linkedin post 2018-08-21 04:45:38

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HUMAN ALU REPEAT. “Over 5% of the mammalian genome consists of short interspersed elements (SINEs), typified by the human Alu repeat. These are RNA polymerase III transcribed sequences whose expression is usually silenced. However, upon prolonged exposure to DNA damaging agents that predominantly cause double strand breaks, transcription from the human Alu elements and murine SINEs is strongly induced.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn
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linkedin post 2018-08-21 04:47:57

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TELOMERES AND DNA DAMAGE. “Telomere length is highly connected with the replicative lifespan of metazoan cells. Telomeres shorten with each successive round of DNA replication until one telomere reaches a threshold of “shortness” that emits a chronic DNA damage signal that causes the cell to cease dividing and enter senescence. Mechanistically, the short telomeres are seen as chronic DNA damage by the cell, resulting in the activation of the DNA damage response, which causes a G1 cell cycle arrest.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn
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linkedin post 2018-08-21 04:49:45

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BACK TO CHROMATIN. “Telomere-mediated activation of the DNA damage response appears to be intimately linked to the chromatin structure. Specifically, it was shown that chronic DNA damage from the processed telomeres also affects histone expression leading to their depletion and to the depletion of the central histone chaperones.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn
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linkedin post 2018-08-21 04:51:15

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JUMPING GENES. “However, in response to a potential decay of the chromatin structure during aging, excess retrotransposon transcription prevents recruitment of cohesion and condensin, causing persistent DNA damage checkpoint activation and senescence.” http://journal.frontiersin.org/article/10.3389/fgene.2013.00136/full View in LinkedIn
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linkedin post 2018-08-22 05:54:57

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TELOMERE METRICS. “Harley et al. observed that the mean telomere length decreased by 2 to 3 kilobase pairs (kbp) during the serial passage of several strains of normal human diploid fibroblasts. The decrease was found to be progressive and averaged 50 base pairs for each population doubling. The telomere shortening seen in aging normal human fibroblasts also occurs in vivo in skin epidermal cells, peripheral blood leukocytes and colon mucosa epithelia.” http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn
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linkedin post 2018-08-22 05:57:08

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CREATIVE SOLUTION. “Eukaryotic cells have evolved a novel solution to the end replication problem in which the specialized chromosome end structures, or telomeres, contain repetitive sequences, some of which are lost at each round of replication. The loss of these sequences, which lack the information contained in downstream genes, acts as a buffer protecting those genes from loss during each round of DNA replication.” http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn
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linkedin post 2018-08-22 06:00:56

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THE AGING CLOCK. “Telomeric shortening, which occurs in several classes of dividing normal somatic cells, may be the replicometer that determines the number of times that a normal cell is able to divide. Once a critical or threshold number of telomeric TTAGGG repeats is reached, cells will then be unable to divide.” http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn
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linkedin post 2018-08-22 06:02:38

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SECOND EXCEPTION. “How do the cells composing immortal populations avoid telomere shortening that, if it occurs, would lead to their demise? They found that telomeres are synthesized de novo by telomerase, a ribonucleoprotein enzyme that extends the 3´ end of telomeres and thus elongates them. This ribonucleoprotein complex contains a reverse transcriptase and RNA template for the synthesis of the repeated sequence. Telomerase was later found to occur in extracts of immortal human cells.” http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn
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