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Article: DNA Methylation, Nuclear Organization, and Cancer.

Madakashira, Bhavani P / Sadler, Kirsten C

2017 Volume 8, Page(s) 76

Abstract: ... LOCKs) and nuclear lamina interactions (LADs). In this review, we focus on a novel perspective that DNA ... of nuclear reorganization in cancer are found in the long regions of chromatin marked by histone methylation ... The dramatic re-organization of the cancer cell nucleus creates telltale morphological features ...

Abstract	The dramatic re-organization of the cancer cell nucleus creates telltale morphological features critical for pathological staging of tumors. In addition, the changes to the mutational and epigenetic landscape in cancer cells alter the structure and stability of the genome and directly contribute to malignancy. DNA methylation is one of the best studied epigenetic changes in cancer, as nearly every type of cancer studied shows a loss of DNA methylation spread across most of the genome. This global hypomethylation is accompanied by hypermethylation at distinct loci, and much of the work on DNA methylation in cancer has focused on how local changes contribute to gene expression. However, the emerging picture is that the changes to DNA methylation in cancer cells has little direct effect on gene expression but instead impacts the organization of the genome in the nucleus. Several recent studies that take a broad view of the cancer epigenome find that the most profound changes to the cancer methylome are spread across large segments of the genome, and that the focal changes are reflective of a whole reorganization of epigenome. Hallmarks of nuclear reorganization in cancer are found in the long regions of chromatin marked by histone methylation (LOCKs) and nuclear lamina interactions (LADs). In this review, we focus on a novel perspective that DNA methylation changes in cancer impact the global structure of heterochromatin, LADs and LOCKs, and how these global changes, in turn, contribute to gene expression changes and genomic stability.
Language	English
Publishing date	2017-06-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2017.00076
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Article ; Online: The impact of DNA methylation on CTCF-mediated 3D genome organization.

Monteagudo-Sánchez, Ana / Noordermeer, Daan / Greenberg, Maxim V C

Nature structural & molecular biology

2024 Volume 31, Issue 3, Page(s) 404–412

Abstract: ... such as cancer, in which the epigenome and 3D genome organization are misregulated. ... of DNA methylation at gene promoters and repetitive elements has been extensively studied, the function ... to both the mammalian DNA methylation and chromatin architecture fields and attempt to assess the extent to which DNA ...

Abstract	Cytosine DNA methylation is a highly conserved epigenetic mark in eukaryotes. Although the role of DNA methylation at gene promoters and repetitive elements has been extensively studied, the function of DNA methylation in other genomic contexts remains less clear. In the nucleus of mammalian cells, the genome is spatially organized at different levels, and strongly influences myriad genomic processes. There are a number of factors that regulate the three-dimensional (3D) organization of the genome, with the CTCF insulator protein being among the most well-characterized. Pertinently, CTCF binding has been reported as being DNA methylation-sensitive in certain contexts, perhaps most notably in the process of genomic imprinting. Therefore, it stands to reason that DNA methylation may play a broader role in the regulation of chromatin architecture. Here we summarize the current understanding that is relevant to both the mammalian DNA methylation and chromatin architecture fields and attempt to assess the extent to which DNA methylation impacts the folding of the genome. The focus is in early embryonic development and cellular transitions when the epigenome is in flux, but we also describe insights from pathological contexts, such as cancer, in which the epigenome and 3D genome organization are misregulated.
MeSH term(s)	Animals ; DNA Methylation ; Repressor Proteins/metabolism ; CCCTC-Binding Factor/metabolism ; Genomic Imprinting ; Chromatin ; Mammals/genetics
Chemical Substances	Repressor Proteins ; CCCTC-Binding Factor ; Chromatin
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/s41594-024-01241-6
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Article ; Online: Circulating DNA fragmentomics and cancer screening.

Thierry, A R

Cell genomics

2023 Volume 3, Issue 1, Page(s) 100242

Abstract: The high fragmentation of nuclear circulating DNA (cirDNA) relies on chromatin organization and ... in the circulation. Fragmentomics can determine tissue of origin and distinguish cancer-derived cirDNA. The screening ... as a strategy for characterizing cancer within individuals and offers an alternative or a synergistic supplement ...

