Our lab studies various aspects of chromosome biology ranging from the maintenance of chromosome ends
by telomerase to meiosis, hybridization and ploidy.
The scientists speculated that when chromosome tips get too stubby — a process that can be reversed
by telomerase, an enzyme made up of protein and RNA — cells cease replicating and enter a state called senescence (see» More Than a Sum of Our Cells»).
The protein produced by this gene protects the chromosome ends of the DNA from damage, and controls telomere maintenance
by the telomerase enzyme.
Not exact matches
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.
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.
For now, the only diseases clearly caused
by shortened telomeres or dysfunctional
telomerase are rare premature aging disorders like dyskeratosis congenita.
The enzyme
telomerase slows this degradation
by adding new DNA to the ends of telomeres.
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.
I also had heard from friends that the
telomerase lab directed
by Carol Greider was a top place.»
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.
With each division the telomere would shorten
by a notch from whatever it had been when we took
telomerase out.
She was given lab space and funding to hire three Ph.D. students to start her own research group on
telomerase activity, her salary being provided
by El Consejo Superior de Investigaciones Científicas (the Spanish National Research Council).
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.
Another biochemical process affected
by smoking is
telomerase activity.
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.
This widespread lack of the need for
telomerase is used
by evolution as a key component of our defense against cancer, because having a limit to the size and renewal of telomeres prevents our cells from replicating themselves indefinitely — the crucial hallmark of cancer.
In 2012, the CNIO Telomeres and
Telomerase Group, headed
by Maria A. Blasco, came up with a strategy to repair telomeres.
«Obviously, this information can be used in our efforts to identify drug therapies that kill cancer cells
by targeting
telomerase activity.»
In their research project in 2012, the researchers substantially delayed the aging of mice
by enabling their cells to produce
telomerase once again for a period of time.
The second animal model attempts to reproduce hereditary aplastic anemia, which is produced
by mutations associated with the telomeres and
telomerase.
But the media hype is that somehow
telomerase can increase our life span
by circumventing the limit on cell replication and halting the aging process.
«We provide proof - of - concept that the
telomerase based treatment -LRB-...) has a therapeutic effect on the type of aplastic anemia caused
by short telomeres,» the authors state in an article in the journal Blood, with Christian Bär among them as the first author, as well as Juan Manuel Povedano.
Telomerase offsets cellular aging
by lengthening the telomeres, adding back lost DNA repeats to add time onto the molecular clock countdown, effectively extending the lifespan of the cell.
By specifically targeting the pause signal that prevents restarting DNA repeat synthesis,
telomerase enzymatic function can be supercharged to better stave off telomere length reduction, with the potential to rejuvenate aging human adult stem cells.
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.
The five - year study, led
by UCLA Jonsson Comprehensive Cancer Center member Dr. Jianyu Rao, measured the ability of TSY - 1 to affect
telomerase activity in cancer cells lines, including one known as HL - 60, as well as normal peripheral blood mononuclear and hematopoietic stem cells.
The ribonucleoprotein enzyme
telomerase synthesizes telomeric DNA
by copying an internal RNA template sequence.
In telomeric DNA mutants of Tetrahymena thermophila, created
by expression of a
telomerase RNA with an altered template sequence, division of the germline nucleus was severely delayed or blocked in anaphase.
As a safeguard, in cells such as egg, sperm, and stem cells, an enzyme called
telomerase is responsible for preventing this wear and tear
by maintaining telomere length.
Up to now, it was assumed that
by suppressing the
telomerase activity, tumor cells might be eliminated due to telomere shortening.
This would have prevented the amplification of the
telomerase signal
by PCR even though the activity was present.
In the case of
telomerase activity, the tissues were divided into central, intermediate and peripheral areas
by the use of trephines.
The data presented in this report (
telomerase activity and BrdU - linked alkaline phosphatase activity staining) suggests that cells in the corneal endothelium may be renewed
by stem - like cells located in a niche at the posterior limbus.
Telomerase activity was assayed
by a commercial version (TRAPeze; Chemicon International, Temecula, CA) of the method described
by Kim et al. [20].
These cells were immortalized
by retroviral transduction of the SV40 T antigen and
Telomerase reverse transcriptase (TERT), the catalytic subunit of the telomerase complex [4], and then termed HMLE (Human Mammary with Large T
Telomerase reverse transcriptase (TERT), the catalytic subunit of the
telomerase complex [4], and then termed HMLE (Human Mammary with Large T
telomerase complex [4], and then termed HMLE (Human Mammary with Large T and TERT).
A study conducted
by California's Preventive Medicine Research Institute saw
telomerase production boosted
by 29 percent in 24 patients who switched from a sedentary lifestyle to one defined
by exercise, healthy diet and stress management.
Huaire, Lilian C. «Telomere and
Telomerase: brief review of a history initiated
by Hermann Müller and Barbara McClintock.»
Various types of meditation have been shown to improve well - being among different populations such as physicians and the general public.14, 15, 16 Preliminary evidence suggests that meditation - based interventions may slow cellular aging rates
by increasing
telomerase activity, but many such studies lacked an active control group.17, 18 Recent randomized trials in breast cancer suggest that long - term intensive meditation interventions might have positive effects on
telomerase activity.
Telomere length predicts both cellular health and disease in rodent models and humans.8 Shorter telomeres predict onset of cardiometabolic diseases of aging.9 Chronic stress is associated with higher inflammation, shorter telomeres, and lower activity levels of
telomerase, the cellular enzyme that elongates telomeric DNA.10, 11 Levels of amyloid beta (Aβ) proteins circulating in the blood appear to be stress - related in rodent models12 and may be affected
by stress reduction, and greater Aβ42 / Aβ40 ratios are associated with lower risk of dementia.13
We also identified a «meditation effect» within the regular meditator group, characterized
by a distinct network of genes with cellular functions that may be relevant to healthy aging, and this network was associated with increased expression of a number of telomere maintenance pathway genes and an increase in measured
telomerase enzymatic activity.
The figure demonstrates both the existence of
telomerase activity in the peripheral endothelium (but not the central endothelium) and the elimination of contamination
by Taq polymerase inhibitors in some tissue samples.
The method
by which
telomerase and associated regulatory factors physically interact and function with each other to maintain appropriate telomere length is poorly understood.
The second animal model attempts to reproduce hereditary aplastic anaemia, which is produced
by mutations associated with the telomeres and
telomerase.
This work, published in «Blood», was carried out
by the CNIO Telomeres and
Telomerase Group The treatment is based on the transport of the telomerase gene to the bone marrow cells using gene therapy, a completely new strategy in the treatment of aplast
Telomerase Group The treatment is based on the transport of the
telomerase gene to the bone marrow cells using gene therapy, a completely new strategy in the treatment of aplast
telomerase gene to the bone marrow cells using gene therapy, a completely new strategy in the treatment of aplastic anaemia
In their research project in 2012, the researchers substantially delayed the ageing of mice
by enabling their cells to produce
telomerase once again for a period of time.
A study
by Dr. Dean Ornish and his team showed that lifestyle changes including diet, exercise, and stress management techniques made a difference in
telomerase levels.
«We provide proof - of - concept that the
telomerase based treatment -LRB-...) has a therapeutic effect on the type of aplastic anaemia caused
by short telomeres,» the authors state in an article in the journal Blood, with Christian Bär among them as the first author, as well as Juan Manuel Povedano.
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.