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/sci/ - Science & Math


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2673644 No.2673644 [Reply] [Original]

Yo chemfags - how does it feel to know that you guys hold the key to mankinds oldest fantasy - immortality?

So what's taking so long? Telomeraze that shit.

>> No.2673669

If it's your fantasy do it yourself

>> No.2673668

I'm on it

>> No.2673684
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2673684

>>2673668

Great! What's the plan?

>> No.2673681
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2673681

o hai der

>> No.2673687

OP's picture is creeping me out for some reason

>> No.2673708

>>2673684
Finish the graduate school that I'll be starting in Fall.

>> No.2673722

sweet room bro...

>> No.2673725

>>2673644

You are now realizing that using telomerase to prevent telomeres from shortening is also called WHAT CAUSES CANCER

>> No.2673734

>>2673725
[citation needed]

>> No.2673743

>>2673734

http://en.wikipedia.org/wiki/Telomere
>Most cancers are the result of "immortal" cells that have ways of evading this programmed destruction.[4]

>[4] Harrison's Principles of Internal Medicine, Ch. 69, Cancer cell biology and angiogenesis, Robert G. Fenton and Dan L. Longo, p. 454.

JFC how am i the first person to say this, is /sci/ retarded?

>> No.2673748

>>2673743
to clarify, "this programmed destruction" is the shortening of telomeres as per the article I linked.

>> No.2673770
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2673770

I'll tell you guys my secret if you give me some microscopic honey.

>> No.2673788

>>2673734

OH GOD YOU GOT SO FUCKING PWNPWNPWNPWNPWNT

>> No.2673790

>>2673725
cancer is caused by cells dividing at an uncontrollable rate. telomeres have nothing to do with it. the source you linked doesnt say telomerase will cause caner. it's saying that telomeres prevent cancerous mutations by preventing chromosomes from fusing. cancer is also associated with shortened telomeres, so lengthened telomeres would prevent certain cancers.

>> No.2673792

>>2673743
so we should find out how to survive as cancerous blobs!

>> No.2673799
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2673799

>>2673788
>didn't know
>provides a source
>"Huh, learn something new erry day."
>some asshat goes PWNTPWNTPWNT

Just another day on /sci/

>> No.2673814

>>2673790

so you didn't read the link all the way through to the point where it said that cancer exists because the telomeres cease to shorten to the point of the cell dying THANSK TO TELOMERASE

>>2673799
brah, I'm not the asshat, someone sarcastically said [citation needed] to a point of biology i learned in my TEXAS JUNIOR HIGH SCHOOL back in 1997

AND WE ALL KNOW HOW RETARD TEXANS ARE

>> No.2673825

>>2673814

tl;dr telomeres do not fully shorten and kill the cell off, thus cell is immortal, and this is by definition a cancerous cell

this was in direct response to someone saying we need to learn how to keep telomeres from shortening,
>implying making immortal cells would give us immortality instead of assloads of cancer

>> No.2673828

>>2673814
>someone sarcastically said [citation needed]
ALL I SAID WAS [CITATION NEEDED]
>i learned in my TEXAS JUNIOR HIGH SCHOOL
>AND WE ALL KNOW HOW RETARD TEXANS ARE
Lol

>> No.2673838
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2673838

>this entire thread
>doesn't know that telomerase overexpression is only part of the requirements for a succesful tumor
>amateur cancer biology at its finest

Stay classy, /sci/.

>> No.2673869

>>2673838

telomerase overexpression results in a hgher incidence of cancer, and the proposed method of immortality ITT is "TELOMERASE OVEREPXRESSION NONSTOP 24/7"

>>2673828
>all i said was [citation needed]
If you aren't smart enough to realize that 100% of the time when this Wikipedia meme is used it is used to
>imply guy is lying through his teeth
then you really are a dumbshit and should killself for getting styled on by me, a cousin fucking sheep fucking inbred yokel redneck who can barely operate a keyboard

>> No.2673877

>So what's taking so long?
>implying it will happen
Wake up and smell the senescence.

>> No.2673884

This thread made the manifold jizz it's pants

>> No.2673891

Richfag here.

a means of immortality has already been discovered and secretly stored away for the worlds finest only. We're going to let the rest die, keep it for the fine and the few. Imagine if we just sold that shit over the counter. Chaos would ensue.

>> No.2673893

>>2673838
Yes, part of the requirement. Now, think about all of the trillions of cells in your body dividing and dividing and dividing to their indomitable little nuclei's content. What do you think the probability of cancer developing in one of them is?
Hint: it's much higher than in cells that aren't dividing forever.

>> No.2673905
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2673905

>>2673869
>telomerase overexpression results in a hgher incidence of cancer, and the proposed method of immortality ITT is "TELOMERASE OVEREPXRESSION NONSTOP 24/7"
One of the things my lab is looking into is the generation of mice that have normally functioning telomerase except in the presence of a certain secret factor, then (by a secret proprietary (not really) process) increase telomerase activity until the factor is removed, because yes, overexpression all day erry day does lead to an increased risk of cancer. See knudson hypothesis.
We're following up on Ron DePinho's paper, "Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice" to see what kind of nifty phenotypes we can generate in mice that don't have conditional telomerase silencing, but instead have conditional overexpression.

