27 replies to this topic

[Lazarus Long]

Scientists: Biological Clock Is Two-Faced Protein
Mon Jan 6, 3:20 PM ET
http://story.news.ya...cience_clock_dc

WEST LAFAYETTE, Ind. (Reuters) - A two-sided protein that tells cells when to grow and when to rest is nature's timepiece, a discovery that offers help to those whose internal clocks have been disrupted by jet lag or health problems, a husband-and-wife scientific team said Monday.

The two-sided, cylindrical protein, which has been recreated in the laboratory and altered by the team to confirm its function, directs 12-minute growth and rest cycles in living cells, the Purdue University researchers said.

"One 'face' handles cell enlargement. Then the protein 'flips over,' allowing the second face to carry out other activities while cell enlargement rests," said James Morre, a medicinal chemist at Purdue's pharmacy school, who has researched the origins of biological clocks since he was a student 40 years ago.

The protein's precise timing and its links to living organisms' biological clocks was tested by altering cloned versions to produce cycles of between 22 and 42 minutes.

"Now we have an opportunity to tell how organisms tell time," said Dorothy Morre, a professor of foods and nutrition at Purdue University.

"This could give us new insights into cellular activity, such as cholesterol synthesis, respiration, heart rhythms, response to drugs, sleep, alertness -- there's so much," she said.

The body's biological clock, sometimes referred to as Circadian rhythm, has been thought to have hormonal and, ultimately, multiple genetic sources -- though it has been tenuously linked to cycles of the moon and to sunspots. The mechanism seems similar in all organisms, directing plants to unfurl leaves or animals to start a mating cycle.

The couple's research, which was published in the journal Biochemistry, was sponsored in part by NASA (news - web sites), the National Institutes of Health (News - Web Sites) and the Purdue Botanicals Center.

The protein's switching mechanism is difficult to see, because it is constantly moving and has not been crystallized to get a closer look at it, James Morre said.

The prospect of speeding up or slowing down the body's biological clock may not be possible, but it should be possible to reset the clock, he said.

"This discovery also affords an opportunity to improve our methods of clock setting, from minimizing jet lag to correcting sleep disorders," he said. "We might even be able to develop simple artificial clock-setting environments to aid astronauts and those living near the Arctic Circle, where day-night cycles are absent for long periods."

[Mondey]

Hi,

Another broad category of analysis that could yield the fruit of understanding is to do long term studies on individual genetics over the full life cycle.

"I admit this would be a very good and badly needed project."


I do not think that a truly in depth analysis has yet to take place and because of the long term aspects of this most investigators would shy away from this kind of study.

Various governmental research institutes and Universities have been taking blood samples that might be useful for establishing a baseline for analysing natural mutation rates and possible "Markers" for the aging process in a single generation.


"This collected blood wouldn't give this much information when you look for markers of aging, because the blood only reflects the daily fitness or age of the body, so you couldn#t realy tell from this kind of samples if one patients is relavtively old or not. If you have taken the blood from the patient after a small influenca, it will reflect an other age/stress point as when you take it after he did eat for a week a lot of healthy food. It would be necessary to take tissues samples from patients over a very long period of time and from many people to execlude such differnces/changes of daily health of the human."



Mondey

[Lazarus Long]

Thanks for noticing.

Now how to organize these kinds of statistical analysies along with access to the dataabse and samples?

[Jay the Avenger]

http://www.ananova.c...nceanddiscovery


Genetic test might tell how long you'll live

Scientists have developed a genetic test which could one day be used to let pensioners know how long they are likely to live.

Scientists in the United States found it is possible to predict death risk by looking at the ends of chromosomes.

The discovery could have big implications for life and health insurance, and people's pension entitlements.

Those with lower life expectancies might find it hard to get insurance, but could be rewarded by higher pensions because they would not be drawing them for so long.

The researchers from the University of Utah studied 143 individuals all over the age of 60.

They focused on the telomeres - caps of DNA at the ends of chromosomes.

Telomeres appear to protect and stabilise the chromosome ends, like the tabs on the end of shoe laces which prevent them fraying.

Over time the telomeres shorten and provide less protection, making cells more vulnerable to degenerative age-related diseases.

The US scientists measured telomere length in cells taken from blood samples and compared them to individuals' life spans.

The findings, reported in the Lancet medical journal, showed that those with the longest telomeres lived the longest. Those in the top half of the range of telomere lengths lived four to five years longer than those in the bottom half.

