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Article ; Online: DNA repair as a shared hallmark in cancer and ageing.

Clarke, Thomas L / Mostoslavsky, Raul

2022 Volume 16, Issue 18, Page(s) 3352–3379

Abstract: Increasing evidence demonstrates that DNA damage and genome instability play a crucial role in ageing. Mammalian cells have developed a wide range of complex and well-orchestrated DNA repair pathways to respond to and resolve many different types of DNA ... ...

Abstract	Increasing evidence demonstrates that DNA damage and genome instability play a crucial role in ageing. Mammalian cells have developed a wide range of complex and well-orchestrated DNA repair pathways to respond to and resolve many different types of DNA lesions that occur from exogenous and endogenous sources. Defects in these repair pathways lead to accelerated or premature ageing syndromes and increase the likelihood of cancer development. Understanding the fundamental mechanisms of DNA repair will help develop novel strategies to treat ageing-related diseases. Here, we revisit the processes involved in DNA damage repair and how these can contribute to diseases, including ageing and cancer. We also review recent mechanistic insights into DNA repair and discuss how these insights are being used to develop novel therapeutic strategies for treating human disease. We discuss the use of PARP inhibitors in the clinic for the treatment of breast and ovarian cancer and the challenges associated with acquired drug resistance. Finally, we discuss how DNA repair pathway-targeted therapeutics are moving beyond PARP inhibition in the search for ever more innovative and efficacious cancer therapies.
MeSH term(s)	Aging/genetics ; Animals ; DNA ; DNA Damage/genetics ; DNA Repair/genetics ; Female ; Humans ; Mammals/genetics ; Ovarian Neoplasms/drug therapy ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use
Chemical Substances	Poly(ADP-ribose) Polymerase Inhibitors ; DNA (9007-49-2)
Language	English
Publishing date	2022-07-28
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13285
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Article ; Online: Resveratrol: Friend or Foe?

Clarke, Thomas L / Mostoslavsky, Raul

Molecular cell

2020 Volume 79, Issue 5, Page(s) 705–707

Abstract: In this issue of Molecular Cell, Benslimane et al. (2020) perform a CRISPR-Cas9 chemogenomic screen, identifying a network of DNA replication and genome integrity genes with the nutraceutical compound Resveratrol and its analog Pterostilbene, linking ... ...

Abstract	In this issue of Molecular Cell, Benslimane et al. (2020) perform a CRISPR-Cas9 chemogenomic screen, identifying a network of DNA replication and genome integrity genes with the nutraceutical compound Resveratrol and its analog Pterostilbene, linking these compounds to the induction of DNA replication stress in mammalian cells.
MeSH term(s)	Animals ; Clustered Regularly Interspaced Short Palindromic Repeats ; DNA Replication ; Humans ; Resveratrol
Chemical Substances	Resveratrol (Q369O8926L)
Language	English
Publishing date	2020-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.08.008
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Article: Resveratrol: Friend or Foe?

Clarke, Thomas L / Mostoslavsky, Raul

Molecular cell. 2020 Sept. 03, v. 79, no. 5

2020

Abstract	In this issue of Molecular Cell, Benslimane et al. (2020) perform a CRISPR-Cas9 chemogenomic screen, identifying a network of DNA replication and genome integrity genes with the nutraceutical compound Resveratrol and its analog Pterostilbene, linking these compounds to the induction of DNA replication stress in mammalian cells.
Keywords	DNA replication ; dietary supplements ; mammals ; pterostilbene ; resveratrol
Language	English
Dates of publication	2020-0903
Size	p. 705-707.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.08.008
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Article ; Online: Assessing kinetics and recruitment of DNA repair factors using high content screens.

Martinez-Pastor, Barbara / Silveira, Giorgia G / Clarke, Thomas L / Chung, Dudley / Gu, Yuchao / Cosentino, Claudia / Davidow, Lance S / Mata, Gadea / Hassanieh, Sylvana / Salsman, Jayme / Ciccia, Alberto / Bae, Narkhyun / Bedford, Mark T / Megias, Diego / Rubin, Lee L / Efeyan, Alejo / Dellaire, Graham / Mostoslavsky, Raul

Cell reports

2021 Volume 37, Issue 13, Page(s) 110176

Abstract: Repair of genetic damage is coordinated in the context of chromatin, so cells dynamically modulate accessibility at DNA breaks for the recruitment of DNA damage response (DDR) factors. The identification of chromatin factors with roles in DDR has mostly ... ...

