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Aravind L, Koonin EV: The DNA-repair protein AlkB, EGL-9, and leprecan define new families of 2-oxoglutarate- and iron-dependent dioxygenases. Genome Biol 2001, 2:research0007.1-0007.8.
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Aravind L, Koonin EV: The DNA-repair protein AlkB, EGL-9, and leprecan define new families of 2-oxoglutarate- and iron-dependent dioxygenases. Genome Biol 2001, 2:research0007.1-0007.8.
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••] were published together and are the first direct demonstration of the repair of 1-methyladenine and 3-methylcytosine by alkB protein by direct reversal of the lesion.
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••] were published together and are the first direct demonstration of the repair of 1-methyladenine and 3-methylcytosine by alkB protein by direct reversal of the lesion.
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Falnes, P.O.1
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Human and bacterial oxidative demethylases repair alkylation damage in both RNA and DNA
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Generation and elimination of 8-oxo-7,8-dihydro-2′-deoxyguanosine 5′-triphosphate, a mutagenic substrate for DNA synthesis, in human cells
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Hayakawa H., Taketomi A., Sakumi K., Kuwano M., Sekiguchi M. Generation and elimination of 8-oxo-7,8-dihydro-2′-deoxyguanosine 5′-triphosphate, a mutagenic substrate for DNA synthesis, in human cells. Biochemistry. 34:1995;89-95.
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Friedberg EC, Walker GC, Siede W: DNA Repair and Mutagenesis. Washington DC: ASM Press; 1995.
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The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by the COP9 signalosome in response to DNA damage
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This study yields new and provocative information concerning the possible role of the COP9 signalosome in nucleotide excision repair. The COP9 signalosome (CSN), a regulator of cullin-based ubiquitin ligases is part of two different complexes - one containing DDB and another containing CSA. Differential regulation of the CSN ubiquitin ligase activity of the DDB2 and CSA complexes in response to UV irradiation is demonstrated.
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Groisman R., Polanowska J., Kuraoka I., Sawada J., Saijo M., Drapkin R., Kisselev A.F., Tanaka K., Nakatani Y. The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by the COP9 signalosome in response to DNA damage. Cell. 113:2003;357-367 This study yields new and provocative information concerning the possible role of the COP9 signalosome in nucleotide excision repair. The COP9 signalosome (CSN), a regulator of cullin-based ubiquitin ligases is part of two different complexes - one containing DDB and another containing CSA. Differential regulation of the CSN ubiquitin ligase activity of the DDB2 and CSA complexes in response to UV irradiation is demonstrated.
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Cell
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Groisman, R.1
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Chromosomal localization and cDNA cloning of the genes (DDB1 and DDB2) for the p127 and p48 subunits of a human damage-specific DNA binding protein
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Dualan R., Brody T., Keeney S., Nichols A.F., Admon A., Linn S. Chromosomal localization and cDNA cloning of the genes (DDB1 and DDB2) for the p127 and p48 subunits of a human damage-specific DNA binding protein. Genomics. 29:1995;62-69.
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0038105065
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True XP group E patients have a defective UV-damaged DNA binding protein complex and mutations in DDB2 which reveal the functional domains of its p48 product
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Rapic-Otrin V., Navazza V., Nardo T., Botta E., McLenigan M., Bisi D.C., Levine A.S., Stefanini M. True XP group E patients have a defective UV-damaged DNA binding protein complex and mutations in DDB2 which reveal the functional domains of its p48 product. Hum. Mol. Genet. 12:2003;1507-1522.
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Rapic-Otrin, V.1
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Genetic predisposition and somatic diversification in tumor development and progression
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Kolodner R. Biochemistry and genetics of eukaryotic mismatch repair. Genes Dev. 10:1996;1433-1442.
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Functional significance of concomitant inactivation of hMLH1 and hMSH6 in tumor cells of the microsatellite mutator phenotype
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Baranovskaya S., Soto J.L., Perucho M., Malkhosyan S.R. Functional significance of concomitant inactivation of hMLH1 and hMSH6 in tumor cells of the microsatellite mutator phenotype. Proc. Natl. Acad. Sci. U.S.A. 98:2001;15107-15112.
