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The protein is named after the fact that it reduces the chances of suppressor mutations in UV-irradiated cells (or rather, knockout cells show higher rates of such mutations). It does not reduce the chance of every kind of mutation. In fact, it seems to increase the chances of mutation in general,
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Animal immune systems try to kill bacteria in a number of ways, one being the release of nitrogen monoxide (NO). NO damages bacterial DNA, but some species can survive this attack by expressing
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discovered that Mfd quickens the bacterial mutation process. This work researches ways to slow the rate of bacterial mutations and to block their evolution, in order to fight against
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to translocate along DNA, most likely forcing RNA polymerase forward and ultimately dissociating it from the DNA template. Mfd also contains binding domains which recruit
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In 2002, it was shown that Mfd may also re-initiate transcription at backtracked RNAP by forcing the polymerase forward and out of its backtracked state.
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In 2022, a small molecule inhibitor of Mfd was identified by the
Merrikh lab. As expected, it slowed down the evolution of antibiotic resistance.
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pathway and was initially discovered when its mutation led to a decrease in mutation rates after irradiation by UV light. Structural studies of
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Deaconescu, Alexandra M.; Chambers, Anna L.; Smith, Abigail J.; Nickels, Bryce E.; Hochschild, Ann; Savery, Nigel J.; Darst, Seth A. (2006).
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Roberts, Jeffrey; Park, Joo-Seop (2004). "Mfd, the bacterial transcription repair coupling factor: translocation, repair and termination".
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have revealed that this molecule is autoinhibited for UvrA-binding in its apo form due to a "clamp" interaction between the
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307:"E. coli Transcription repair coupling factor (Mfd protein) rescues arrested complexes by promoting forward translocation"
23:) is the gene which encodes the protein Mfd (also known as Transcription Repair Coupling Factor, TRCF). Mfd functions in
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Deaconescu, Alexandra M.; Artsimovitch, Irina; Grigorieff, Nikolaus (December 2012).
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that has encountered DNA damage and is unable to continue translocating.
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Park, Joo-Seop; Marr, Michael T.; Roberts, Jeffrey W. (2002-06-14).
266:"Structural Basis for Bacterial Transcription-Coupled DNA Repair"
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helping to evolve new traits such as antimicrobial resistance.
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149:"Merrikh Lab Working to Defeat Drug-Resistant Superbugs"
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147:Palisoc, Mhean (2019-01-03).
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69:UvrB-homology module and the
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25:transcription-coupled repair
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51:and trigger the associated
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53:nucleotide excision repair
17:Mutation Frequency Decline
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186:10.1016/j.mib.2004.02.014
91:University of Washington
89:In 2015, Merrikh Lab at
469:Molecular biology stubs
361:(in French). 2018-12-31
95:antibiotic resistance
63:X-ray crystallography
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71:C-terminal
67:N-terminal
333:0092-8674
233:0968-0004
464:Mutation
359:Slate.fr
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