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10.15252/msb.20177974 http://scihub22266oqcxt.onion/10.15252/msb.20177974 C5866917!5866917!29572294     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Syst+Biol 2018 ; 14 (3): ä Nephropedia Template TP {{tp|p=29572294|t=2018. Systematic characterization of pan?cancer mutation clusters |pdf=|usr=}}{{29572294}} gab.com Text Systematic characterization of pan cancer mutation clusters JO: Mol Syst Biol http://www.kidney.de/pget.php?&tw=1&pmid=29572294 #FOAvip Cancer genome sequencing has shown that driver genes can often be distinguished not only by the elevated mutation frequency but also by specific nucleotide positions that accumulate changes at a high rate. However, properties associated with a residue's potential to drive tumorigenesis when mutated have not yet been systematically investigated. Here, using a novel methodological approach, we identify and characterize a compendium of 180 hotspot residues within 160 human proteins which occur with a significant frequency and are likely to have functionally relevant impact. We find that such mutations (i) are more prominent in proteins that can exist in the on and off state, (ii) reflect the identity of a tumor of origin, and (iii) often localize within interfaces which mediate interactions with other proteins or ligands. Following, we further examine structural data for human protein complexes and identify a number of additional protein interfaces that accumulate cancer mutations at a high rate. Jointly, these analyses suggest that disruption and dysregulation of protein interactions can be instrumental in switching functions of cancer proteins and activating downstream changes. Twit Text FOAVip Systematic characterization of pan cancer mutation clusters ????Mol Syst Biol http://www.kidney.de/pget.php?&tw=1&pmid=29572294 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29572294 #FOAvip English Wikipedia <ref>{{Cite pmid|29572294}}</ref> Systematic characterization of pan?cancer mutation clusters #MMPMID29572294 Buljan M; Blattmann P; Aebersold R; Boutros M Mol Syst Biol 2018[Mar]; 14 (3): ä PMID29572294show ga Cancer genome sequencing has shown that driver genes can often be distinguished not only by the elevated mutation frequency but also by specific nucleotide positions that accumulate changes at a high rate. However, properties associated with a residue's potential to drive tumorigenesis when mutated have not yet been systematically investigated. Here, using a novel methodological approach, we identify and characterize a compendium of 180 hotspot residues within 160 human proteins which occur with a significant frequency and are likely to have functionally relevant impact. We find that such mutations (i) are more prominent in proteins that can exist in the on and off state, (ii) reflect the identity of a tumor of origin, and (iii) often localize within interfaces which mediate interactions with other proteins or ligands. Following, we further examine structural data for human protein complexes and identify a number of additional protein interfaces that accumulate cancer mutations at a high rate. Jointly, these analyses suggest that disruption and dysregulation of protein interactions can be instrumental in switching functions of cancer proteins and activating downstream changes. äSystematic characterization of pan?cancer mutation clusters (epmc).pdf DeepDyve Pubget Overpricing