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Baranovskaya, S.1
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Perucho, M.3
Malkhosyan, S.R.4
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18
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0037716637
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Cadmium is a mutagen that acts by inhibiting mismatch repair
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A fascinating study on the apparent direct effect of cadmium on mismatch repair. The results illustrate that exogenous agent can directly interfere with DNA-repair pathways and enhance genomic instability.
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Jin Y.H., Clark A.B., Slebos R.J., Al-Refai H., Taylor J.A., Kunkel T.A., Resnick M.A., Gordenin D.A. Cadmium is a mutagen that acts by inhibiting mismatch repair. Nat. Genet. 34:2003;326-329 A fascinating study on the apparent direct effect of cadmium on mismatch repair. The results illustrate that exogenous agent can directly interfere with DNA-repair pathways and enhance genomic instability.
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Jin, Y.H.1
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Resnick, M.A.7
Gordenin, D.A.8
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19
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0035917489
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Artemis, a novel DNA double-strand break repair/V(D)J recombination protein, is mutated in human severe combined immune deficiency
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Moshous D., Callebaut I., de Chasseval R., Corneo B., Cavazzana-Calvo M., Le Deist F., Tezcan I., Sanal O., Bertrand Y., Philippe N.et al. Artemis, a novel DNA double-strand break repair/V(D)J recombination protein, is mutated in human severe combined immune deficiency. Cell. 105:2001;177-186.
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Moshous, D.1
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Sanal, O.8
Bertrand, Y.9
Philippe, N.10
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20
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0037155703
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Hairpin opening and overhang processing by an Artemis/DNA-dependent protein kinase complex in nonhomologous end joining and V(D)J recombination
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cs, Artemis gains endonucleolytic activity on 5′ and 3′ overhangs, as well as hairpins. In addition, the complex can open hairpins generated by the RAG complex.
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cs, Artemis gains endonucleolytic activity on 5′ and 3′ overhangs, as well as hairpins. In addition, the complex can open hairpins generated by the RAG complex.
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Cell
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Ma, Y.1
Pannicke, U.2
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Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions
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Sharpless N.E., Ferguson D.O., O'Hagan R.C., Castrillon D.H., Lee C., Farazi P.A., Alson S., Fleming J., Morton C.C., Frank K.et al. Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions. Mol. Cell. 8:2001;1187-1196.
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Sharpless, N.E.1
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Farazi, P.A.6
Alson, S.7
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Morton, C.C.9
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22
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Specialized DNA polymerases, cellular survival, and the genesis of mutations
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Friedberg E.C., Wagner R., Radman M. Specialized DNA polymerases, cellular survival, and the genesis of mutations. Science. 296:2002;1627-1630.
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Science
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Friedberg, E.C.1
Wagner, R.2
Radman, M.3
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23
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0038377325
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The dinB operon and spontaneous mutation in Escherichia coli
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A study showing that the dinB gene is part of a polycistronic operon. Some mutations in dinB affect down-stream genes, whereas others do not. These results account for conflicting data regarding the role of Pol IV in spontaneous mutagenesis in E. coli.
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McKenzie G.J., Magner D.B., Lee P.L., Rosenberg S.M. The dinB operon and spontaneous mutation in Escherichia coli. J. Bacteriol. 185:2003;3972-3977 A study showing that the dinB gene is part of a polycistronic operon. Some mutations in dinB affect down-stream genes, whereas others do not. These results account for conflicting data regarding the role of Pol IV in spontaneous mutagenesis in E. coli.
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J. Bacteriol.
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Mckenzie, G.J.1
Magner, D.B.2
Lee, P.L.3
Rosenberg, S.M.4
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24
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0037799191
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Uncoupling of leading- and lagging-strand DNA replication during lesion bypass in vivo
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This study examines the kinetics of leading and lagging strand DNA synthesis in vivo, indicating that the synthesis of the two strands is uncoupled when a blocking lesion is on either strand. The replicative machinery does not appear to disengage from the arrested fork while the bypass polymerase performs translesion DNA synthesis.
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Pages V., Fuchs R.P. Uncoupling of leading- and lagging-strand DNA replication during lesion bypass in vivo. Science. 300:2003;1300-1303 This study examines the kinetics of leading and lagging strand DNA synthesis in vivo, indicating that the synthesis of the two strands is uncoupled when a blocking lesion is on either strand. The replicative machinery does not appear to disengage from the arrested fork while the bypass polymerase performs translesion DNA synthesis.
