[mage lang=”en|es|fr|en” source=”flickr”]telomerase disease[/mage]
[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: email@example.com
[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 detection[/mage]
[mage lang=”en|es|fr|en” source=”flickr”]telomerase replication[/mage]
HELP multiple choice?
The enzyme telomerase solves the problem of replication at the ends of linear chromosomes by which method?
A)adding a single 5′ cap structure that resists degradation by nucleases
B)adding numerous GC pairs which resist hydrolysis and maintain chromosome integrity
C)adding numerous short DNA sequences such as TTAGGG, which form a hairpin turn
D)causing specific double strand DNA breaks that result in blunt ends on both strands
Telomere Replication Made Easy
[mage lang=”en|es|fr|en” source=”flickr”]telomerase in cancer[/mage]
Potential new approach for treating myelofibrosis
A new study conducted by a team of researchers at Boston University School of Medicine (BUSM) sheds light on a possible new approach to treat the bone marrow disease known as myelofibrosis by inhibiting an enzyme that connects extracellular fibers.
Lung Cancer: Recharge Biomedical – Dr Ed Park’s Podcast 4 (short version)
[mage lang=”en|es|fr|en” source=”flickr”]cells with telomerase[/mage]
Pourquoi ne pas les dernières cellules de la vie d'un organisme?
a. L'élimination de la réplication de l'ADN suivantes ARN primaire conduit à une raccourcissement des chromosomes et finalement la mort cellulaire. b. l'enzyme télomérase est facilement détruit par l'environnement, résultant dans la mort cellulaire. C. Réplication L'ADN est sujet à des erreurs, ce qui provoque une mort cellulaire prématurée d. Fragments d'Okazaki la synthèse des protéines modifiées, ce qui entraîne une mort cellulaire prématurée. e. Répétez la séquence télomérique TTAGGG interfère avec la réplication d'ADN normal et entraîne la mort cellulaire
C. Réplication de l'ADN est soumis erreurs, peut causer la mort cellulaire apoptose, la mort cellulaire programmée survient lorsque dommages à l'ADN est réparé et ne peuvent être adéquatement
Three Scientists Win Nobel Prize in Medicine
Two defective genes may cause telomere elongations in cancer cells: Study
Scientists at Johns Hopkins have provided more clues to one of the least understood phenomena in some cancers: why the “ends caps” of cellular DNA, called telomeres, lengthen instead of shorten.
Dr. Edmund Chein,MD on 2009 Nobel Prize in Medicine pt 3
[mage lang=”en|es|fr|en” source=”flickr”]rna telomerase[/mage]
How is telomerase RNA synthesized?
telomerase RNA component (TERC) is transcribed from the TERC gene.
the TERC gene is located –
Cytogenetic Location: 3q26
Molecular Location on chromosome 3: base pairs 169,482,397 to 169,482,847
Tom Cech Part 1
[mage lang=”en|es|fr|en” source=”flickr”]green tea telomerase[/mage]