[ocsrazor]

I just caught the original article in this weeks Lancet. Not really anything new, but it is nice to see statistical confirmation that telomeres are likely involved in aging of the immune system. My guess is that the involvement with heart disease is likely linked to bacterial infection as well, as there is a large body of evidence suggesting this. Suprising the authors don't draw this conclusion themselves. So, the take home message is that if you have short telomeres, you better do everything you can to maintain the health of your immune system.

It is likely that telomeres are limited to affecting the aging of a limited # of cell types (i.e. the fast dividing ones) . I certainly don't buy the argument that telomeres are the root cause of all aging.

Best,
OcsRazor

[Mind]

Here is a recent article about how cells keep time. I am not sure at this point if this discovery has applications in life extension. The discovery is of a protien that drives cells on a 24 minute cycle. This timing can vary up to 42 minutes long. Perhaps if our cells ran on the "slow" 42 minute clock we would would live longer. Anyway, here is a link.

New Protien Discovered

[ocsrazor]

Good Post!

Biologically very interesting, might be applicable to CR and other metabolic studies of aging, but you definitely wouldn't want to slow your cell clocks down which would result in your normal body rythms being altered and a loss of control by the higher systems (neurologic, hormonal, etc.) which regulate metabolism and depend on cellular processes being what they expect. Besides, that would result in a much slower metabolism, and who wants to be a slug for their whole life? ;^)

Best Stuff,
Ocsrazor

[Lazarus Long]

It is a great article and a wonderful follow up on the fact that I mentioned this research over two weeks ago in the other thread on: How does the body know its age?

Yahoo Article & Links

Parallel Thread

This one does give more depth and I suggest we watch Nature Magazine, Science, and Scientific American, etc. to see where the full text of their research gets published. I concur completely on the vitally important aspect of this discovery.

I should add that I think this couple belongs in the Hall of Mention at the Gilgamesh Project.

[ocsrazor]

Hi Gang,

Lazarus brought this thread to my attention, and this reply should probably be cross posted in both the thread about aging theories by Caliban and the new one started today by Mind about the biological clock. The new research about a cellular biological clock is important for general metabolism research and understanding cellular energy processes, but this should not be confused with a global body clock for aging, the idea of which most aging researchers finally rejected about ten years ago.

There is a developmental program for getting us to adulthood, but all the data suggests that after that it is just systems wearing out, there is no program anymore. Even telomeres, which only affect a limited number of cell types are just an example of a component with a limited lifetime going past its warranty. There just isn't any data for a prgrammed (or clocked) theory of aging, despite many years of looking for one. The strongest refutation of this idea was by Michael Rose, who is the foremost evolutionary thinker on aging, see his book for a complete explanation:

Evolutionary Biology of Aging, by M.R. Rose
http://www.amazon.co...il/-/0195095308

So the short answer to the question the original post asked is for development to adulthood, there is highly networked spatio-temporal system that uses certain key events for doing things such as starting production of certain hormones, or starting and stopping bone growth. There is no central clock, just a highly evolved interconnected system. For aging, there is no timing mechanism at all, because there was never any selective pressure to create it, we have only very recently been able to live beyond ~35-40 years, not enough time for evolution to act. We just have a system whose components become damaged by use and eventually lose the ability to repair themselves. (OK maybe that wasn't so short)

Best,
Ocsrazor

[ocsrazor]

Hi Gang,

I just wanted to make absolutely clear what the impact on aging research is for this publication. The importance is that this may lead to more fundamental understanding of how the cellular metabolic processes operate, and this is important for aging because senescence is most likely the result of accumulated damage, a good deal of which is caused by these metabolic processes. This wil NOT lead to the discovery of a global aging clock. For further information why, please see my post here:

http://www.imminst.o...=44&t=681&st=12

I'm going off on this because the clock or programmed hypothesis of aging is just blatantly wrong and it needs to be made clear that it is just not true. Talking about this to an aging researcher is similar to saying the Earth is flat. It just ain't so.

Best,
Ocsrazor

[Jay the Avenger]

Here is a recent article about how cells keep time. I am not sure at this point if this discovery has applications in life extension. The discovery is of a protien that drives cells on a 24 minute cycle. This timing can vary up to 42 minutes long.

Could it be that "42" really *is* the answer to all questions in the Universe? [B)]

[Lazarus Long]

Note from Ocsrazor: Lazarus originally posted this piece to the Aging Theories Thread. I felt it deserved its own thread because it has some complex issues outside of just aging and is a whole discussion in its own right. The first six posts here are the original part of the discussion between Lazarus and I. Please post your own insights on biological timing as well.