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(2003)
Science
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Pages, V.1
Fuchs, R.P.2
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25
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0037453719
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DnaE2 polymerase contributes to in vivo survival and the emergence of drug resistance in Mycobacterium tuberculosis
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An interesting study, suggesting a possible mechanism of antibiotic resistance during infection with M. tuberculosis. This appears to result from the upregulation of dnaE2, a gene with homology to the major replicative polymerase, in response to DNA damage.
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Boshoff H.I., Reed M.B., Barry C.E. III, Mizrahi V. DnaE2 polymerase contributes to in vivo survival and the emergence of drug resistance in Mycobacterium tuberculosis. Cell. 113:2003;183-193 An interesting study, suggesting a possible mechanism of antibiotic resistance during infection with M. tuberculosis. This appears to result from the upregulation of dnaE2, a gene with homology to the major replicative polymerase, in response to DNA damage.
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(2003)
Cell
, vol.113
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Boshoff, H.I.1
Reed, M.B.2
Barry III, C.E.3
Mizrahi, V.4
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26
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0037849904
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Stress-induced mutagenesis in bacteria
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This study supports the notion that adaptive mutagenesis associated with stress-induced mutations is a general evolutionary strategy in E. coli.
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Bjedov I., Tenaillon O., Gerard B., Souza V., Denamur E., Radman M., Taddei F., Matic I. Stress-induced mutagenesis in bacteria. Science. 300:2003;1404-1409 This study supports the notion that adaptive mutagenesis associated with stress-induced mutations is a general evolutionary strategy in E. coli.
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Science
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Bjedov, I.1
Tenaillon, O.2
Gerard, B.3
Souza, V.4
Denamur, E.5
Radman, M.6
Taddei, F.7
Matic, I.8
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27
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0038681901
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DNA deamination mediates innate immunity to retroviral infection
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(2003)
Cell
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Harris, R.S.1
Bishop, K.N.2
Sheehy, A.M.3
Craig, H.M.4
Petersen-Mahrt, S.K.5
Watt, I.N.6
Neuberger, M.S.7
Malim, M.H.8
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29
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0038681023
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Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts
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•] suggest a role of the deamination of cytosine in the generation of mutations in lentiviruses. The gene product of APOBEC3G is a cytidine deaminase that generates G→A mutations in viral DNA. This gene might have evolved as a viral defense, however, it may contribute to viral diversity.
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•] suggest a role of the deamination of cytosine in the generation of mutations in lentiviruses. The gene product of APOBEC3G is a cytidine deaminase that generates G→A mutations in viral DNA. This gene might have evolved as a viral defense, however, it may contribute to viral diversity.
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Nature
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Mangeat, B.1
Turelli, P.2
Caron, G.3
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Perrin, L.5
Trono, D.6
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The DNA damage response: Putting checkpoints inperspective
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Zhou B.B., Elledge S.J. The DNA damage response: putting checkpoints inperspective. Nature. 408:2000;433-439.
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Nature
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Zhou, B.B.1
Elledge, S.J.2
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31
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Cell cycle checkpoint signaling through the ATM and ATR kinases
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Abraham R.T. Cell cycle checkpoint signaling through the ATM and ATR kinases. Genes Dev. 15:2001;2177-2196.
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Genes Dev.
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Abraham, R.T.1
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32
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0037567268
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Sensing DNA damage through ATRIP recognition of RPA-ssDNA complexes
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This study proposes that RPA, bound to single-stranded DNA, initiates a signal transduction cascade that effects checkpoint regulation by the ATR-ATRIP recruitment to the site by RPA.
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Zou L., Elledge S.J. Sensing DNA damage through ATRIP recognition of RPA-ssDNA complexes. Science. 300:2003;1542-1548 This study proposes that RPA, bound to single-stranded DNA, initiates a signal transduction cascade that effects checkpoint regulation by the ATR-ATRIP recruitment to the site by RPA.
