Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM

Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spo...
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Autor*in:	Hirano, Seiki [verfasserIn] Yamamoto, Kazuhiko [verfasserIn] Ishiai, Masamichi [verfasserIn] Yamazoe, Mitsuyoshi [verfasserIn] Seki, Masayuki [verfasserIn] Matsushita, Nobuko [verfasserIn] Ohzeki, Mioko [verfasserIn] Yamashita, Yukiko M [verfasserIn] Arakawa, Hiroshi [verfasserIn] Buerstedde, Jean‐Marie [verfasserIn] Enomoto, Takemi [verfasserIn] Takeda, Shunichi [verfasserIn] Thompson, Larry H [verfasserIn] Takata, Minoru [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2004

Schlagwörter:	Bloom syndrome Fanconi anemia homologous recombination sister chromatid exchange translesion synthesis

Anmerkung:	© European Molecular Biology Organization 2005

Übergeordnetes Werk:	Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 24(2004), 2 vom: 23. Dez., Seite 418-427
Übergeordnetes Werk:	volume:24 ; year:2004 ; number:2 ; day:23 ; month:12 ; pages:418-427

Links:	Volltext

DOI / URN:	10.1038/sj.emboj.7600534

Katalog-ID:	SPR057950709

Internformat


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024	7		\|a 10.1038/sj.emboj.7600534 \|2 doi
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100	1		\|a Hirano, Seiki \|e verfasserin \|4 aut
245	1	0	\|a Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
264		1	\|c 2004
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520			\|a Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair.
650		4	\|a Bloom syndrome \|7 (dpeaa)DE-He213
650		4	\|a Fanconi anemia \|7 (dpeaa)DE-He213
650		4	\|a homologous recombination \|7 (dpeaa)DE-He213
650		4	\|a sister chromatid exchange \|7 (dpeaa)DE-He213
650		4	\|a translesion synthesis \|7 (dpeaa)DE-He213
700	1		\|a Yamamoto, Kazuhiko \|e verfasserin \|4 aut
700	1		\|a Ishiai, Masamichi \|e verfasserin \|4 aut
700	1		\|a Yamazoe, Mitsuyoshi \|e verfasserin \|4 aut
700	1		\|a Seki, Masayuki \|e verfasserin \|4 aut
700	1		\|a Matsushita, Nobuko \|e verfasserin \|4 aut
700	1		\|a Ohzeki, Mioko \|e verfasserin \|4 aut
700	1		\|a Yamashita, Yukiko M \|e verfasserin \|4 aut
700	1		\|a Arakawa, Hiroshi \|e verfasserin \|4 aut
700	1		\|a Buerstedde, Jean‐Marie \|e verfasserin \|4 aut
700	1		\|a Enomoto, Takemi \|e verfasserin \|4 aut
700	1		\|a Takeda, Shunichi \|e verfasserin \|4 aut
700	1		\|a Thompson, Larry H \|e verfasserin \|4 aut
700	1		\|a Takata, Minoru \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t The EMBO Journal \|d Nature Publishing Group UK, 2023 \|g 24(2004), 2 vom: 23. Dez., Seite 418-427 \|w (DE-627)266022529 \|w (DE-600)1467419-1 \|x 1460-2075 \|7 nnns
773	1	8	\|g volume:24 \|g year:2004 \|g number:2 \|g day:23 \|g month:12 \|g pages:418-427
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912			\|a GBV_ILN_31
912			\|a GBV_ILN_32
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_70
912			\|a GBV_ILN_72
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_90
912			\|a GBV_ILN_95
912			\|a GBV_ILN_100
912			\|a GBV_ILN_101
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_120
912			\|a GBV_ILN_138
912			\|a GBV_ILN_150
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_168
912			\|a GBV_ILN_170
912			\|a GBV_ILN_171
912			\|a GBV_ILN_187
912			\|a GBV_ILN_213
912			\|a GBV_ILN_224
912			\|a GBV_ILN_230
912			\|a GBV_ILN_252
912			\|a GBV_ILN_266
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_636
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2004
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2007
912			\|a GBV_ILN_2008
912			\|a GBV_ILN_2009
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2018
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2025
912			\|a GBV_ILN_2026
912			\|a GBV_ILN_2027
912			\|a GBV_ILN_2034
912			\|a GBV_ILN_2037
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2049
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2055
912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2108
912			\|a GBV_ILN_2110
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2113
912			\|a GBV_ILN_2118
912			\|a GBV_ILN_2119
912			\|a GBV_ILN_2122
912			\|a GBV_ILN_2129
912			\|a GBV_ILN_2143
912			\|a GBV_ILN_2144
912			\|a GBV_ILN_2147
912			\|a GBV_ILN_2148
912			\|a GBV_ILN_2152
912			\|a GBV_ILN_2153
912			\|a GBV_ILN_2188
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_2232
912			\|a GBV_ILN_2336
912			\|a GBV_ILN_2470
912			\|a GBV_ILN_2472
912			\|a GBV_ILN_2507
912			\|a GBV_ILN_2522
912			\|a GBV_ILN_2548
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4029
912			\|a GBV_ILN_4035
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4046
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4116
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4155
912			\|a GBV_ILN_4242
912			\|a GBV_ILN_4246
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4251
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4311
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4314
912			\|a GBV_ILN_4318
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4326
912			\|a GBV_ILN_4328
912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4336
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4393
912			\|a GBV_ILN_4598
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 24 \|j 2004 \|e 2 \|b 23 \|c 12 \|h 418-427