Abstract	The high fragmentation of nuclear circulating DNA (cirDNA) relies on chromatin organization and protection or packaging within mononucleosomes, the smallest and the most stabilized structure in the bloodstream. The detection of differing size patterns, termed fragmentomics, exploits information about the nucleosomal packing of DNA. Fragmentomics not only implies size pattern characterization but also considers the positioning and occupancy of nucleosomes, which result in cirDNA fragments being protected and persisting in the circulation. Fragmentomics can determine tissue of origin and distinguish cancer-derived cirDNA. The screening power of fragmentomics has been considerably strengthened in the omics era, as shown in the ongoing development of sophisticated technologies assisted by machine learning. Fragmentomics can thus be regarded as a strategy for characterizing cancer within individuals and offers an alternative or a synergistic supplement to mutation searches, methylation, or nucleosome positioning. As such, it offers potential for improving diagnostics and cancer screening.
Language	English
Publishing date	2023-01-11
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2666-979X
ISSN (online)	2666-979X
DOI	10.1016/j.xgen.2022.100242
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Article ; Online: Evaluation of DNA Methylation Profiles of LINE-1, Alu and Ribosomal DNA Repeats in Human Cell Lines Exposed to Radiofrequency Radiation.

Ravaioli, Francesco / Bacalini, Maria Giulia / Giuliani, Cristina / Pellegrini, Camilla / D'Silva, Chiara / De Fanti, Sara / Pirazzini, Chiara / Giorgi, Gianfranco / Del Re, Brunella

International journal of molecular sciences

2023 Volume 24, Issue 11

Abstract: ... such as long interspersed nuclear elements-1 (LINE-1), Alu short interspersed nuclear elements and ribosomal ... in terms of both average profiles and organisation of methylated and unmethylated CpG sites, in different ... repeats. To this purpose, we analysed DNAm profiles of cervical cancer and neuroblastoma cell lines (HeLa ...

Abstract	A large body of evidence indicates that environmental agents can induce alterations in DNA methylation (DNAm) profiles. Radiofrequency electromagnetic fields (RF-EMFs) are radiations emitted by everyday devices, which have been classified as "possibly carcinogenic"; however, their biological effects are unclear. As aberrant DNAm of genomic repetitive elements (REs) may promote genomic instability, here, we sought to determine whether exposure to RF-EMFs could affect DNAm of different classes of REs, such as long interspersed nuclear elements-1 (LINE-1), Alu short interspersed nuclear elements and ribosomal repeats. To this purpose, we analysed DNAm profiles of cervical cancer and neuroblastoma cell lines (HeLa, BE(2)C and SH-SY5Y) exposed to 900 MHz GSM-modulated RF-EMF through an Illumina-based targeted deep bisulfite sequencing approach. Our findings showed that radiofrequency exposure did not affect the DNAm of Alu elements in any of the cell lines analysed. Conversely, it influenced DNAm of LINE-1 and ribosomal repeats in terms of both average profiles and organisation of methylated and unmethylated CpG sites, in different ways in each of the three cell lines studied.
MeSH term(s)	Humans ; DNA Methylation ; DNA, Ribosomal ; Neuroblastoma/genetics ; Cell Line ; Alu Elements/genetics
Chemical Substances	DNA, Ribosomal
Language	English
Publishing date	2023-05-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24119380
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Article ; Online: Evaluation of DNA Methylation Profiles of LINE-1, Alu and Ribosomal DNA Repeats in Human Cell Lines Exposed to Radiofrequency Radiation

Francesco Ravaioli / Maria Giulia Bacalini / Cristina Giuliani / Camilla Pellegrini / Chiara D’Silva / Sara De Fanti / Chiara Pirazzini / Gianfranco Giorgi / Brunella Del Re