Abstract	Repair of genetic damage is coordinated in the context of chromatin, so cells dynamically modulate accessibility at DNA breaks for the recruitment of DNA damage response (DDR) factors. The identification of chromatin factors with roles in DDR has mostly relied on loss-of-function screens while lacking robust high-throughput systems to study DNA repair. In this study, we have developed two high-throughput systems that allow the study of DNA repair kinetics and the recruitment of factors to double-strand breaks in a 384-well plate format. Using a customized gain-of-function open-reading frame library ("ChromORFeome" library), we identify chromatin factors with putative roles in the DDR. Among these, we find the PHF20 factor is excluded from DNA breaks, affecting DNA repair by competing with 53BP1 recruitment. Adaptable for genetic perturbations, small-molecule screens, and large-scale analysis of DNA repair, these resources can aid our understanding and manipulation of DNA repair.
Language	English
Publishing date	2021-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110176
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Article ; Online: Histone Lysine Methylation Dynamics Control

Clarke, Thomas L / Tang, Ran / Chakraborty, Damayanti / Van Rechem, Capucine / Ji, Fei / Mishra, Sweta / Ma, Anqi / Kaniskan, H Ümit / Jin, Jian / Lawrence, Michael S / Sadreyev, Ruslan I / Whetstine, Johnathan R

Cancer discovery

2019 Volume 10, Issue 2, Page(s) 306–325

Abstract: Acquired chromosomal DNA copy gains are a feature of many tumors; however, the mechanisms that underpin oncogene amplification are poorly understood. Recent studies have begun to uncover the importance of epigenetic states and histone lysine ... ...

Abstract	Acquired chromosomal DNA copy gains are a feature of many tumors; however, the mechanisms that underpin oncogene amplification are poorly understood. Recent studies have begun to uncover the importance of epigenetic states and histone lysine methyltransferases (KMT) and demethylases (KDM) in regulating transient site-specific DNA copy-number gains (TSSG). In this study, we reveal a critical interplay between a myriad of lysine methyltransferases and demethylases in modulating H3K4/9/27 methylation balance to control extrachromosomal amplification of the
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Hypoxia/genetics ; Cell Line, Tumor ; DNA Copy Number Variations/drug effects ; DNA Methylation/drug effects ; DNA Methylation/genetics ; Epigenesis, Genetic/drug effects ; ErbB Receptors/antagonists & inhibitors ; ErbB Receptors/genetics ; Gene Amplification/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Histone-Lysine N-Methyltransferase/antagonists & inhibitors ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/metabolism ; Humans ; Jumonji Domain-Containing Histone Demethylases/antagonists & inhibitors ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Lysine/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Histones ; Protein Kinase Inhibitors ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2019-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-19-0463
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Book ; Conference proceedings: Distributed interactive simulation systems for simulation and training in the aerospace environment

Clarke, Thomas L

proceedings of a conference held 19-20 April 1995, Orlando, Florida

(Critical reviews of optical science and technology ; v. CR58)

1995

Institution	Society of Photo-Optical Instrumentation Engineers
Event/congress	Conference (1995.04.19-20, Orlando)
Author's details	Thomas L. Clarke, editor
Series title	Critical reviews of optical science and technology ; v. CR58
Language	English
Size	xii, 327 p, ill, 26 cm
Publisher	SPIE Optical Engineering Press
Publishing place	Bellingham, Wash
Document type	Book ; Conference proceedings
Note	Includes bibliographical references and index
ISBN	0819418501 ; 9780819418500
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Cross-talk between Lysine-Modifying Enzymes Controls Site-Specific DNA Amplifications.

Mishra, Sweta / Van Rechem, Capucine / Pal, Sangita / Clarke, Thomas L / Chakraborty, Damayanti / Mahan, Sarah D / Black, Joshua C / Murphy, Sedona E / Lawrence, Michael S / Daniels, Danette L / Whetstine, Johnathan R

Cell

2018 Volume 175, Issue 6, Page(s) 1716

Language	English
Publishing date	2018-12-13
Publishing country	United States
Document type	Published Erratum
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2018.11.018
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cross-talk between Lysine-Modifying Enzymes Controls Site-Specific DNA Amplifications.

Cell

2018 Volume 174, Issue 4, Page(s) 803–817.e16

Abstract: Acquired chromosomal DNA amplifications are features of many tumors. Although overexpression and stabilization of the histone H3 lysine 9/36 (H3K9/36) tri-demethylase KDM4A generates transient site-specific copy number gains (TSSGs), additional ... ...

Abstract	Acquired chromosomal DNA amplifications are features of many tumors. Although overexpression and stabilization of the histone H3 lysine 9/36 (H3K9/36) tri-demethylase KDM4A generates transient site-specific copy number gains (TSSGs), additional mechanisms directly controlling site-specific DNA copy gains are not well defined. In this study, we uncover a collection of H3K4-modifying chromatin regulators that function with H3K9 and H3K36 regulators to orchestrate TSSGs. Specifically, the H3K4 tri-demethylase KDM5A and specific COMPASS/KMT2 H3K4 methyltransferases modulate different TSSG loci through H3K4 methylation states and KDM4A recruitment. Furthermore, a distinct chromatin modifier network, MLL1-KDM4B-KDM5B, controls copy number regulation at a specific genomic locus in a KDM4A-independent manner. These pathways comprise an epigenetic addressing system for defining site-specific DNA rereplication and amplifications.
MeSH term(s)	Cell Cycle ; Chromatin/metabolism ; DNA Copy Number Variations ; DNA Methylation ; HEK293 Cells ; Histones/metabolism ; Humans ; Lysine/metabolism ; Retinoblastoma-Binding Protein 2/genetics ; Retinoblastoma-Binding Protein 2/metabolism
Chemical Substances	Chromatin ; Histones ; KDM5A protein, human (EC 1.14.11.-) ; Retinoblastoma-Binding Protein 2 (EC 1.14.11.27) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2018-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2018.06.018
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Article: Cross-talk between Lysine-Modifying Enzymes Controls Site-Specific DNA Amplifications