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Science
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Zou, L.1
Elledge, S.J.2
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33
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0037446871
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Evidence that the retroviral DNA integration process triggers an ATR-dependent DNA damage response
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Retroviral integration can, apparently, activate the checkpoint response. ATR kinase, but not ATM kinase, is required for completion of retroviral integration into the genome.
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Daniel R., Kao G., Taganov K., Greger J.G., Favorova O., Merkel G., Yen T.J., Katz R.A., Skalka A.M. Evidence that the retroviral DNA integration process triggers an ATR-dependent DNA damage response. Proc. Natl. Acad. Sci. U.S.A. 100:2003;4778-4783 Retroviral integration can, apparently, activate the checkpoint response. ATR kinase, but not ATM kinase, is required for completion of retroviral integration into the genome.
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Proc. Natl. Acad. Sci. U.S.A.
, vol.100
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Daniel, R.1
Kao, G.2
Taganov, K.3
Greger, J.G.4
Favorova, O.5
Merkel, G.6
Yen, T.J.7
Katz, R.A.8
Skalka, A.M.9
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34
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0036679130
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Previously uncharacterized genes in the UV- and MMS-induced DNA damage response in yeast
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This study identified novel genes involved in biological responses to DNA damage in yeast. Screening of 2,827 yeast gene deletion strains identified six novel genes that were not previously known to be involved in DNA damage. Deletion of these genes results in UV and MMS sensitivity.
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Hanway D., Chin J.K., Xia G., Oshiro G., Winzeler E.A., Romesberg F.E. Previously uncharacterized genes in the UV- and MMS-induced DNA damage response in yeast. Proc. Natl. Acad. Sci. U.S.A. 99:2002;10605-10610 This study identified novel genes involved in biological responses to DNA damage in yeast. Screening of 2,827 yeast gene deletion strains identified six novel genes that were not previously known to be involved in DNA damage. Deletion of these genes results in UV and MMS sensitivity.
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Proc. Natl. Acad. Sci. U.S.A.
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Hanway, D.1
Chin, J.K.2
Xia, G.3
Oshiro, G.4
Winzeler, E.A.5
Romesberg, F.E.6
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35
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0037443054
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Identification of genes that protect the C. elegans genome against mutations by genome-wide RNAi
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This study identified multiple genes in C. elegans that are required for genomic stability, using an RNAi strategy. 61 genes were identified, many of which were novel.
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Pothof J., van Haaften G., Thijssen K., Kamath R.S., Fraser A.G., Ahringer J., Plasterk R.H., Tijsterman M. Identification of genes that protect the C. elegans genome against mutations by genome-wide RNAi. Genes Dev. 17:2003;443-448 This study identified multiple genes in C. elegans that are required for genomic stability, using an RNAi strategy. 61 genes were identified, many of which were novel.
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(2003)
Genes Dev.
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Pothof, J.1
Van Haaften, G.2
Thijssen, K.3
Kamath, R.S.4
Fraser, A.G.5
Ahringer, J.6
Plasterk, R.H.7
Tijsterman, M.8
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36
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18444362122
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Biallelic inactivation of BRCA2 in Fanconi anemia
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Most of the genes responsible for the eight FA complementation groups have been identified and belong to the same protein complex that direct the monoubiquitination of FA-D2. The resulting protein interacts with BRCA1, with subsequent signaling through BRCA2 and RAD51. This study identified mutations in the BRCA2 gene in FANCD1 and FANCB patients.
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Howlett N.G., Taniguchi T., Olson S., Cox B., Waisfisz Q., De Die-Smulders C., Persky N., Grompe M., Joenje H., Pals G.et al. Biallelic inactivation of BRCA2 in Fanconi anemia. Science. 297:2002;606-609 Most of the genes responsible for the eight FA complementation groups have been identified and belong to the same protein complex that direct the monoubiquitination of FA-D2. The resulting protein interacts with BRCA1, with subsequent signaling through BRCA2 and RAD51. This study identified mutations in the BRCA2 gene in FANCD1 and FANCB patients.
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(2002)
Science
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Howlett, N.G.1
Taniguchi, T.2
Olson, S.3
Cox, B.4
Waisfisz, Q.5
De Die-Smulders, C.6
Persky, N.7
Grompe, M.8
Joenje, H.9
Pals, G.10
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