Pretty srs.
So yeah, you're kinda right, it does sorta cause cancer, but it's not HURP DURP OVEREXPRESSION DIRECTLY IMPLIES CANCER IMMORTAL CANCER-RIDDLED PPL LOL as your first post seemed to imply.
>using telomerase to prevent telomeres from shortening is also called WHAT CAUSES CANCER

>> No.2673907

>>2673814
"Advocates of human life extension promote the idea of lengthening the telomeres in certain cells through temporary activation of telomerase (by drugs), or possibly permanently by gene therapy. They reason that this would extend human life because it would extend the Hayflick Limit. So far these ideas have not been proven in humans, but it has been demonstrated that telomere extension has successfully reversed some signs of aging in laboratory mice and the nematode worm species Caenorhabditis elegans. However, it has been hypothesized that longer telomeres and especially telomerase activation might cause increased cancer (e.g. Weinstein and Ciszek, 2002). Paradoxically, longer telomeres might also protect against cancer, because short telomeres are associated with cancer. It has also been suggested that longer telomeres might cause increased energy consumption"
>the effects of telomere lengthening on cancers are not known

"As a cell begins to become cancerous, it divides more often and its telomeres become very short. If its telomeres get too short, the cell may die. It can escape this fate by up-regulating an enzyme called telomerase, which can prevent telomeres from getting shorter and even elongate them."
>extremely shortened telomeres can help prevent some cancers if the right genetic information is impacted, but cancer is caused by cells dividing too fast, which is regulated by MPFs, not DNA. cancer cells can continue to live and divide with very little DNA.

>> No.2673910

>>2673905
And the entire point of that post was, conditional overexpression does not lead to increased cancer rates.

>> No.2673913

>>2673907

"Studies have found shortened telomeres in many cancers, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck. In addition, people with many types of cancer have been found to possess shorter leukocyte telomeres than healthy controls"
>shortened telomeres are definitely linked to cancer. not longer ones.

"a sizeable fraction of cancerous cells employ alternative lengthening of telomeres (ALT), a non-conservative telomere lengthening pathway involving the transfer of telomere tandem repeats between sister-chromatids"
>many cancerous cells have telomerase active to allow them to build more useless DNA, but this is in cells that are already cancerous. adding telomerase to somatic cells will not cause them to be cancerous. it can instead reduce, if not remove entirely, the affects of aging, as well as reducing risks for cardiovascular disease and other things

>quoting wikipedia is pro. also basing molecular biology opinions on a textbook that's fourteen years old is sketchy at best. read some up to date stuff

>> No.2673918

>>2673644
>rape sux
i chuckled a bit

>> No.2673932

>>2673770
The bears know.
They hold the future.

>> No.2673961

Chemfag here
Back when we were still called alchemfags we found it, but you bastards think its too expensive and lethal.

>> No.2673972

>>2673961
Are you referring to the philosopher's stone?

>> No.2673974

its already been created by logic, its just a matter of finding out how to make one.

>> No.2673980

>>2673972
Nope i'm referring to the wondrous art of scamming kings out of money with mercury poisoning, while also developing basics of a science.

>> No.2673998

When telomere sequences are exposed they are subject to DNA repair machinery which leads to end to end fusion of chromosomes and this leads to cell death. There is a process known as capping where telomeric DNA is bound to proteins that protect it from repair mech. The probability of UNcapping increases as telomere length decreases.

Somatic cells of multicell org. have no telomerase activity (thus the cells are limited to about 50 doublings). This is where the aging thing comes from.

There is a correlation between telomere length and proliferation capacity (as has been shown with progeria - premature aging) where fibroblast cells have observed short tel sequ. and there is decreased proliferation.

Some cancer cells have active telomerase that leads to uncontrolled proliferation and immortality.

Just wanted to clear some stuff up.

>> No.2674013

>>2673998
>When telomere sequences are exposed they are subject to DNA repair machinery which leads to end to end fusion of chromosomes and this leads to cell death. There is a process known as capping where telomeric DNA is bound to proteins that protect it from repair mech. The probability of UNcapping increases as telomere length decreases.
It's also significantly tied to the ability of telomerase sequences to form highly stable quadruplex structures, which are not able to be acted upon by DNA repair machinery. Whether or not this protection is COMPLETELY protein independent, I can't really say.

>> No.2674020

>>2674013
Do you mean G-quartets? I thought that's the structure the capping proteins binded to.

>> No.2674042

>>2674020
G quartets are a big reason behind quadruplex stability, but the issue of the structure is more complex than just 4G tetramers.
I was under the impression that those quadruplex regions, which have a vastly different tertiary structure than the rest of the DNA, simply don't present the topology to be recognized by DNA repair mechanisms, and that the capping proteins weren't the main mechanism of telomere function.
Quadruplex structures are srs business. Shit won't denature at temperatures of 100C or higher in the buffers I've studied. Most complexes I've studied and/or heard about can't unwind it.