Well we have an observable fact. There seems to be a chemical clock in the cells.

This begs at least two questions (probably more) Why? And what is it controlling?

Let us step back and also ask a different question, is it the only observable clock that we can recognize which effects human metabolism?

For those of you that don’t see where this is going, let me spell out the obvious for most of my male counterparts here studying this with their built in gender bias, menstruation already has a clock and it appears to coincide with the findings suggested.

Why would male physiology have a menstrual cycle?

Because gender isn’t as concrete as we are lead to believe through memetic understanding, male physiology can be seen genetically as simply a specialized variant on female physiology.

Testable hypothesis:

Examine the cellular chronological system for coincidence with menstruation, and determine if what we are seeing is in fact the timekeeper for ovulation AND longer periodicity phase change with regard to sexual maturation and post partum behavioral/physiological change (for BOTH genders).

Corollary question of arcane interest, determine how a cellular mechanism is sensitive to tidal, and/or other factors such that it can be responding to Lunar Cycles as has been an observable fact for thousands of years, or is this just a Cosmic Coincidence?

[>] How does the body know its age?

[>] Cell Clock Discovered

Hope From Telomeres?

Edited by ocsrazor, 03 March 2003 - 03:50 PM.

[ocsrazor]

Hi Lazarus,

Just a quick response, it is extremely unlikely that the cellular clock you mention is related to the menstrual clock. Female hormonal cycling is caused by a complex central nervous system clock which is well understood and is not dependent on cellular metabolic clocking. It is an emergent system property which cannot be extrapolated from single cell behavior.

Best,
Ocsrazor

[Lazarus Long]

I don't think it is off topic and I included the other links because I see them as merging for discussion. Funny I was doing it before but while you were writing you post.

Synchronicity?

Or at least I anticipated your concern.

Here is why: We need to test the arguments that aging is directly a consequence of sexual maturation and progenitive physiology.

If it is, and if the phases can be seen as predominantly for that purpose then many alternative approaches to modifying the process may become more apparant. This is a challenge to paradigms and perhaps that is why you are (too) quick to offer a change of thread.

I suggest that we fly these ideas together a bit and break formation later after we have a chance to see what level of parallelism is observable. But you are correct that I too think it is relevant to the Cell Clock argument and that is why I too included those links.

[ocsrazor]

Hi Lazarus,

I was also adding an edit to my last post

General notes on timing and aging:
The best place to look for timing mechanisms for aging are in the complex system clocks for development. The clock is a bad metaphor for aging though, because these systems set up a trajectory which can be altered by environmental influence, but the body is not a strict timekeeper. The menstrual cycle is a downstream effect of these systems, and can give you insight into where the trajectory is going and if it is running optimally, but it will not give you an explanation of the higher level system.

To reiterate some of my earlier posts, telomeres are not a timing mechanism at all, but are a damage control mechanism (one of the last damage control mechanisms to fail as we age)

Cellular level clocks are not affecting aging trajectory except in the way they feed into the higher order system, but this is not a linear system and it has emergent properties at every level. Damage to cells does affect the trajectory because large parts of the system are no longer functioning in the way the system was evolved to handle and so coordination is lost.

Higher central nervous systems/hormonal systems may use cellular metabolic clocks to respond appropriately to environmental conditions, which may have the pleasant side effect of extending development time and lifespan. As an example, caloric restriction does cause some other developmental program to start running.

So Laz, what I am saying is that there is no direct connection between cellular metabolic timing and menstruation. Cellular timing is a low level control point for the developmental system, and menstruation is an indicator of the health of the system and can yield information about what the local (monthly) rate of the system is. The highly networked system controlling all of this is the appropriate place to look for explanation.

Best,
Ocsrazor

[Lazarus Long]

So Laz, what I am saying is that there is no direct connection between cellular metabolic timing and menstruation. Cellular timing is a low level control point for the developmental system, and menstruation is an indicator of the health of the system and can yield information about what the local (monthly) rate of the system is. The highly networked system controlling all of this is the appropriate place to look for explanation.

This is assumption not validated fact and deserves a more deeper test of both hypotheses.

That is also my point about scientific methods as well, herein is the test of character that determines the difference between good scientists and bottlewashers that are comfortable with their accepted assumptions.

[ocsrazor]

Hi Lazarus,

The system controlling menstruation is very well understood and is regulated by a network of coupled oscillators (system level oscillators, not single cells) in the central nervous system (hypothalamus mainly) whose inputs are hormonal and neural signals. Something as low level as timing of cell metabolism is unlikely to provide information to this system. I'm not ruling it out completely, but according to what we know about molecular physiology, this doesn't happen in large multicellular animals.

