A portion of
the telomere DNA is lost during cell division.
Not exact matches
In a related development in 2008, a group of psychologists concluded in a research paper that a sense of purpose and direction prolongs life and we can see evidence of this in our
DNA — specifically our
telomeres.
Doing so keeps the
telomeres found on the ends of your
DNA strands long and able to protect chromosomes from deterioration.
Telomeres are repetitive stretches of
DNA that cap natural chromosome ends to protect them from being damaged or fused together during
DNA replication.
Researchers from several institutions, including, UCLA, Boston University, Stanford University and the Institute for Aging Research at Hebrew SeniorLife, analyzed blood samples from nearly 10,000 people to find that genetic markers in the gene responsible for keeping
telomeres (tips of chromosomes) youthfully longer, did not translate into a younger biologic age as measured by changes in proteins coating the
DNA.
Telomeres provide protection to chromosomes during the replication process to prevent the loss of
DNA strands.
Blackburn and Szostak determined that it was a specific
DNA sequence in the
telomeres that kept chromosomes from fraying whenever they were copied when a cell splits in two.
The parts affected are the
telomeres — stretches of
DNA that cap the ends of chromosomes.
Telomere proteins from ciliated protozoa bind to the single - stranded G - rich
DNA extensions at the ends of macronuclear chromosomes.
The boosted genes had three main beneficial effects: improving the efficiency of mitochondria, the powerhouse of cells; boosting insulin production, which improves control of blood sugar; and preventing the depletion of
telomeres, caps on chromosomes that help to keep
DNA stable and so prevent cells wearing out and ageing.
Because of a quirk in the way the
DNA is replicated, the ends are not completely copied, and that information would gradually be lost if not for the
telomeres.
Cech was collaborating with the younger professor on research involving
telomeres, the
DNA - and - protein caps that guard chromosome tips.
Austad recalls one conversation in which Muller made an insightful connection about
telomeres, the
DNA - and - protein caps at the ends of chromosomes that shorten with every cell division, eventually pushing cells into a nondividing state called senescence.
«The mean difference in leukocyte
telomere length between the most active and least active subjects was 200 nucleotides (chemical structural units of
DNA and RNA), which means that the most active subjects had
telomeres the same length as sedentary individuals up to 10 years younger, on average.»
12
Telomeres, sequences of
DNA at the tips of chromosomes, get shorter every time a cell divides; when they get too short, the cell dies.
Chromosomes are capped by
telomeres, tightly wound strands of
DNA.
They specifically studied the length of
telomeres (repeated
DNA sequences) on the ends of chromosomes in leukocytes (white blood cells); the protective caps are believed to be markers of biological aging, because they shrink over time.
Greider and Hackett wondered whether short
telomeres might render chromosomes vulnerable to a type of enzyme called an exonuclease, which degrades
DNA.
Every time linear chromosomes are replicated during late S phase, the
DNA polymerase complex is incapable of replicating all the way to the end of the chromosome; if it were not for
telomeres, this would quickly result in the loss of vital genetic information, which is needed to sustain a cell's activities.
The enzyme telomerase slows this degradation by adding new
DNA to the ends of
telomeres.
The
telomere prevents this problem by employing a different mechanism to synthesize
DNA at this point, thereby preserving the sequence at the terminal of the chromosome.
Telomeres are protective caps of
DNA that prevent damage to the ends of chromosomes.
The key to cancer cell immortality are the cell's
telomeres, repetitive stretches of
DNA at the ends of chromosomes that may protect the chromosomes when they divide.
This top view of a G - quadruplex shows its structure in the
DNA of a human
telomere, where they frequently form.
Telomeres are pieces of
DNA that protect the ends of chromosomes.
Telomeres, the caps of
DNA which protect the ends of chromosomes, shorten every time cells divide.
Telomeres are composed of double - stranded
DNA with terminal 3» single - stranded G - rich overhangs called
telomere G - tails.
Individuals carrying the variant had shorter
telomeres, stretches of
DNA at the ends of chromosomes that protect them from daily wear — and also aging
Some of the sequence matched repetitive
DNA in
telomeres, the caps of chromosomes, which often shorten each time a cell divides and play an important role in aging.
Telomeres are bits of
DNA that protect the ends of chromosomes from unraveling or degrading.
Telomeres are the protective tips found at the end of each
DNA strand and are indicative of cellular aging.
Telomeres are tiny fragments of
DNA at the end of each chromosome.
These tiny strips of
DNA, called
telomeres, cap the end of chromosomes.
«Cells do not repair damage to
DNA during mitosis because
telomeres could fuse together.»
This revealed
telomeres as dangerous structures during mitosis, because the cells momentarily lost the ability to distinguish between damaged
DNA strands and normal
telomeres.
They took
DNA samples from Nicoya residents who were older than 60 to measure the length of their
telomeres.
To evaluate whether the experimental treatment is safe and whether it might be able to reduce frailty, Maharaj plans to run a battery of baseline testing on each clinical trial participant before they get their first infusion of young plasma and then monitor their changes for two years: That means cognitive exams, questionnaires about their quality of life and their indicators of frailty, and tests to measure biomarkers he believes are linked with aging, such as
telomere lengths and
DNA methylation.
«In other words, at that moment of cell division, the cell miss - identified its own
telomeres as damaged
DNA, which it then «repaired,» Dr. Orthwein says.
When imposing repair on broken
DNA strands during mitosis, some
telomeres are seen to fuse together (one dot).
Klingelhutz and his team immortalized immature precursor fat cells by adding in two genes from HPV (the virus that causes cervical cancer) along with a gene for part of an enzyme that controls the length of cells»
telomeres — the pieces of
DNA that protect chromosome tips from deterioration.
The protein produced by this gene protects the chromosome ends of the
DNA from damage, and controls
telomere maintenance by the telomerase enzyme.
The shortening of
telomeres is a process that occurs naturally in the body each time that a cell divides: during cell division the
DNA, which is tightly packaged into chromosomes, must be duplicated but the
DNA - copying machinery design itself, prevents the full replication of the ends of the chromosomes.
Fossel believes the first viable antiaging therapy will target
telomeres, which are repeating
DNA sequences at the ends of chromosomes.
Telomerase is an enzyme that replicates the ends of chromosomes (sections of
DNA called
telomeres), replacing the
DNA lost when chromosomes are copied before cell division and, therefore, maintaining the stability of the genome.
Biological age, Samani says, is related to the length of
telomeres — stretches of
DNA at the ends of chromosomes, which protect these precious packages of genes from daily wear and tear.
O'Sullivan came to the Karlseder lab seven years ago to explore whether histone /
DNA interactions in nucleosomes altered
telomere function.
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.
These
DNA repeats are part of the protective capping structures, termed «
telomeres,» which safeguard the ends of chromosomes from unwanted and unwarranted
DNA rearrangements that destabilize the genome.
The offshore bird's secret, revealed for the first time in May by zoologists at Iowa State University, is in the storm petrel's
telomeres, repetitive bits of
DNA that sit on the ends of the chromosomes in each cell like protective caps.