The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer
Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Guppy, Brent J. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer International Publishing AG 2017 |
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| Übergeordnetes Werk: |
Enthalten in: Current molecular biology reports - Berlin : Springer, 2015, 3(2017), 1 vom: 26. Jan., Seite 18-27 |
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| Übergeordnetes Werk: |
volume:3 ; year:2017 ; number:1 ; day:26 ; month:01 ; pages:18-27 |
| Links: |
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| DOI / URN: |
10.1007/s40610-017-0051-0 |
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| Katalog-ID: |
SPR036748773 |
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| 024 | 7 | |a 10.1007/s40610-017-0051-0 |2 doi | |
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| 041 | |a eng | ||
| 100 | 1 | |a Guppy, Brent J. |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
| 264 | 1 | |c 2017 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a © Springer International Publishing AG 2017 | ||
| 520 | |a Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. | ||
| 650 | 4 | |a DOT1L |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a H3K79me1 |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a H3K79me3 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Genome stability |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cancer |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Jeusset, Lucile M-P. |4 aut | |
| 700 | 1 | |a McManus, Kirk J. |4 aut | |
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10.1007/s40610-017-0051-0 doi (DE-627)SPR036748773 (SPR)s40610-017-0051-0-e DE-627 ger DE-627 rakwb eng Guppy, Brent J. verfasserin aut The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Jeusset, Lucile M-P. aut McManus, Kirk J. aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 1 vom: 26. Jan., Seite 18-27 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:1 day:26 month:01 pages:18-27 https://dx.doi.org/10.1007/s40610-017-0051-0 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_2190 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 3 2017 1 26 01 18-27 |
| spelling |
10.1007/s40610-017-0051-0 doi (DE-627)SPR036748773 (SPR)s40610-017-0051-0-e DE-627 ger DE-627 rakwb eng Guppy, Brent J. verfasserin aut The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Jeusset, Lucile M-P. aut McManus, Kirk J. aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 1 vom: 26. Jan., Seite 18-27 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:1 day:26 month:01 pages:18-27 https://dx.doi.org/10.1007/s40610-017-0051-0 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_2190 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 3 2017 1 26 01 18-27 |
| allfields_unstemmed |
10.1007/s40610-017-0051-0 doi (DE-627)SPR036748773 (SPR)s40610-017-0051-0-e DE-627 ger DE-627 rakwb eng Guppy, Brent J. verfasserin aut The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Jeusset, Lucile M-P. aut McManus, Kirk J. aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 1 vom: 26. Jan., Seite 18-27 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:1 day:26 month:01 pages:18-27 https://dx.doi.org/10.1007/s40610-017-0051-0 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_2190 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 3 2017 1 26 01 18-27 |
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10.1007/s40610-017-0051-0 doi (DE-627)SPR036748773 (SPR)s40610-017-0051-0-e DE-627 ger DE-627 rakwb eng Guppy, Brent J. verfasserin aut The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Jeusset, Lucile M-P. aut McManus, Kirk J. aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 1 vom: 26. Jan., Seite 18-27 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:1 day:26 month:01 pages:18-27 https://dx.doi.org/10.1007/s40610-017-0051-0 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_2190 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 3 2017 1 26 01 18-27 |
| allfieldsSound |
10.1007/s40610-017-0051-0 doi (DE-627)SPR036748773 (SPR)s40610-017-0051-0-e DE-627 ger DE-627 rakwb eng Guppy, Brent J. verfasserin aut The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 Jeusset, Lucile M-P. aut McManus, Kirk J. aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 1 vom: 26. Jan., Seite 18-27 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:1 day:26 month:01 pages:18-27 https://dx.doi.org/10.1007/s40610-017-0051-0 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_2190 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 3 2017 1 26 01 18-27 |
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Enthalten in Current molecular biology reports 3(2017), 1 vom: 26. Jan., Seite 18-27 volume:3 year:2017 number:1 day:26 month:01 pages:18-27 |
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Guppy, Brent J. @@aut@@ Jeusset, Lucile M-P. @@aut@@ McManus, Kirk J. @@aut@@ |
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We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. 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| author |
Guppy, Brent J. |
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Guppy, Brent J. misc DOT1L misc H3K79me1 misc H3K79me2 misc H3K79me3 misc Genome stability misc Cancer The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
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The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer DOT1L (dpeaa)DE-He213 H3K79me1 (dpeaa)DE-He213 H3K79me2 (dpeaa)DE-He213 H3K79me3 (dpeaa)DE-He213 Genome stability (dpeaa)DE-He213 Cancer (dpeaa)DE-He213 |
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misc DOT1L misc H3K79me1 misc H3K79me2 misc H3K79me3 misc Genome stability misc Cancer |
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The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
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The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
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relationship between dot1l, histone h3 methylation, and genome stability in cancer |
| title_auth |
The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
| abstract |
Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. © Springer International Publishing AG 2017 |
| abstractGer |
Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. © Springer International Publishing AG 2017 |
| abstract_unstemmed |
Purpose of Review This review describes how disruptor of telomeric silencing 1-like (DOT1L) and histone H3 at lysine 79 (H3K79) methylation maintain genome stability under normal conditions and discusses the consequences of their dysregulation. We highlight the roles that DOT1L and H3K79 methylation have in various cellular processes and detail their roles in the DNA damage response and mitotic fidelity. Recent Findings DOT1L is currently the only known enzyme capable of catalyzing the methylation of H3K79. DOT1L activity and H3K79 methylation regulate a number of key cellular processes required to maintain genome stability, including transcription, cell cycle progression, and the DNA damage response. Consequently, alterations of DOT1L activity and H3K79 methylation patterning are predicted to compromise genome stability. Summary Consistent with a putative role in oncogenesis, aberrant DOT1L expression and function occur in a wide range of cancer types including breast, colorectal, and lung, yet the exact mechanisms linking altered DOT1L expression and H3K79 methylation to genome instability remain poorly understood. © Springer International Publishing AG 2017 |
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The Relationship Between DOT1L, Histone H3 Methylation, and Genome Stability in Cancer |
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https://dx.doi.org/10.1007/s40610-017-0051-0 |
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Jeusset, Lucile M-P. McManus, Kirk J. |
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10.1007/s40610-017-0051-0 |
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2024-07-03T19:26:06.607Z |
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|
| score |
7.399976 |