Alternative excision repair of topoisomerase inhibitor-induced DNA damage
Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kuraoka, Isao [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Anmerkung: |
© Archana Sharma Foundation of Calcutta 2018 |
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| Übergeordnetes Werk: |
Enthalten in: The nucleus - [New Delhi] : Springer India, 2010, 61(2018), 3 vom: 12. Okt., Seite 235-240 |
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| Übergeordnetes Werk: |
volume:61 ; year:2018 ; number:3 ; day:12 ; month:10 ; pages:235-240 |
| Links: |
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| DOI / URN: |
10.1007/s13237-018-0248-5 |
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| Katalog-ID: |
SPR030980437 |
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| 100 | 1 | |a Kuraoka, Isao |e verfasserin |0 (orcid)0000-0001-6391-3411 |4 aut | |
| 245 | 1 | 0 | |a Alternative excision repair of topoisomerase inhibitor-induced DNA damage |
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| 520 | |a Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. | ||
| 650 | 4 | |a Topoisomerase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a TOPO damage |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Nucleotide excision repair |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Base excision repair |7 (dpeaa)DE-He213 | |
| 773 | 0 | 8 | |i Enthalten in |t The nucleus |d [New Delhi] : Springer India, 2010 |g 61(2018), 3 vom: 12. Okt., Seite 235-240 |w (DE-627)644282746 |w (DE-600)2589081-5 |x 0976-7975 |7 nnns |
| 773 | 1 | 8 | |g volume:61 |g year:2018 |g number:3 |g day:12 |g month:10 |g pages:235-240 |
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| 912 | |a GBV_ILN_2034 | ||
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| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2065 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2070 | ||
| 912 | |a GBV_ILN_2086 | ||
| 912 | |a GBV_ILN_2088 | ||
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| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2107 | ||
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| 912 | |a GBV_ILN_2446 | ||
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| 951 | |a AR | ||
| 952 | |d 61 |j 2018 |e 3 |b 12 |c 10 |h 235-240 | ||
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10.1007/s13237-018-0248-5 doi (DE-627)SPR030980437 (SPR)s13237-018-0248-5-e DE-627 ger DE-627 rakwb eng Kuraoka, Isao verfasserin (orcid)0000-0001-6391-3411 aut Alternative excision repair of topoisomerase inhibitor-induced DNA damage 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Archana Sharma Foundation of Calcutta 2018 Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 Enthalten in The nucleus [New Delhi] : Springer India, 2010 61(2018), 3 vom: 12. Okt., Seite 235-240 (DE-627)644282746 (DE-600)2589081-5 0976-7975 nnns volume:61 year:2018 number:3 day:12 month:10 pages:235-240 https://dx.doi.org/10.1007/s13237-018-0248-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 61 2018 3 12 10 235-240 |
| spelling |
10.1007/s13237-018-0248-5 doi (DE-627)SPR030980437 (SPR)s13237-018-0248-5-e DE-627 ger DE-627 rakwb eng Kuraoka, Isao verfasserin (orcid)0000-0001-6391-3411 aut Alternative excision repair of topoisomerase inhibitor-induced DNA damage 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Archana Sharma Foundation of Calcutta 2018 Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 Enthalten in The nucleus [New Delhi] : Springer India, 2010 61(2018), 3 vom: 12. Okt., Seite 235-240 (DE-627)644282746 (DE-600)2589081-5 0976-7975 nnns volume:61 year:2018 number:3 day:12 month:10 pages:235-240 https://dx.doi.org/10.1007/s13237-018-0248-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 61 2018 3 12 10 235-240 |
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10.1007/s13237-018-0248-5 doi (DE-627)SPR030980437 (SPR)s13237-018-0248-5-e DE-627 ger DE-627 rakwb eng Kuraoka, Isao verfasserin (orcid)0000-0001-6391-3411 aut Alternative excision repair of topoisomerase inhibitor-induced DNA damage 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Archana Sharma Foundation of Calcutta 2018 Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 Enthalten in The nucleus [New Delhi] : Springer India, 2010 61(2018), 3 vom: 12. Okt., Seite 235-240 (DE-627)644282746 (DE-600)2589081-5 0976-7975 nnns volume:61 year:2018 number:3 day:12 month:10 pages:235-240 https://dx.doi.org/10.1007/s13237-018-0248-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 61 2018 3 12 10 235-240 |
