Cancer and p53
In the blog 'Intelligently Sequenced' there appears a post entitled 'The Notorious p53.' The post, most of which is quoted below, refers to an article appearing at the website of St. Jude Children’s Research Hospital. The focus of the article is a protein known as p53 which has a function related to damaged DNA. Mutations involving the gene coding for this protein are common among cancer patients. The article:
"The website for St. Jude Children’s Research Hospital features an article about p53 levels. P53 is associated with responses to damaged DNA occasioned by radiation and chemicals. More than any other gene, the gene that codes for the p53 protein is found mutated in cancer patients.
As the article entitled 'Mechanism controlling DNA damage response has potential novel medical applications' indicates, p53 is associated with cellular responses to stress. Research connected with it is linked to efforts to improve cancer therapies. A cause of cancer is believed to be damage to DNA brought about through radiation and chemical reactions.
An impact of the St. Jude study was a finding thatDNA damage led to an increase in p53 protein synthesis. This finding ran counter to a previously held notion that enhanced p53 levels resulted from a decrease in the rate in which the protein is broken down. A practical benefit to the discovery is apparant namely, a potential to manipulate the synthesis rate to occasion positive results following damage to DNA.
Following damage to DNA p53 can either prevent cellular division or trigger apoptosis or cellular suicide. In so doing p53 inhibits the proliferation of damaged cells which in turn can inhibit cancer.
The specifics of the mechanism controling the rate of p53 synthesis involve an untranslated region of mRNA coding for p53. This UTR acts as a control switch. A protein known as nucleolin suppresses synthesis of p53 by binding to the UTR of p53 mRNA. When DNA damage occurs however, another protein known as RPL26 binds the UTR and causes accelerated translation of the mRNA resulting in more p53.
Researchers were able to document the link between the regulating proteins and synthesis levels by inhibiting RPL26 production which short circuits an increase in p53 following damage to DNA. The p53 functions of halting cellular proliferation or apoptosis were correspondingly compromised. Likewise reduced nucleolin levels increase p53 production in response to DNA damage.
The article goes on to indicate a general approach to the phenomenon of protein synthesis shutdown which can result from damaged DNA or other factors like hypoxia- too little oxygen. By utilizing specific regulatory binding proteins a bypass strategy might be realized."
"The website for St. Jude Children’s Research Hospital features an article about p53 levels. P53 is associated with responses to damaged DNA occasioned by radiation and chemicals. More than any other gene, the gene that codes for the p53 protein is found mutated in cancer patients.
As the article entitled 'Mechanism controlling DNA damage response has potential novel medical applications' indicates, p53 is associated with cellular responses to stress. Research connected with it is linked to efforts to improve cancer therapies. A cause of cancer is believed to be damage to DNA brought about through radiation and chemical reactions.
An impact of the St. Jude study was a finding thatDNA damage led to an increase in p53 protein synthesis. This finding ran counter to a previously held notion that enhanced p53 levels resulted from a decrease in the rate in which the protein is broken down. A practical benefit to the discovery is apparant namely, a potential to manipulate the synthesis rate to occasion positive results following damage to DNA.
Following damage to DNA p53 can either prevent cellular division or trigger apoptosis or cellular suicide. In so doing p53 inhibits the proliferation of damaged cells which in turn can inhibit cancer.
The specifics of the mechanism controling the rate of p53 synthesis involve an untranslated region of mRNA coding for p53. This UTR acts as a control switch. A protein known as nucleolin suppresses synthesis of p53 by binding to the UTR of p53 mRNA. When DNA damage occurs however, another protein known as RPL26 binds the UTR and causes accelerated translation of the mRNA resulting in more p53.
Researchers were able to document the link between the regulating proteins and synthesis levels by inhibiting RPL26 production which short circuits an increase in p53 following damage to DNA. The p53 functions of halting cellular proliferation or apoptosis were correspondingly compromised. Likewise reduced nucleolin levels increase p53 production in response to DNA damage.
The article goes on to indicate a general approach to the phenomenon of protein synthesis shutdown which can result from damaged DNA or other factors like hypoxia- too little oxygen. By utilizing specific regulatory binding proteins a bypass strategy might be realized."
posted by Paul at 10:27 AM
0 Comments:
Post a Comment
<< Home