

Mouse model: Telomeres and telomerase in stem cell and cancer.

Telomeres and telomerase in cancer stem cells.

Telomeres and Telomerase in Cancer.

They found shorter telomeres and decreased telomerase in spouses who were caring for mates with dementia and in mothers of children with chronic diseases.

In this study, the reaction for telomerase in the peripheral corneal endothelium was manifest (Figure 2).

Other investigations suggest that telomerase activity that is associated with adult stem cells may reside preferentially in transient amplifying cells, the stem cell daughters that are on the way to commitment and that, in fact, the telomerase in quiescent stem cells is repressed [22,25].

With arsenic forcing the production of largely useless telomerase in cell lines that simulate acute promyelocytic leukemia, the chromosomes in cancer cells fuse together, causing the cell death that helps fight the cancer.

Preliminary evidence suggests that arsenic may have the same effect on telomerase in other cancers; human trials are ongoing.

They have become a valuable resource for biologists, enabling momentous scientific breakthroughs including the development of the polio vaccine the Nobel Prize winning studies defining the role of telomerase in aging, and research on the causative role of human papillomavirus (HPV) in some types of cervical cancer.

Building on this «telomere hypothesis,» Geron's big idea was that tinkering with telomerase in cells could stave off their senescence — and prevent aging.

The activity of telomerase in adult stem cells merely slows down the countdown of the molecular clock and does not completely immortalize these cells.

An estimated 90 percent of all malignant tumors use telomerase to achieve immortality, and various proposed cancer therapies focus on turning down the production of telomerase in tumors.

Not exact matches

The underlying reason is that Geron and partner Johnson & Johnson (NYSE: JNJ) are developing a first - in - class telomerase inhibitor called imetelstat for the rare blood disorders myelodysplastic syndromes (MDS) and myelofibrosis (MF).

In the Zakian group, he focused on the PIFI gene, a telomerase inhibitor.

Variants in the gene called Telomerase Reverse Transcriptase (TERT) on chromosome 5 that were associated with older IEAA were also associated with longer telomeres indicating a critical role for TERT in regulating the epigenetic clock, in addition to its established role of compensating for cell replication - dependent telomere shortening.

By 1985, Blackburn, who had started her own lab at UC Berkeley, and Carol Greider, a grad student in Blackburn's group, had discovered telomerase, an enzyme that synthesizes and preserves telomeric DNA.

Although de Lange notes that telomere shortening needs further investigation, she says there's now no doubt that telomeres play a critical role in limiting human cell division and that telomerase can reactivate the process.

The grueling 18 months unearthed a gold mine: Lundblad's team found three genes that are crucial for telomerase function, results that generated a flurry of groundbreaking papers from the members of her group in 1996 and 1997.

Voice: The 2009 Nobel Prize in Physiology or Medicine goes to Harvard's Jack Szostak, Johns Hopkins's Carol Greider and Elizabeth Blackburn at U.C. San Francisco for their work on how chromosomes are protected by telomeres and the enzyme telomerase.

Working in Berkeley, Lundblad discovered that even without telomerase, yeast cells can sustain their chromosome tips — the first example of an alternative telomere - lengthening pathway.

Researchers at Geron Corp. of Menlo Park, California, and the University of Texas Southwestern Medical Center in Dallas wondered whether telomerase might delay this fate.

Alteration of the template region in vivo generated altered telomerase products.

Sequence comparisons placed the telomerase proteins in the reverse transcriptase family but revealed hallmarks that distinguish them from retroviral and retrotransposon relatives.

Thus, the proposed telomerase catalytic subunits are phylogenetically conserved and represent a deep branch in the evolution of reverse transcriptases.

Amounts of telomerase RNA increased in immortal cells derived from primary mouse fibroblasts.

In August, 1997, Nobelist Thomas Cech of the University of Colorado at Boulder and colleagues at Geron isolated the human gene for telomerase reverse transcriptase (hTRT)-- an enzyme that reknits loosening telomeres and extends a cell's life.

Mariela Jaskelioff and her colleagues at the Dana Farber Cancer Institute in Boston, Massachusetts, engineered mice with short telomeres and inactive telomerase to see what would happen when they turned the enzyme back on.

By reactivating telomerase activity in stem - cell derived tissue transplants, Geron could provide patients with a life - time warranty on their new parts.

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.

Removing telomerase from every cell in our body would preempt cancer before it had a chance to get started.

According to the new theory, the telomeres are short in precancerous cells because telomerase is turned on just enough to maintain but not lengthen the telomeres.

So, the effect of telomerase deletion on frequently dividing cells would be very serious indeed — fatal, in fact.

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.

Hockemeyer says that it's unlikely to be another mutation, but rather an epigenetic change that affects expression of the telomerase gene, or a change in the expression of a transcription factor or other regulatory proteins that binds to the promoter upstream of the telomerase gene.

Hockemeyer and his UC Berkeley colleagues, in collaboration with dermatopathologist Boris Bastian and his colleagues at UCSF, found that immortalization is a two - step process, driven initially by a mutation that turns telomerase on, but at a very low level.

The discovery of telomerase and its role in replenishing the caps on the ends of the chromosomes, made by Elizabeth Blackburn and Carol Greider at UC Berkeley and John Szostak at Harvard University in the 1980s, earned them a Nobel Prize in Physiology or Medicine in 2009.

The reason, he said, is that if a TERT promoter mutation arises to push a precancerous lesion — the mole or nevus — toward a melanoma, the chances are greater in someone with short telomeres that the cell will die before it up - regulates telomerase and immortalizes the cells.

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.

Some would simply crank their telomerase activity up even further; some would enhance the activity of drug - metabolizing enzymes that degrade the inhibitor; still others would change their cell surface proteins in ways that would make it harder for the drug to penetrate into the cell.

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.

«Two - step process leads to cell immortalization and cancer: Clearer view of the role telomere length and telomerase play in cell immortalization.»

If it weren't for telomerase, this gradual shortening would eventually lead to the complete loss of the telomeres in cells that replicate frequently during a life span, and thus the gradual erosion of the genes themselves.

As with all of our other genes, the DNA that encodes the telomerase enzyme is present in all of our cells — but because it's needed only after quite a few cell divisions have occurred, it's not needed in most cells for most or all of the time, so it's turned off.

The year 1993 was also about the same time that an enzyme close to the one she was working on, telomerase, was first associated with the development of cancer in humans.

By measuring telomerase activity, investigators determined that the group that smoked without drinking red wine showed a 56 % decrease in telomerase activity while the drinking group showed only a 20 % decrease.

So the molecular cause is exactly the same base pair change in a telomerase gene.