Best,
Ocsrazor

[Lazarus Long]

I am saying to test this conclusion you are drawing not assume or discount the question. There is a strong overlap between the timing of this cellular cycle, and basic neurochemistry doesn't explain Alpha Cycling and Lunar Rhythm. Something at a much more fundamental level must be interacting with broader environmental features.

If the mechanism we understand takes its measure from the cellular clock we are observing then we are seeing a "Timed Reaction" which triggers Ovum Planting and Cycling.

I don't disagree with a word you have said describing the "known" system of Hypothalamic Control; I am only describing a possibility that the newly discovered cellular cycling functions as a systems "timer".

In this case the clock mechanism is probably a redundancy built in to every cell. They don't all need the specific meter of menstrual cycling but like a bios they all need a BIOS Clock, so nature just makes the same model do it all. DNA is a living computer and I DON'T think it s pushing the analogy to a computational device to suggest the need for a basic systems timers that aligns each cells Nuclei operating system

Such a mechanism wouldn't have to very noticeable, any more than your alarm clock is in your room as a cell would see it. A sort of oscillating organic crystal triggered at the birth of each cell and running like a bios clock for the DNA software.

Now you can argue that what I am saying about Alpha Alignment of Menstrual Cycling for small groups is anecdotal and I will say test it.

You can argue that Lunar Coincidence of Menstrual Cycling is anecdotal and I believe I will look for papers on this one. There is a meter that must interact on an unseen tidal and sociopsychological level for there to be interaction.

On a basic level this cellular clock might be sensitive to tidal force. On a behavioral level something about behavior causes the biorhythmic patterns of small grouped females to coincide for menstrual cycle with certain specific members of the female group. Anthropological study confirms this actually. The data is from tribal studies and the behavioral link to hormone production suggets the linkage.

Hormones probably operate to regulate the cell clocks rate and is interactive with Body Metabolism such that the rate of cell production can be altered to lie within a powerband in proportion to the Physiological Paramters of each individual. This may describe how we change complex cellular output based on neural input of command.

Otherwise the bodies ability to adapt rapidly over all its systems wouldn't be able to change its power output as easilly it does yet keep synchronized heart rate, respiratory, digestive, etc.

I understand all these have hormonal and synaptic connectors that transmit information I am suggesting a reason that the signals are understood on a "Program Level" that allows complex neural dominance very much of the bodies mechanisms, but keeps its own meter for general cell reproduction, general physiology, as well as the species level of reproduction cycling.

Here is an hypothesis that I should now have to test.

Or as Another God says it: Prove me wrong!

My point is we are as a species behaiorally outgrowing dependence on menstrual cycling and adapting over millennium and eons as we become more evolutionarilly complex but this is a "cellular level of physiology" we are describing. Such as a limbic system it will be more basic in principle and more an evolutionary consequence of what we possess at a primal physiological level, as might even control procreative physiology and basic cellular division and nuclear systems control over the cell. Male anatomy wouldn't need a different meter then the cellular timer women do need so again all cells get the same timer. I am proposing a different perspective on the same processes not an overall challenge to basic female physiology as it is well understood.

The brain is a DNA based Quantum Computer. Synaptic firings probably represent the energy, or current of the Command but the Software Language of the Command must have a kind of BIOS like Clock of its own too. Something that keeps all our cells of a complex mulitcellular organism singing to the same cellular tune

[ocsrazor]

Hi Gang,

Me and Lazarus Long had a chat last night about the issues in his last post, I'll try to summarize some of the ideas here.

Lazarus believes that the cell metabolism clock maybe acting as a low level general system clock off of which much of the general physiological system of an organism is basing its timing. I agree completely with that idea, but from what I know of molecular physiology, I think that this system is utilized in a top down fashion, i.e. the local cell clock timing is being adjusted by hormonal influences from the central nervous system and general physiological network systems. Lazarus feels there may still be some upstream timing signal from the cells to higher level systems. I don't think there is a need for such a signal or any evidence for such, but I would need to do a detailed literature search or experiments to really answer the question.

When Lazarus mentions Alpha alignment, he is referring to that strange phenomenon of multiple females living in close proximity to each other tend to synchronize their menstrual cycles. That has been well documented, but is not fully explained and is thought to be pheromone related. Lazarus points out that they tend to synchronize to an alpha (dominant) female, I have never read this, but would be very interested in seeing some literature on this. I suggested that the timing mechanism is probably higher level coupled oscillators, i.e. the neuro/hormonal systems of multiple women jointly affecting each other until a consensus timing is reached.

