RNAinterference

[immortal]

Is these ideas going to work.

 

As we all know that the life span of chromosomes depend on their telomere length. With the help of RNAinterference can we switch on the gene in humans which synthesises the enzyme telomerase and live forever.

Or else

You can overexpress the Klotho gene to produce more klotho protein to increase your life span.

[ecoli]

except, that telomerase tends to promote cancer as well, at least in humans... So much for the fountain of youth.

 

Even, with telomerase, this just means the cells don't age as quickly, not that they'll live forever.

[immortal]

except, that telomerase tends to promote cancer as well, at least in humans... So much for the fountain of youth.

 

Even, with telomerase, this just means the cells don't age as quickly, not that they'll live forever.

 

You can always switch off the gene as soon as the average telomere length is achieved and prevent cancerous cells.

[Dak]

our cells also produce telomerase-inhibitase, which slows down the action of telomerase.

 

this means that telomerase can keep up with normal cell duplication, but not with cancer's duplication; anything that inhibits or removes telomerase-inhibitase (and thus allows telomerase to keep up with cancers replication) is, in actual fact, a (secondary?) carsonogen.

 

so yeah, making there effectively be more telomerase action would probably be a bad idea, possibly even over the short-term.

 

with ageing, is it actually anything to do with telomerase action that iliminates telomeres?

 

when a telomere is copied, it's length goes up or down by a few repetitions.

when you're old and lose your telomeres, is that because your telomerase isn't functinoing properly, or is it because, given enough time, you'll get several duplications in a row where the telomere just happens to shrink?

[Prewitt]

telomere length is just a thesis. there is probably a lot more to limitations of the lifespan of cells than just telomeres. besides - you cannot manipulate genes that easily in living humans. if you could - hellooooooooo nobel prize.

[Paralith]

telomere length is just a thesis. there is probably a lot more to limitations of the lifespan of cells than just telomeres. besides - you cannot manipulate genes that easily in living humans. if you could - hellooooooooo nobel prize.

 

there are definitely many more factors in aging than just telomeres, even if they are one of the larger factors.

 

also, though still in the process of development, the possiblity of gene replacement (or at least, gene addition) is increasing with the use of retroviruses. still a very long way from implementation, but it is in the works.

[immortal]

We can use nonviral delivery systems such as polyethylenimine(PEI), a synthetic polymer which can deliver gene safely into the cells. Since the efficiency of this polymer is low it is a long way from implementation.

[Prewitt]

the problem is not really to manipulate the gen but to target cells specificly. there have been deaths because artificial viruses targeted the wrong cells in some patients. imo that is the major problem. once you can specificly target your cells of intereset in vivo (meaning them and only them) medicine will enter a new century.

[immortal]

Sooner or later medicine will enter a new century with innovative technologies evoving all the time.

Here is a link of a company which uses electroporation technology to deliver genes safely and efficiently.

http://www.inovio.com/technology/genedelivery.htm

[Prewitt]

sadly enough, this is not necessarily true. there are some problems in science that can not be solved by solely working on them. eg. the development of a fusion reactor. there are profound problems that might be solved by the discovery of a totally new technique. unfortunatly those discoveries happen by accident rather than systematic research. therefore in vivo cell targeting might be invented one day, but might also not at all. electroporation is a rather old in vitro technique for dna uptake that does not contribute the the mentioned problem of specific targeting of in vivo cells which is without doubt a necessity. therefore to my mind all thought about the topic are pure science fiction. and it'll stay that way until something like a revolutionary discovery is made. as i already said this discovery can occur but doesn't have to. you can but a million highly skilled scientists in a garden eden of research - they might work several hundred years and still not make the discovery - that's the way my math teacher used to explain this kind of discovery.

[Dak]

wait, we can target vectors in vivo, can't we?

 

maybe not with 100% accuracy, but the fact that we can kinda sujjests that attaining ~100% accuracy is just a matter of time.

[Prewitt]

last thing i've heard were experiments in the states who thought they could and some patients died. because the vector worked well in just a part of the patients. also the problem is that it's just modified viruses afaik and you can't make them specific for any cell you like.

[immortal]

our cells also produce telomerase-inhibitase, which slows down the action of telomerase.

 

this means that telomerase can keep up with normal cell duplication, but not with cancer's duplication; anything that inhibits or removes telomerase-inhibitase (and thus allows telomerase to keep up with cancers replication) is, in actual fact, a (secondary?) carsonogen.