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10.1007/s13237-018-0248-5 doi (DE-627)SPR030980437 (SPR)s13237-018-0248-5-e DE-627 ger DE-627 rakwb eng Kuraoka, Isao verfasserin (orcid)0000-0001-6391-3411 aut Alternative excision repair of topoisomerase inhibitor-induced DNA damage 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Archana Sharma Foundation of Calcutta 2018 Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 Enthalten in The nucleus [New Delhi] : Springer India, 2010 61(2018), 3 vom: 12. Okt., Seite 235-240 (DE-627)644282746 (DE-600)2589081-5 0976-7975 nnns volume:61 year:2018 number:3 day:12 month:10 pages:235-240 https://dx.doi.org/10.1007/s13237-018-0248-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 61 2018 3 12 10 235-240 |
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10.1007/s13237-018-0248-5 doi (DE-627)SPR030980437 (SPR)s13237-018-0248-5-e DE-627 ger DE-627 rakwb eng Kuraoka, Isao verfasserin (orcid)0000-0001-6391-3411 aut Alternative excision repair of topoisomerase inhibitor-induced DNA damage 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Archana Sharma Foundation of Calcutta 2018 Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 Enthalten in The nucleus [New Delhi] : Springer India, 2010 61(2018), 3 vom: 12. Okt., Seite 235-240 (DE-627)644282746 (DE-600)2589081-5 0976-7975 nnns volume:61 year:2018 number:3 day:12 month:10 pages:235-240 https://dx.doi.org/10.1007/s13237-018-0248-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 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_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 61 2018 3 12 10 235-240 |
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Enthalten in The nucleus 61(2018), 3 vom: 12. Okt., Seite 235-240 volume:61 year:2018 number:3 day:12 month:10 pages:235-240 |
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Enthalten in The nucleus 61(2018), 3 vom: 12. Okt., Seite 235-240 volume:61 year:2018 number:3 day:12 month:10 pages:235-240 |
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Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). 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Kuraoka, Isao |
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Kuraoka, Isao misc Topoisomerase misc TOPO damage misc Nucleotide excision repair misc Base excision repair Alternative excision repair of topoisomerase inhibitor-induced DNA damage |
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Alternative excision repair of topoisomerase inhibitor-induced DNA damage Topoisomerase (dpeaa)DE-He213 TOPO damage (dpeaa)DE-He213 Nucleotide excision repair (dpeaa)DE-He213 Base excision repair (dpeaa)DE-He213 |
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alternative excision repair of topoisomerase inhibitor-induced dna damage |
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Alternative excision repair of topoisomerase inhibitor-induced DNA damage |
| abstract |
Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. © Archana Sharma Foundation of Calcutta 2018 |
| abstractGer |
Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. © Archana Sharma Foundation of Calcutta 2018 |
| abstract_unstemmed |
Abstract Topoisomerase 1 (Top1) and 2 (Top2) are common targets of anti-cancer drugs, which induce specific DNA lesions that are thought to lead to cell death in tumour cells. Camptothecin blocks DNA religation in the Top1–DNA complex and induces Top1-attached nick DNA lesions (Top1–DNA damage). We propose that nucleotide excision repair (NER) factors, excision repair cross complementing 1 protein-xeroderma pigmentosum group F (ERCC1–XPF) endonuclease, and replication protein A (RPA), participate in the repair of Top1-attached nick DNA lesions. ERCC1–XPF exhibits nuclease activity in the presence of RPA on a 3′-phosphotyrosyl bond nick-containing DNA (3′-Tyr-nick DNA) substrate, which mimics a Top1-attached nick DNA lesion. Moreover, repair of the 3′-Tyr-nick DNA occurred in the presence of NER factors, including ERCC1–XPF, RPA, DNA polymerase delta, flap endonuclease 1 (FEN1) and DNA ligase 1 (LIG1). We also illustrate a repair model for DNA lesions induced by Top2 inhibitor etoposide (VP-16), Top2-attached nick DNA (Top2-DNA damage). FEN1 participates in the cleavage of the 5′-phosphotyrosyl bond nick-containing DNA (5′-Tyr-nick DNA) substrates, which mimic Top2-attached nick DNA lesions. Under DNA repair synthesis conditions, FEN1 efficiently repaired the 5′-Tyr-nick DNA substrates in the presence of other base excision repair (BER) factors, LIG1 and DNA polymerase beta (POLB). Taken together, some of the NER and BER machinery might represent an alternative repair pathway for Top1- and Top2-DNA damage. © Archana Sharma Foundation of Calcutta 2018 |
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| title_short |
Alternative excision repair of topoisomerase inhibitor-induced DNA damage |
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https://dx.doi.org/10.1007/s13237-018-0248-5 |
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10.1007/s13237-018-0248-5 |
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2024-07-03T21:17:38.820Z |
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| score |
7.398242 |