International Journal of Molecular Sciences, Vol 24, Iss 9380, p

2023 Volume 9380

Abstract	A large body of evidence indicates that environmental agents can induce alterations in DNA methylation (DNAm) profiles. Radiofrequency electromagnetic fields (RF-EMFs) are radiations emitted by everyday devices, which have been classified as “possibly carcinogenic”; however, their biological effects are unclear. As aberrant DNAm of genomic repetitive elements (REs) may promote genomic instability, here, we sought to determine whether exposure to RF-EMFs could affect DNAm of different classes of REs, such as long interspersed nuclear elements-1 (LINE-1), Alu short interspersed nuclear elements and ribosomal repeats. To this purpose, we analysed DNAm profiles of cervical cancer and neuroblastoma cell lines (HeLa, BE(2)C and SH-SY5Y) exposed to 900 MHz GSM-modulated RF-EMF through an Illumina-based targeted deep bisulfite sequencing approach. Our findings showed that radiofrequency exposure did not affect the DNAm of Alu elements in any of the cell lines analysed. Conversely, it influenced DNAm of LINE-1 and ribosomal repeats in terms of both average profiles and organisation of methylated and unmethylated CpG sites, in different ways in each of the three cell lines studied.
Keywords	radiofrequency electromagnetic field ; DNA methylation ; neuroblastoma ; LINE-1 ; Alu ; ribosomal DNA ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	612
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genome-wide mapping of genomic DNA damage: methods and implications.

Amente, Stefano / Scala, Giovanni / Majello, Barbara / Azmoun, Somaiyeh / Tempest, Helen G / Premi, Sanjay / Cooke, Marcus S

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 21-22, Page(s) 6745–6762

Abstract: ... of forms of DNA damage, to specific locations across the nuclear and mitochondrial genomes. We propose ... Exposures from the external and internal environments lead to the modification of genomic DNA ... mutation, microsatellite instability, altered methylation and gene expression) on cellular function will be ...

Abstract	Exposures from the external and internal environments lead to the modification of genomic DNA, which is implicated in the cause of numerous diseases, including cancer, cardiovascular, pulmonary and neurodegenerative diseases, together with ageing. However, the precise mechanism(s) linking the presence of damage, to impact upon cellular function and pathogenesis, is far from clear. Genomic location of specific forms of damage is likely to be highly informative in understanding this process, as the impact of downstream events (e.g. mutation, microsatellite instability, altered methylation and gene expression) on cellular function will be positional-events at key locations will have the greatest impact. However, until recently, methods for assessing DNA damage determined the totality of damage in the genomic location, with no positional information. The technique of "mapping DNA adductomics" describes the molecular approaches that map a variety of forms of DNA damage, to specific locations across the nuclear and mitochondrial genomes. We propose that integrated comparison of this information with other genome-wide data, such as mutational hotspots for specific genotoxins, tumour-specific mutation patterns and chromatin organisation and transcriptional activity in non-cancerous lesions (such as nevi), pre-cancerous conditions (such as polyps) and tumours, will improve our understanding of how environmental toxins lead to cancer. Adopting an analogous approach for non-cancer diseases, including the development of genome-wide assays for other cellular outcomes of DNA damage, will improve our understanding of the role of DNA damage in pathogenesis more generally.
MeSH term(s)	Animals ; Chromosome Mapping/methods ; DNA/genetics ; DNA Damage/genetics ; Genome/genetics ; Genome-Wide Association Study/methods ; Genomics/methods ; Humans ; Mutation/genetics ; Neoplasms/genetics
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2021-08-31
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03923-6
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Article ; Online: Lung mitochondrial DNA copy number, inflammatory biomarkers, gene transcription and gene methylation in vapers and smokers.

