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10.1002/em.22023 http://scihub22266oqcxt.onion/10.1002/em.22023 C4945469!4945469 !27273795     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27273795 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Environ+Mol+Mutagen 2016 ; 57 (6 ): 421-34 Nephropedia Template TP {{tp|p=27273795 |t=2016. Better living with hyper-mutation |pdf=|usr=}}{{27273795 }} gab.com Text Better living with hyper-mutation JO: Environ Mol Mutagen http://www.kidney.de/pget.php?&tw=1&pmid=27273795 #FOAvip The simplest forms of mutations, base substitutions, typically have negative consequences, aside from their existential role in evolution and fitness. Hypermutations, mutations on steroids, occurring at frequencies of 10(-2) -10(-4) per base pair, straddle a domain between fitness and death, depending on the presence or absence of regulatory constraints. Two facets of hypermutation, one in Escherichia coli involving DNA polymerase V (pol V), the other in humans, involving activation-induced deoxycytidine deaminase (AID) are portrayed. Pol V is induced as part of the DNA-damage-induced SOS regulon, and is responsible for generating the lion's share of mutations when catalyzing translesion DNA synthesis (TLS). Four regulatory mechanisms, temporal, internal, conformational, and spatial, activate pol V to copy damaged DNA and then deactivate it. On the flip side of the coin, SOS-induced pols V, IV, and II mutate undamaged DNA, thus providing genetic diversity heightening long-term survival and evolutionary fitness. Fitness in humans is principally the domain of a remarkably versatile immune system marked by somatic hypermutations (SHM) in immunoglobulin variable (IgV) regions that ensure antibody (Ab) diversity. AID initiates SHM by deaminating C ? U, favoring hot WRC (W?=?A/T, R?=?A/G) motifs. Since there are large numbers of trinucleotide motif targets throughout IgV, AID must exercise considerable catalytic restraint to avoid attacking such sites repeatedly, which would otherwise compromise diversity. Processive, random, and inefficient AID-catalyzed dC deamination simulates salient features of SHM, yet generates B-cell lymphomas when working at the wrong time in the wrong place. Environ. Mol. Mutagen. 57:421-434, 2016. © 2016 Wiley Periodicals, Inc. Twit Text FOAVip Better living with hyper-mutation ????Environ Mol Mutagen http://www.kidney.de/pget.php?&tw=1&pmid=27273795 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27273795 #FOAvip English Wikipedia <ref>{{Cite pmid|27273795 }}</ref> Better living with hyper-mutation #MMPMID27273795 Goodman MF Environ Mol Mutagen 2016[Jul]; 57 (6 ): 421-34 PMID27273795 show ga The simplest forms of mutations, base substitutions, typically have negative consequences, aside from their existential role in evolution and fitness. Hypermutations, mutations on steroids, occurring at frequencies of 10(-2) -10(-4) per base pair, straddle a domain between fitness and death, depending on the presence or absence of regulatory constraints. Two facets of hypermutation, one in Escherichia coli involving DNA polymerase V (pol V), the other in humans, involving activation-induced deoxycytidine deaminase (AID) are portrayed. Pol V is induced as part of the DNA-damage-induced SOS regulon, and is responsible for generating the lion's share of mutations when catalyzing translesion DNA synthesis (TLS). Four regulatory mechanisms, temporal, internal, conformational, and spatial, activate pol V to copy damaged DNA and then deactivate it. On the flip side of the coin, SOS-induced pols V, IV, and II mutate undamaged DNA, thus providing genetic diversity heightening long-term survival and evolutionary fitness. Fitness in humans is principally the domain of a remarkably versatile immune system marked by somatic hypermutations (SHM) in immunoglobulin variable (IgV) regions that ensure antibody (Ab) diversity. AID initiates SHM by deaminating C ? U, favoring hot WRC (W?=?A/T, R?=?A/G) motifs. Since there are large numbers of trinucleotide motif targets throughout IgV, AID must exercise considerable catalytic restraint to avoid attacking such sites repeatedly, which would otherwise compromise diversity. Processive, random, and inefficient AID-catalyzed dC deamination simulates salient features of SHM, yet generates B-cell lymphomas when working at the wrong time in the wrong place. Environ. Mol. Mutagen. 57:421-434, 2016. © 2016 Wiley Periodicals, Inc. |*Mutation [MESH] |*Somatic Hypermutation, Immunoglobulin [MESH] |AICDA (Activation-Induced Cytidine Deaminase) [MESH] |Cytidine Deaminase/*genetics [MESH] |DNA-Directed DNA Polymerase/*genetics [MESH] |Escherichia coli Proteins/*genetics [MESH] |Escherichia coli/genetics [MESH] |Genetic Fitness/immunology [MESH] |Humans [MESH] |Immunoglobulin Variable Region/*genetics [MESH] |Models, Genetic [MESH] |Mutation Rate [MESH] |SOS Response, Genetics [MESH]Better living with hyper-mutation (epmc).pdf DeepDyve Pubget Overpricing