tag:blogger.com,1999:blog-7447544468792389936.post2949422581382707340..comments2024-02-26T21:18:23.165-08:00Comments on CHIMERAS: The missing heritabilityAnonymoushttp://www.blogger.com/profile/09922888671399516573noreply@blogger.comBlogger5125tag:blogger.com,1999:blog-7447544468792389936.post-45156998917137206832011-10-25T08:23:46.584-07:002011-10-25T08:23:46.584-07:00Shoot, my lab doesn't have access to Oncogene....Shoot, my lab doesn't have access to Oncogene. Does yours? I found this 2008 paper: PMID:18840648 instead. I think I'm going to discuss it in a separate post. Again, many thanks -- feel free to pitch in your input again!Anonymoushttps://www.blogger.com/profile/09922888671399516573noreply@blogger.comtag:blogger.com,1999:blog-7447544468792389936.post-82344776193720338102011-10-24T20:04:08.375-07:002011-10-24T20:04:08.375-07:00Glad to be useful.
FYI: Off the top of my head p...Glad to be useful. <br /><br />FYI: Off the top of my head p53 intercepts signals from the DNA damage proteins like ATM in the event of double-strand breaks to arrest cell cycle progression. So it would be a broad spectrum situation rather that a one-on-one gene balance. However that ANKRD11 thing looks mighty interesting. I might have to look up that paper myself tomorrow in lab.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-7447544468792389936.post-88041173567591241212011-10-24T19:22:49.744-07:002011-10-24T19:22:49.744-07:00So, come to think of it, that last paper I mention...So, come to think of it, that last paper I mentioned is along the lines of what I was looking for: a gene that counter-effects the negative allele of another gene. I can't access the full article from home. I'll take a better look tomorrow and add it to the references above.<br /><br />Thanks so much!Anonymoushttps://www.blogger.com/profile/09922888671399516573noreply@blogger.comtag:blogger.com,1999:blog-7447544468792389936.post-11827806246393499042011-10-24T19:12:06.076-07:002011-10-24T19:12:06.076-07:00Hi, excellent point! My understanding is that the ...Hi, excellent point! My understanding is that the protein p53 is considered a "tumor suppressant," but as far as I know wild-type mutations in the p53 coding gene have been found to be associated with cancer, as for example in this paper: PMID:21989411, or in this: PMID:21986947, where they say "Mutations of p53 in cancer can result in a gain of function associated with tumour progression and metastasis." This paper, actually, is quite interesting because, if I understand it correctly, they found an interaction between p53 and the gene ANKRD11, and apparently this can restore the tumor suppressant function of p53: "ANKRD11 restores a native conformation to the mutant p53 protein and causes dissociation of the mutant p53–p63 complex. This represents the first evidence of an endogenous protein with the capacity to suppress the oncogenic properties of mutant p53."Anonymoushttps://www.blogger.com/profile/09922888671399516573noreply@blogger.comtag:blogger.com,1999:blog-7447544468792389936.post-76013896606995376562011-10-24T17:57:43.152-07:002011-10-24T17:57:43.152-07:00I may have missed something in the description. Wo...I may have missed something in the description. Wouldn't a tumor suppressor (like p53) count as a protective allele though it's not explicitly refered to as one? Or even a heterozygously expressed dominant negative or dominant positive mutation? I know there are minimized disease phenotypes that can occur in that situation. Or I could be entirely off base, in which case I apologize.Anonymousnoreply@blogger.com