The Nobel Prize in Medicine was awarded for the year two thousand and the discovery of the enzyme telomerase. On this occasion (yes, just like that for a while, but recently contracted for the year Zweitausendundzehn is anyway not worth mentioning) is here once the dementia is corrected, the number of consumers of the mainstream media of which to learn about telomeres and telomerase . believe
telomeres are indeed the ends of chromosomes. The enzyme telomerase is able to extend and comes in tumor cells in particularly large quantities. That is all what is wrong with the presentation of the main stream media. The mainstream media have described the enzyme as a fountain of enzyme. By then it is nonsensical. Actually provide some biotechnologists telomerase was already making a large scale in order to sell gullible. But what if you had more of telomerase?
telomeres consist of repeats of the same old sequence that is species specific. In the kind of person that is the sequence TTAGGG. The sequence is a nucleotide, not an amino acid sequence as can unfortunately foolishly now and then must read. In cells in cell cultures has been observed, that the telomeres were shorter after each cell division. That must be so because the replication of the chromosomes are not exactly start with the first nucleotide pairs and not exactly end with the last nucleotide pairs can. That would be an enzyme that obeys only the laws of nature and simply can not make decisions, too much to ask. Bacteria solved the problem by its single chromosome have joined together to form a ring molecule that is replicated through again and again and again. Multicellular organisms need to share too many genes to copy the model. Therefore, multicellular organisms solve the problem by treating all the chromosomes with telomeres from repetitive sequences, the no genes contain , covered on all sides. Thus it will not interfere when lost a few nucleotide pairs, or even a few repeats of the telomeric sequence. In cell culture that takes place until the cells do not divide further, because they lack the telomeric sequence as the initial signal. That the cells in cell culture at some point the ability to divide is lost, one has already been observed long before the telomeres and telomerase and before they knew the chromosomes. This could be seen easily because the ability to divide entered ten times after changing the culture medium and the match around with a division of cultured cells should, at least in mammalian cells. This was called the Hayflick limit, after the former record holder in the duration of mammalian cell culture. In other experimenters the ability to divide was still lost in the past. So it was obvious that the cell culture technique was not perfect (nor is it today), and attempts were made to improve the cell culture technique. The next record was fifty cell divisions or Nährmediumswechsel a cell culture was lost before their ability to divide. do this is regarded today as the Hayflick limit, although some experimenters can achieve already sixty cell divisions. The history of the Hayflick cup record proves already that cell proliferation in vivo, ie in a living organism, must proceed differently in vitro, ie in cell culture, and that has little or nothing to do with the telomerase and telomeres. Nevertheless, both are happy for each other in one context and as a cause seen, of course, mainly of biological laity, which includes, unfortunately, many doctors, which of course should not be so.
In vivo are only a few cells in the embarrassment of having to divide again and again. These are the stem cells. Other cells do during the work to which they themselves are specialized. Because it would be fatal for a living, if they share a stem cell could no longer (the division of human cells to fifty to sixty division operations would be limited, then would everyone not later than six months after his birth, already dead), so was obliged nature to think of something to the telomeres and over again to regenerate. That is why evolution has produced the telomerase, which always attaches repetitions of the sequence TTAGGG (human, other sequences in other animals) to the ends of chromosomes. People have individual differences in many repetitions of the sequence in their telomeres. People from long-lived families actually have more of it and tumors that survive their means, made it earmarked for stem cells activate telomerase genes (as it were illegal). A stem cell can divide, but at each telomere length even further, because the human telomerase with short telomeres always appends the nucleotide sequence TTAGGG to the telomere. But why then are calculated, the longer telomeres an indication of longevity? The answer to the question is, after all, been known well over ten years, but is ignored and mainly by those who report to you on the telomerase.
addition to the telomeres contain human chromosomes (and chromosomes of other animals), other places where there are no genes. These include the centromeres and chromosome to chromosome individually distributed, long, repetitive sequences. The latter decide the way, very much with it looks like a genetic fingerprint. In aged cells, plasmids are also observed. Because plasmids but only in passing on the bacteria used genetic information that they had been taken as evidence of pathogens. That is why they wanted to identify those. It turned out that the cells were not infected with pathogens, but passed the plasmids from repetitive sequences. The plasmids were dropped out during previous cell divisions of the chromosomes and were then combined to form ring-shaped molecules perhaps they had tangled with in the first ring-shaped molecules and were cut out of it. An aged animal cell is thus characterized by the fact that, in addition to oxidation caused by metabolic products, animal containing plasmids. It contains all the more animal plasmids, the older it is. Both the animal and the Centromere plasmids and the telomeres as well as other repetitive sequences can not be interpreted by the synthesizing enzymes as genes, because that would be fatal for the cell metabolism. But an enzyme can not make the decision, it can only obey the laws of nature. That is why nature has solved the problem in another way. She has developed for repetitive Desoxyribonukleïnsäuresequenzen a protein that sits on top those no longer disappears from there and see how others enzymes on the sequence hindrance. The protein is called S ilent I nformation R egulator or shortly SIR (which do incidentally, nothing with the protein SIRT or SIRT Proteïnklasse or SIR-Proteïnklasse which it belongs, is somewhere in the signal transduction one that begins the reading of genes). The silent information regulator protein must therefore sit at all repetitive Desoxyribonukleïnsäuresequenzen. But a cell may only a limited amount of it produced. The older a cell, to the more animal protein, the plasmids must be distributed. For old cells that is a problem. They can not produce enough Silent Information Regulator for all repetitive Desoxyribonukleïnsäuresequenzen, then the cells attempt to resolve the problem by switching off telomerase and telomeres no longer complement the other repeats of the nucleotide sequence. Consequently, telomeres shorten so that a cell after them (by number of previous cell divisions) has grown old.
What would happen now if in fact the production of telomerase could fire up again in old cells or to introduce additional telomerase into the cells? First, the telomeres would actually be extended again. Therefore, the cell would not be enough Silent Information Regulator for all repetitive Desoxyribonukleïnsäuresequenzen. So not all be occupied with it. The new telomere should be to come as the latest, so it is most likely the ones now be readable by other enzymes. The sequence TTAGGG and any combination of the repetitions (TAGGGT, AGGGTT, GGGTTA, GGTTAG, GTTAGG) it will ribonucleic acid and finally converted into amino acid sequences the garbage floating around as in the cells and results are unpredictable. Thus, the cell is not getting any younger, the whole organism is not at all already, but the cell works only worse. Evidence of how such a manipulated cell is generally behave, provide us with so far only the existing cells with an unnaturally high level of telomerase. They are tumor cells. They are even exclusively tumor cells. Let her provide you so sometime in the future with additional telomerase, then are ye only sooner or later provide additional tumors. Anyone who sees this as a fountain of youth, which I can help (or anyone else) any more.
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