[mage lang=”en|es|fr|en” source=”flickr”]telomerase aging mice[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase disease[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase in mice[/mage]
Watch this remarkable video from ABC Television showing the lab results of two mice.
One was treated with a telomerase suppliment and the other was not. Both mice are the same age and you can see the results of the mouse that was treated showing signs of age reversal.
The mouse’s hair is growing back from where it was once going bald. The grey hairs have been replaced with normal color hair of a younger mouse.
This holds a great deal of promise for human response to telomere suppliment treatments.
[mage lang=”en|es|fr|en” source=”flickr”]telomere telomerase and cancer[/mage]
If telomere shortening could be avoided (eg, telomerase), what do you think the benefits and risks would be?
Do you think cell senescence or slow or stop the aging increased cancer mechanical, such as longer life cells encourage such developments. Do you think you that any significant changes would occur?
A variety of syndromes of accelerated aging are associated with short telomeres. These include Werner syndrome syndrome, ataxia telangiectasia, Bloom, Fanconi anemia, Nijmegen breakage syndrome and ataxia telangiectasia, a disorder. The genes that are mutated in these diseases have a role in the repair of damage to DNA, and their precise roles in maintaining telomere length is an active area of research. While it is unknown extent of erosion telomeres contributes to the normal aging process, maintenance of DNA, in general, and specifically to telomeric DNA, have emerged as key players. Dr. Michael Fossel has been suggested that telomerase therapy (see link) can be used not only to fight cancer, but to really get on aging and prolonging human life significantly. He believes that human trials of telomerase therapies based on extending the life occur in the next 10 years. This chronology is important because it coincides with the retirement of baby boomers United States and Europe. When cells are approaching the Hayflick limit in cell culture, the aging time can be extended by inactivation the tumor suppressor protein – TP53 and retinoblastoma protein (pRb). Cells that have been modified so eventually undergo an event called a "crisis" when the majority of cells in culture die. Sometimes a cell will stop dividing once they reach the crisis. Normally, the telomeres are lost, and the integrity of chromosomes is reduced at each subsequent cell division. Chromosome ends are exposed interpreted as a double-strand breaks (DSB) of DNA, this damage is usually repaired by reconnecting (religation) the broken ends together. When the cell is due to telomeres shortened, the ends of chromosomes may be set. This temporarily solves the problem of lack of telomeres, but during the anaphase of cell division the chromosomes fused randomly broken causing many mutations and chromosomal abnormalities. As this process continues, the genome of the cell becomes unstable. Over time, if enough damage will occur in the chromosomes of the cell so the cell dies (for programmed cell death (apoptosis or not), or an additional mutation with activities of telomerase.
Telomerase.org Intro: firstname.lastname@example.org
questions ….( 3)?
11. What enzyme is present in cancer cells, which scientists believe, allows cancer cells continue to grow indefinitely? Morphogenic BA Glucagon C. Oxytocin D. 12.Which of the following telomerase by itself can lead to information? AB genome chromosomes C. Codon D. 13 nucleotides. The process by which a web tour is a "sketch" of a web design before making permanent Internet called A.lock-step sequence. B.simulation. C.trial and error. D.cinch and tie. 14.To produce a specific protein, ribosomes, a set of twenty lines of tRNA, and a strand of messenger RNA work together in a process called A.translation. B.transcription.C.replication. D.reproduction. 15. Through a series of experiments with sterilized broth, Louis Pasteur disproved the idea of A. Gene sequencing. B. DNA. C.spontaneous generation. D.evolution.
11.D.Telomerase 13.B.simulation 12.D.Nucleotide (guess …) generation 14.A.translation 15.C.spontaneous.
Dr. Laura Niklason on the importance of her AFAR grants for telomerase gene therapy research
[mage lang=”en|es|fr|en” source=”flickr”]telomerase cells[/mage]
what enzyme is present in cancer cells, which, scientists believe, allows the cancer cells to keep growing ?
morphogen, oxytocin, glucagon, telomerase
In normal cells, the telomeres (segment of DNA at the end of the chromosomes) shorten following each cell division thus limiting the life span of the cell. Due to the nature of the lagging strand after each cell division some DNA is lost, once the telomeres are gone, slowly genes of the chromosome disappear until the point that the cell cannot make proteins that it needs to survive, then the cell dies. This is very important in cell ageing. Most fully differentiated somatic cells do not express the enzyme, however, for some reason cancer cells do, thus allowing them to be immortal and replicate indefinetly
Elizabeth Blackburn Part 3 Stress, Telomeres and Telomerase in Humans
[mage lang=”en|es|fr|en” source=”flickr”]telomerase process[/mage]
Could increased cell senescence be avoided during healing process by activating the telomerase gene?
During a healing process, our cells divide to repair a damaged area of our body. Telomere sequences are therefore shortened by this process, reducing the lifespan of the newly created cells.
Theoretically, could this be avoided by enabling the telomerase gene in the cells as they reproduce and then disabled upon successful completion of the process or would it be impossible to disable the gene in such a large amount of cells?
(Obviously the cells would need to be monitored to ensure that any defective cells are removed to avoid cancer developing.)
I think, theoretically, this may be feasible. But remember that the effect of activating the telomerase doesn’t apply to all cells. Our body is composed of so many complex tissues and cells. An effect on one cell doesn’t necessarily mean the same effect to all other cells.
Yes, I agree that you must first remove any defective cells to avoid cancer development since activation of telomerase makes some cells immortal (that is, if there are cancer cells, it will multiply and live forever making it hard to destroy them). However, detection of defective cells involves a very tedious and complex process and you might end up destroying the good cells.
Besides, our body needs cell senescence. The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. Senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species as a mechanism to prevent the onset of cancer. In a few simple species, senescence is negligible and cannot be detected. All such species have no “post-mitotic” cells; they reduce the effect of damaging free radicals by cell division and dilution.
These are just my thoughts. Please feel free to correct me if I misunderstood some of the terms.
What’s a Telomere and Why is it Important to the Aging Process
[mage lang=”en|es|fr|en” source=”flickr”]telomerase evolution[/mage]
SENS4 – Evolution of Anticancer Mechanisms (3/3)
[mage lang=”en|es|fr|en” source=”flickr”]harvard telomerase[/mage]
Carol Greider, Ph.D., Q&A Part 4
[mage lang=”en|es|fr|en” source=”flickr”]telomerase research nature[/mage]