Posted on 03/29/2011 10:54:05 AM PDT by decimon
Protein aggregation, generally associated with Alzheimer’s and mad cow disease, turns out to play a significant role in cancer. In a paper published in Nature Chemical Biology, Frederic Rousseau and Joost Schymkowitz of VIB, K.U.Leuven and Vrije Universiteit Brussel describe that certain mutations of p53, an important tumor suppressor, cause the protein to misfold in a way that the proteins start to aggregate. This not only disrupts the protective function of normal p53, but of other related proteins as well.
p53 plays a central role in protection against cancer In the study, the focus was on the p53 protein which plays a key role in protecting the body against cancer. If p53 works normally, it controls cell division. If p53 control ceases - e.g. when there is a mutation in the protein - the cells start to divide in an uncontrolled manner and this may result in a tumor. Mutations in p53 are observed in about half of cancer cases, making the protein an important target in the development of new cancer therapies.
Mutated p53 aggregates “We have revealed a new mechanism for the action of mutant p53,” Joost Schymkowitz and Frederic Rousseau of VIB, Vrije Universiteit Brussel and K.U. Leuven say. “Mutations in p53 cause the protein to lose its protective function. The proteins change in shape, hook into each other and begin to aggregate. The active p53 disappears from the cell and can no longer carry out its control function properly." The mechanism has been encountered in about one third of p53 mutations.
(Excerpt) Read more at vib.be ...
Ping
In other words, Cancer gets away with being a ‘high crime neighborhood’ because they ‘shot the local cop’. p53 being the local policeman in this scenario.
Looks like a Salvadore Dali painting....
Worse, it says the mutated p53 goes Quisling to aid the cancerous tumor.
Van Gogh. It copies Starry Night.
Remarkable!! Right down to the smoke curling out of the building chimney, too!
Aggregates of the protein Huntingtinin in the brain are what causes the eventual insanity and death of Huntington's disease. This is because the codon triplet “CAG” (that specifies the amino acid glutamine) is ‘slippery’ and DNA polymerase will sometimes add an extra one. The gene for Huntingtinin usually has a few “CAG” repeats in normal people, those with the disease have many “CAG” repeats.
Worse still is the propensity of a long chain of “CAG”’s to become even MORE inclined to ‘slip in’ an extra “CAG” or two when the DNA is copied. Sort of like if I said “cat cat cat cat cat cat cat cat cat cat cat” really fast, you might not be sure if I said it 11 times or 12 times - so DNA polymerase becomes even MORE likely to add a “CAG” every time - and soon like a ‘crazy cat lady’ you have WAY TOO MANY “CAG”’s.
Hyper glutanation of proteins (CAG ‘spells’ glutamine in the language of genetics) commonly causes aggregation of proteins - glutamine to glutamine, in more than just Huntingtinin.
SAVE
And what effect does beer have on this aggregation?
bump
It aggrivates it..not to mention the wife.
You’re right, it’s ear-ily similar.....What a razor sharp observation....snicker :^)
“Worse, it says the mutated p53 goes Quisling to aid the cancerous tumor.”
You mean RINO!
bttt
A distributed program from Stanford University called Folding@Home has worked on p53 aggregation, as part of a larger search for the science behind Alzheimer's Disease, Huntington’s Disease and others.
Please check out the thread above and consider donating your unused computer cycles to research.
The team (# 36120) has been around for about 10 years and over 500 FReepers have participated.
We would love to have you join us!
Ping for later.
I have a server that could be of assistance here.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.