DialysisBag

p53 gene... Controls apoptosis and including PCD (programmed cell-death); cancer mutates this gene so it doesn't respond to signals propagating PCD. ~db

Hmmmm... Don't we produce telomerase? I thought I saw that we produce small amounts right before the Go phase. Compared to carcinoma, it produces it excessively in all phases. When you think about it, I think it is all but possible for us to mass produce this 'magic bullet'. This is of course refering to the gene we haven't found yet that controls telomerase. In order to take advantage of this gene besides reducing cancer, would be quite possibly mutate it ourselves (like how cancer does it). No. The reason we age is BECAUSE of telomeres. We lose efficiency as we get closer and closer to our deaths. Many would agrue that free radicals accumalate over time, propagating mutations and errors within our complex systems, eventually leading to death. But our bodies have ways to counter oxidants (I know there are, but I don't remember). Just as we age, we lose functionality due to deteriorating telomeres, therefore the systems that control oxidant concentrations become lacks and less able to do their jobs. In a co-effort, DNA destruction and oxidants perform well to end the living. But. If this were the case, and if telomerase were to be used to improve longevity of the human multicellular organism, then several issues arise. Like what was stated earlier, there are periods of time that activate and initiate processes as we 'age'. Hormones are released to start puberty, and to end it. How does the body know when to start and end these crucial times in our lives? Maybe at the peak of maturity, cells start responding by PCD, who knows? By inducting this enzyme we could very well start living in 'Neverland' at the point we switch on this enzyme. Ever seen 'Spirited Away'? You might be able to produce telomerase as a new born, but may forever look like that huge baby in that movie. Just maybe, 'aging' is really the time sheet everyone talks about. But a time sheet of activation and production too. Another thing to think about. Once we have this (I call it cellulare longevity) there comes a time where you wonder about the cells that don't replicate and undergo mitosis. Neurons and muscular tissue for an example. Cardiac muscle replaces (if there is need to God forbit) damaged tissue with scar tissue (aka connective tissue) and not by replication of initial cells. Don't muscle cells fuse with one another, containing multiple nuclei? I might be having a bad trip, but it's been awhile since I thought about muscle cellularity. There is no proliferation, so there is no need for telomerase. Same thing with neurons, but at a complexity that is making me dizzy. With the form agelessness, there will be (I think) an advanced form of Alzheimer's Disease that contributes to nerve tissue deterioration. Since replication (if at all in nerve cells) is so slow, the amount of cellular death surpases cellular life in the CNS. Maybe by that time we will have stem cells that enable faster neuron replacements that enact our past neurons so we don't loose information. Just my idea... *blushes* ~db

Sorry, someone delete this for me... There is another topic very similiar to this one. My bad. ~db

Hi, I'm a new member and currently starting my first year in college since graduating HS last spring. I plan to get a BA in Molecular and Cell Biology, and then continue to UCSF as a graduate. My question for you all; I assume everyone knows about carcinoma telomerase production in all phases of the cell cycle. What small part of the cell cycle do 'normal' cells produce telomerase in? This is of course if normal cells indeed produce telomerase at all, but I heard rumors that they do (only in a tiny part right before the Go phase?). And I haven't surfed up any information on which gene is actually mutated to excessively produce telomerase (I doubt there is any...), but wouldn't this gene initially produce telomerase if it has been mutated to 'stream-line' cancer? Meaning that research is correct in its hypothesis that normal cells produce it? Thanks. ~db