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10.1007/s00018-014-1722-0 http://scihub22266oqcxt.onion/10.1007/s00018-014-1722-0 C4233150!4233150!25283145     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25283145&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Life+Sci 2014 ; 71 (23): 4577-87 Nephropedia Template TP {{tp|p=25283145|t=2014. The FHIT gene product: tumor suppressor and genome ?caretaker? |pdf=|usr=}}{{25283145}} gab.com Text The FHIT gene product: tumor suppressor and genome caretaker JO: Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=25283145 #FOAvip The FHIT gene at FRA3B is one of the earliest and most frequently altered genes in the majority of human cancers. It was recently discovered that the FHIT gene is not the most fragile locus in epithelial cells, the cell of origin for most Fhit negative cancers, eroding support for past claims that deletions at this locus are simply passenger events that are carried along in expanding cancer clones, due to extreme vulnerability to DNA damage rather than to loss of FHIT function. Indeed, recent reports have reconfirmed FHIT as a tumor suppressor gene with roles in apoptosis and prevention of the epithelial-mesenchymal transition. Other recent works have identified a novel role for the FHIT gene product, Fhit, as a genome ?caretaker.? Loss of this caretaker function leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks. Because Fhit loss-induced DNA damage is ?checkpoint blind,? cells accumulate further DNA damage during subsequent cell cycles, accruing global genome instability that could facilitate oncogenic mutation acquisition and expedite clonal expansion. Loss of Fhit activity therefore induces a mutator phenotype. Evidence for FHIT as a mutator gene is discussed in light of these recent investigations of Fhit loss and subsequent genome instability. Twit Text FOAVip The FHIT gene product: tumor suppressor and genome caretaker ????Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=25283145 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25283145 #FOAvip English Wikipedia <ref>{{Cite pmid|25283145}}</ref> The FHIT gene product: tumor suppressor and genome ?caretaker? #MMPMID25283145 Waters CE; Saldivar JC; Hosseini SA; Huebner K Cell Mol Life Sci 2014[Dec]; 71 (23): 4577-87 PMID25283145show ga The FHIT gene at FRA3B is one of the earliest and most frequently altered genes in the majority of human cancers. It was recently discovered that the FHIT gene is not the most fragile locus in epithelial cells, the cell of origin for most Fhit negative cancers, eroding support for past claims that deletions at this locus are simply passenger events that are carried along in expanding cancer clones, due to extreme vulnerability to DNA damage rather than to loss of FHIT function. Indeed, recent reports have reconfirmed FHIT as a tumor suppressor gene with roles in apoptosis and prevention of the epithelial-mesenchymal transition. Other recent works have identified a novel role for the FHIT gene product, Fhit, as a genome ?caretaker.? Loss of this caretaker function leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks. Because Fhit loss-induced DNA damage is ?checkpoint blind,? cells accumulate further DNA damage during subsequent cell cycles, accruing global genome instability that could facilitate oncogenic mutation acquisition and expedite clonal expansion. Loss of Fhit activity therefore induces a mutator phenotype. Evidence for FHIT as a mutator gene is discussed in light of these recent investigations of Fhit loss and subsequent genome instability. äThe FHIT gene product: tumor suppressor and genome ?caretaker? (epmc).pdf DeepDyve Pubget Overpricing