Lazarus also mentions Lunar clocking, which is the tendency for a majority of the female population to clock to the lunar cycle with their menstrual timing. Is the 28 day cycle just a coincidence? I haven't heard anything about this either, but would love to see some research. I am very interested in the rhythms in nature that affect our development and basic biological timing.

I still find it hard to believe that cell metabolic timing is related to menstruation except in an extremely general way, because these two systems are on the opposite ends of the complexity scale in an organism and are probably not "talking" to each other in any direct fashion. As for aging, the cell metabolic clocks could be important, but I think that would only be in the way that they are "set" by higher level commands from physiologic & neural systems in response to environmental conditions (diet, stress, etc).

One thing we didn't get to talk about is Laz's comment about the brain being a DNA based Quantum computer. I strongly object to this statement Laz, as there is no evidence at all for quantum effects playing a role in brain based computing. This is the argument of the mathematician Roger Penrose, who understands quantum physics, but who is pretty clueless about neurobiology. This would be another whole thread though

Best Ocsrazor

[Lazarus Long]

One thing we didn't get to talk about is Laz's comment about the brain being a DNA based Quantum computer. I strongly object to this statement Laz, as there is no evidence at all for quantum effects playing a role in brain based computing. This is the argument of the mathematician Roger Penrose, who understands quantum physics, but who is pretty clueless about neurobiology. This would be another whole thread though

Agreed Occam.

And as I was also about to create there is another topic which parallels the discussion and deserves a full area to itself, "Immunology" and its corollary "Healing".

I will get the Immunology topic started for articles after I post this.

Funny thing my sharp edged friend, I was about to also post a follow up to this thread when you did, and in a similar vein.

[Lazarus Long]

As regards menstruation I would also like to see further discusion about Menopause. Clearly again we have a cycle and we are NOT fully aware of WHY it stops, and does so for different women at different times.

I have to agree beforehand that there must be a question of accumulated damage to the sytem, but how does the Body know that?

And is this the only measure or are there more subtleties to the system then we at first perceive?

[ocsrazor]

Hi Laz,

Tom Kirkwood has done alot of thinking about the evolutionary WHY of menopause see:
Evolution of the Human Menopause

As to the how of the mechanism, its pretty clear that the depletion of oocytes initiates the process of menopause. When women get down to a certain level of oocytes remaining, hormonal changes kick in and start the process. Human menopause is unique in the animal kingdom and therefore has raised some question that this may be the only example of anything being "programmed" in human aging, and that there must be some evolutionary pressure for this to occur. Kirkwood explores these ideas in detail.

Best,
Peter
P.S. let me know if you need the full text

[Cyto]

A team led by Francis Collins of the National Human Genome Research Institute, in Maryland, USA, announced last night that a single letter change in the code for a single gene on chromosome 1 which makes the lamin A protein was enough to set the child on a path to early death. The abnormality was found in 18 out of 20 cases of HGPS. (Hutchinson-Gilford progeria syndrome)

Ageing gene identified

Gene work may help treat aging

Edited by XxDoubleHelixX, 18 April 2003 - 03:50 AM.

[Lazarus Long]

Very good articles and I think we would all be well served to access the original study and analyze the methods, conclusions and implications.

[Lazarus Long]

Here is the source study and I suggest that we read this very carefully, and repeatedly. They are staking out a position similar to what Occam, to his credit predicted, but I still feel that it is "premature" to draw too many conclusions as yet about the importance of the directions this discovery will result in. For now however, it appears they have isolated a gene sequence that DOES appear important to the "process" of aging, if not a specific clock. And anyway it is nice for me to see my sense of the importance of areas of study vindicated so quickly.

Also the source links in this article and the related ones lead to are so good that it is like striking a "motherlode" for genetic research datamining. Enjoy them everyone [!]

LL/kxs

http://www.nature.co...4/030414-8.html

Premature-ageing gene found
Single letter change in DNA hints at basic biology of getting old.
17 April 2003
HELEN R. PILCHER


By the age of 6, this girl with HGPS shows signs of ageing.
© Science

Two studies have found that a single letter change in the genetic code is responsible for a premature ageing condition. The finding could hold hints on the processes that underpin ageing.