Cell. 2018 Aug. 09, v. 174, no. 4

2018

Abstract	Acquired chromosomal DNA amplifications are features of many tumors. Although overexpression and stabilization of the histone H3 lysine 9/36 (H3K9/36) tri-demethylase KDM4A generates transient site-specific copy number gains (TSSGs), additional mechanisms directly controlling site-specific DNA copy gains are not well defined. In this study, we uncover a collection of H3K4-modifying chromatin regulators that function with H3K9 and H3K36 regulators to orchestrate TSSGs. Specifically, the H3K4 tri-demethylase KDM5A and specific COMPASS/KMT2 H3K4 methyltransferases modulate different TSSG loci through H3K4 methylation states and KDM4A recruitment. Furthermore, a distinct chromatin modifier network, MLL1-KDM4B-KDM5B, controls copy number regulation at a specific genomic locus in a KDM4A-independent manner. These pathways comprise an epigenetic addressing system for defining site-specific DNA rereplication and amplifications.[Display omitted]
Keywords	DNA ; chromatin ; epigenetics ; gene overexpression ; genomics ; histones ; loci ; lysine ; methylation ; methyltransferases ; neoplasms
Language	English
Dates of publication	2018-0809
Size	p. 803-817.e16.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2018.06.018
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Article ; Online: PRMT5-Dependent Methylation of the TIP60 Coactivator RUVBL1 Is a Key Regulator of Homologous Recombination.

Clarke, Thomas L / Sanchez-Bailon, Maria Pilar / Chiang, Kelly / Reynolds, John J / Herrero-Ruiz, Joaquin / Bandeiras, Tiago M / Matias, Pedro M / Maslen, Sarah L / Skehel, J Mark / Stewart, Grant S / Davies, Clare C

Molecular cell

2017 Volume 65, Issue 5, Page(s) 900–916.e7

Abstract: Protein post-translation modification plays an important role in regulating DNA repair; however, the role of arginine methylation in this process is poorly understood. Here we identify the arginine methyltransferase PRMT5 as a key regulator of homologous ...

Abstract	Protein post-translation modification plays an important role in regulating DNA repair; however, the role of arginine methylation in this process is poorly understood. Here we identify the arginine methyltransferase PRMT5 as a key regulator of homologous recombination (HR)-mediated double-strand break (DSB) repair, which is mediated through its ability to methylate RUVBL1, a cofactor of the TIP60 complex. We show that PRMT5 targets RUVBL1 for methylation at position R205, which facilitates TIP60-dependent mobilization of 53BP1 from DNA breaks, promoting HR. Mechanistically, we demonstrate that PRMT5-directed methylation of RUVBL1 is critically required for the acetyltransferase activity of TIP60, promoting histone H4K16 acetylation, which facilities 53BP1 displacement from DSBs. Interestingly, RUVBL1 methylation did not affect the ability of TIP60 to facilitate ATM activation. Taken together, our findings reveal the importance of PRMT5-mediated arginine methylation during DSB repair pathway choice through its ability to regulate acetylation-dependent control of 53BP1 localization.
MeSH term(s)	ATPases Associated with Diverse Cellular Activities ; Acetylation ; Animals ; Arginine ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; DNA Breaks, Double-Stranded ; DNA Helicases/genetics ; DNA Helicases/metabolism ; Genomic Instability ; HEK293 Cells ; HeLa Cells ; Histone Acetyltransferases/genetics ; Histone Acetyltransferases/metabolism ; Histones/metabolism ; Humans ; Lysine Acetyltransferase 5 ; Methylation ; Mice ; Mice, Transgenic ; Protein Processing, Post-Translational ; Protein-Arginine N-Methyltransferases/genetics ; Protein-Arginine N-Methyltransferases/metabolism ; RNA Interference ; Recombinational DNA Repair ; Time Factors ; Transfection ; Tumor Suppressor p53-Binding Protein 1/genetics ; Tumor Suppressor p53-Binding Protein 1/metabolism
Chemical Substances	Carrier Proteins ; Histones ; TP53BP1 protein, human ; Tumor Suppressor p53-Binding Protein 1 ; Arginine (94ZLA3W45F) ; PRMT5 protein, human (EC 2.1.1.319) ; Prmt5 protein, mouse (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319) ; Histone Acetyltransferases (EC 2.3.1.48) ; KAT5 protein, human (EC 2.3.1.48) ; Lysine Acetyltransferase 5 (EC 2.3.1.48) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; ATPases Associated with Diverse Cellular Activities (EC 3.6.4.-) ; DNA Helicases (EC 3.6.4.-) ; RUVBL1 protein, human (EC 3.6.4.12)
Language	English
Publishing date	2017-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2017.01.019
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