 

so yeah, making there effectively be more telomerase action would probably be a bad idea, possibly even over the short-term.

 

with ageing, is it actually anything to do with telomerase action that iliminates telomeres?

 

when a telomere is copied, it's length goes up or down by a few repetitions.

when you're old and lose your telomeres, is that because your telomerase isn't functinoing properly, or is it because, given enough time, you'll get several duplications in a row where the telomere just happens to shrink?

 

Telomerase has nothing to do with the abnormalities that occur in cancer cells it just helps the cells to divide infinitely. The abnormalities occur due to some mutations in the cells.

[Prewitt]

that is...well...not completely correct. there is a reason that cells do not have a telomerase. if a normally non-proliferative tissue get by whatever means proliferative in a cancerous way, it's proliferative potency is limited to the normally lacking telomerase. if you artifically give all your cells a telomerase, cancer prevalence among your cells will drastically increase.

 

may i ask what relation you have to the topic? are you a student?

[CharonY]

While the precise connection to cancer is not clear, it is known that cancer and tumour cells in general usually have overactive telomerases as compared to normal somatic cells.

Also enlarging telomeres would be detrimental in general as different cells in your body must proliferate in a coordinated manner. Telomeres apparently also play a role in regulating this proliferation. A deregulation, even if not leading to cancer, is surely to be disadvantageous.

Finally, another widely acknowledge factor of aging, the oxidative stress, would not be addressed by this at all.

[immortal]

that is...well...not completely correct. there is a reason that cells do not have a telomerase. if a normally non-proliferative tissue get by whatever means proliferative in a cancerous way, it's proliferative potency is limited to the normally lacking telomerase. if you artifically give all your cells a telomerase, cancer prevalence among your cells will drastically increase.

 

may i ask what relation you have to the topic? are you a student?

 

Yes I am a student willing to take up molecular biology as my future career.

I know there are different causes for cancer and plenty of mutated genes that lead to the abnormalities but if we can somehow prevent the primary tumour cell from spreading to other cells, the cancerous cell would die as it is alone. It takes a number of mutations for cells to be cancerous and it is not a problem if these cells die as cells are not very important (because new cells will arise all the time) and coming to my topic now I do agree that adding telomerase will be a bad idea because there is lot of uncertainity in it.

[Prewitt]

also that is not entierly true. it is pretty often just ONE cell that makes a cancer, since most are monoclonal. the point is that cancerous cells arise all the time and degrate by various means, being limited by telomorases being probably one mean, and nothing happens. but if just ONE cell does survive that is cancerous, you will get a solid cancer. that is the way it happens. it's all just statistics. there is a large number of cells that mutate. few of these mutations are sufficient for cancer. and few of these survive to actually cause cancer. but if ONE does, you get cancer. normally that numbers are so small that you probably don't get cancer. once on of the numbers increase, the probability does too. it just matters if one cell in the end survives.

[immortal]

I do agree that without new technologies for gene therapy and a universal vaccine for cancer the probability of me getting attacked by cancer is very huge. I know that the road to achieve immortality has some ups and downs. There are genes like KLOTHO and MORF4, there are antioxidants, there are stem cell enhancers but I think these things are not sufficient to achieve immortality.

[Paralith]

last thing i've heard were experiments in the states who thought they could and some patients died. because the vector worked well in just a part of the patients. also the problem is that it's just modified viruses afaik and you can't make them specific for any cell you like.

 

Well, the beauty of some viruses is that they already target specific tissues and/or cell types. Viruses have a "preferred" range of hosts for which they have been selected to target. And if viruses have a means of targeting cell types, then there probably will some day be a way to adjust that means to target the cells we want them to target. (Just used the word target(ing) five times! yerk.)

[muchado]

Interesting discussion...it is really important to be open minded when talking about actual cause of cancer....many in the field will tell you that telomere dysfunction (i.e. shortening, missing proteins in the 'cap'), which leads to end-to-end fusion of chormosome and self perpetuating bridge-fusion-break cycles, is the main cause of cancer and genome instability. Since these events lead to amplification, deletion, and addition of different parts in the genome.

 

As for the original question..turning back telomerase will not give you immortality. As Prewitt pointed out before, telomerase is selectively turned off in our cells. This feedback mechanism is extremely important for tumorgenesis..while telomerase must be turned on to develop tumor, it must be turned off before a tumor can take its mature form. There are plentiful of literatures supporting this. Ask for reference if you are interested.

 

Cheers!