Indexfelder

author_variant	s h sh k y ky m i mi m y my m s ms n m nm m o mo y m y ym ymy h a ha j b jb t e te s t st l h t lh lht m t mt
matchkey_str	article:14602075:2004----::ucinleainhpofncoooooseobntotas
hierarchy_sort_str	2004
publishDate	2004
allfields	10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427
spelling	10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427
allfields_unstemmed	10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427
allfieldsGer	10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427
allfieldsSound	10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427
language	English
source	Enthalten in The EMBO Journal 24(2004), 2 vom: 23. Dez., Seite 418-427 volume:24 year:2004 number:2 day:23 month:12 pages:418-427
sourceStr	Enthalten in The EMBO Journal 24(2004), 2 vom: 23. Dez., Seite 418-427 volume:24 year:2004 number:2 day:23 month:12 pages:418-427
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Bloom syndrome Fanconi anemia homologous recombination sister chromatid exchange translesion synthesis
isfreeaccess_bool	false
container_title	The EMBO Journal
authorswithroles_txt_mv	Hirano, Seiki @@aut@@ Yamamoto, Kazuhiko @@aut@@ Ishiai, Masamichi @@aut@@ Yamazoe, Mitsuyoshi @@aut@@ Seki, Masayuki @@aut@@ Matsushita, Nobuko @@aut@@ Ohzeki, Mioko @@aut@@ Yamashita, Yukiko M @@aut@@ Arakawa, Hiroshi @@aut@@ Buerstedde, Jean‐Marie @@aut@@ Enomoto, Takemi @@aut@@ Takeda, Shunichi @@aut@@ Thompson, Larry H @@aut@@ Takata, Minoru @@aut@@
publishDateDaySort_date	2004-12-23T00:00:00Z
hierarchy_top_id	266022529
id	SPR057950709
language_de	englisch
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author	Hirano, Seiki
spellingShingle	Hirano, Seiki misc Bloom syndrome misc Fanconi anemia misc homologous recombination misc sister chromatid exchange misc translesion synthesis Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
authorStr	Hirano, Seiki
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topic_title	Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213
topic	misc Bloom syndrome misc Fanconi anemia misc homologous recombination misc sister chromatid exchange misc translesion synthesis
topic_unstemmed	misc Bloom syndrome misc Fanconi anemia misc homologous recombination misc sister chromatid exchange misc translesion synthesis
topic_browse	misc Bloom syndrome misc Fanconi anemia misc homologous recombination misc sister chromatid exchange misc translesion synthesis
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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title	Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
ctrlnum	(DE-627)SPR057950709 (SPR)sj.emboj.7600534-e
title_full	Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
author_sort	Hirano, Seiki
journal	The EMBO Journal
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author_browse	Hirano, Seiki Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru
container_volume	24
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author-letter	Hirano, Seiki
doi_str_mv	10.1038/sj.emboj.7600534
author2-role	verfasserin
title_sort	functional relationships of fancc to homologous recombination, translesion synthesis, and blm
title_auth	Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
abstract	Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005
abstractGer	Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005
abstract_unstemmed	Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005
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container_issue	2
title_short	Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
url	https://dx.doi.org/10.1038/sj.emboj.7600534
remote_bool	true
author2	Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru
author2Str	Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru
ppnlink	266022529
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doi_str	10.1038/sj.emboj.7600534
up_date	2024-10-22T04:52:01.598Z
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Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM

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