Since it was first described in 1886, more than 100 cases of Hutchinson-Gilford progeria syndrome (HGPS) have been reported worldwide. Sufferers seem to age up to ten times faster than normal. Children develop pinched and wrinkled skin, lose their hair and grow slowly. They are prone to ailments more common in the elderly, such as stiff joints and hip dislocations. Most die by the age of 13, usually from a heart attack or stroke.

Researchers hope that the discovery of the syndrome's genetic basis will aid the development of tests and therapies for the condition. It is "the first piece in solving the tragic puzzle of progeria", says geneticist Francis Collins, director of the National Human Genome Research Institute in Bethesda, Maryland, who led one of the studies1.

Children with HGPS commonly suffer severe muscle pain. Diagnosing the disorder correctly means that doctors can prescribe the most appropriate drugs, explains Nicolas Levy of the Timone Hospital in Marseille, France, co-author of the second study2.

"Identifying the gene responsible for the disease is the first step towards possible therapies," says Levy, although their development is likely to take time.

HGPS may not be a model for
normal ageing
Lenny Guarente
MIT



Between them, the two groups studied DNA from 21 patients. They spotted an abnormality in the LMNA gene, which helps to make the membrane around a cell's nucleus. The nuclei of HGPS patients' cells are often misshapen.

The genes involved in premature ageing may shed light on how we age normally. Understanding their effects may help researchers to clarify the "cellular mechanisms" that underpin ageing, says molecular gerontologist Thomas von Zglinicki of the University of Newcastle-upon-Tyne, UK.

But children with progeria do not display all of the symptoms of normal ageing - they do not become demented, for example. So HGPS "may not be a model for normal ageing," warns ageing researcher Lenny Guarente of the Massachusetts Institute of Technology in Cambridge.


References
Collins, F.S. et al. Recurrent de novo point mutations in Lamin A cause Hutchinson-Gilford Progeria Syndrome. Nature, 422, published online, doi:10.1038/ (2003).
De Sandre-Giovannoli, A., Cau, P. , Navarro, C., Boccaccio, I. & Lévy, N. Lamin A Truncation in Hutchinson-Gilford Progeria. Science, published online, doi:10.1126/science.1084125 (2003). |Article|


© Nature News Service / Macmillan Magazines Ltd 2003

Edited by Lazarus Long, 18 April 2003 - 03:04 PM.

[Cyto]

Sir2 helps DNA pack tightly which can prevent reshuffling and thus prevent aging. So adding more copies to yeast cells increases their lifespan.
Now Sir2 needs help for NAD, which is made by nicotinamide. Now when the amount of NAD was increased it actually repressed the tight packing of chromatin, from this we can see that Sir2 has evolved a sensitivity. Now looking at another area of this array we are brought to Pnc1, which breaks down nicotinamide. The researchers upregulated the gene to overproduce the protein Pnc1 thus resulting in a longer life. Come to find out the Pnc12 also plays a role in glucose reduction. Now without the researchers help it was found that Pnc1 production rises when stresses such as: salt, heat, glucose and [amino acid restriction] are in place. So we have a protein that cuts down nicotinamide but doesn't up the NAD amount, which results in a long-lived yeast cell. So, since we know that Pnc1 isn't going to be the whole bag you could say this is "just another one" but finding these genes and learning if we should overexpress/underexpress them will lead to one tough cookie. The understanding that overexpressing Excision repair proteins so that nicks etc are repaired faster will come in handy when understanding other genes that can cut down the workload of the XP proteins will only exponentially increase cell fidelity.

Source of information:

http://sciencenow.sc...full/2003/508/3

Edited by XxDoubleHelixX, 14 May 2003 - 06:03 PM.

[kevin]

Cancer Linked to Aging

I just came across this press release which discusses a paper by Dr. Carla Grandori which links the expression of the myc oncogene with tumor formation. It seems that myc binds directly to the promoter of the gene WRN, which causes Werner's syndrome...a premature form of aging. Werner's gene, WRN, is a DNA helicase responsible for the unwinding of DNA during proliferation and repair. Cells deficient in the expression of WRN , senesce when the myc oncogene is overexpressed. The discovery further underlines the implication that genes oriented to maintaining the youth of an organism, such as WRN, are also involved in the formation of tumours and that cellular senescence is a protective mechanism designed to prevent tumour formation.

Scientists identify genetic link between cancer and aging

[Infernity]

Could it be that "42" really *is* the answer to all questions in the Universe?  [B)]

Well, it seems you read the books ... heh, nice, nice.
Don't forget to hang around with towel [lol] [sfty]

~Infernity