Mori, Kellie M / McElroy, Joseph P / Weng, Daniel Y / Chung, Sangwoon / Fadda, Paolo / Reisinger, Sarah A / Ying, Kevin L / Brasky, Theodore M / Wewers, Mark D / Freudenheim, Jo L / Shields, Peter G / Song, Min-Ae

EBioMedicine

2022 Volume 85, Page(s) 104301

Abstract: ... is linked to nuclear DNA methylation and gene expression. Increased mtCN in the blood is associated ... immune responses, nuclear DNA methylation and gene expression using linear regression. Ingenuity pathway analysis ... Background: Mitochondrial DNA copy number (mtCN) maintains cellular function and homeostasis, and ...

Abstract	Background: Mitochondrial DNA copy number (mtCN) maintains cellular function and homeostasis, and is linked to nuclear DNA methylation and gene expression. Increased mtCN in the blood is associated with smoking and respiratory disease, but has received little attention for target organ effects for smoking or electronic cigarette (EC) use. Methods: Bronchoscopy biospecimens from healthy EC users, smokers (SM), and never-smokers (NS) were assessed for associations of mtCN with mtDNA point mutations, immune responses, nuclear DNA methylation and gene expression using linear regression. Ingenuity pathway analysis was used for enriched pathways. GEO and TCGA respiratory disease datasets were used to explore the involvement of mtCN-associated signatures. Findings: mtCN was higher in SM than NS, but EC was not statistically different from either. Overall there was a negative association of mtCN with a point mutation in the D-loop but no difference within groups. Positive associations of mtCN with IL-2 and IL-4 were found in EC only. mtCN was significantly associated with 71,487 CpGs and 321 transcripts. 263 CpGs were correlated with nearby transcripts for genes enriched in the immune system. EC-specific mtCN-associated-CpGs and genes were differentially expressed in respiratory diseases compared to controls, including genes involved in cellular movement, inflammation, metabolism, and airway hyperresponsiveness. Interpretation: Smoking may elicit a lung toxic effect through mtCN. While the impact of EC is less clear, EC-specific associations of mtCN with nuclear biomarkers suggest exposure may not be harmless. Further research is needed to understand the role of smoking and EC-related mtCN on lung disease risks. Funding: The National Cancer Institute, the National Heart, Lung, and Blood Institute, the Food and Drug Administration Center for Tobacco Products, the National Center For Advancing Translational Sciences, and Pelotonia Intramural Research Funds.
MeSH term(s)	Humans ; DNA, Mitochondrial/genetics ; Smokers ; DNA Copy Number Variations ; Electronic Nicotine Delivery Systems ; Biomarkers ; DNA Methylation ; Lung ; Transcription, Genetic
Chemical Substances	DNA, Mitochondrial ; Biomarkers
Language	English
Publishing date	2022-10-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2022.104301
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Article ; Online: Treating ARID1A mutated cancers by harnessing synthetic lethality and DNA damage response.

Mandal, Jayaprakash / Mandal, Prativa / Wang, Tian-Li / Shih, Ie-Ming

Journal of biomedical science

2022 Volume 29, Issue 1, Page(s) 71

Abstract: ... replication, methylation, and damage repair. Aberrations in this activity have emerged as epigenomic mechanisms in cancer ... for regulating cell cycle, facilitating DNA damage repair, and controlling expression of genes that are essential ... in understanding the biology of ARID1A in cancer development, with special emphasis on its roles in DNA damage ...

Abstract	Chromatin remodeling is an essential cellular process for organizing chromatin structure into either open or close configuration at specific chromatin locations by orchestrating and modifying histone complexes. This task is responsible for fundamental cell physiology including transcription, DNA replication, methylation, and damage repair. Aberrations in this activity have emerged as epigenomic mechanisms in cancer development that increase tumor clonal fitness and adaptability amidst various selection pressures. Inactivating mutations in AT-rich interaction domain 1A (ARID1A), a gene encoding a large nuclear protein member belonging to the SWI/SNF chromatin remodeling complex, result in its loss of expression. ARID1A is the most commonly mutated chromatin remodeler gene, exhibiting the highest mutation frequency in endometrium-related uterine and ovarian carcinomas. As a tumor suppressor gene, ARID1A is essential for regulating cell cycle, facilitating DNA damage repair, and controlling expression of genes that are essential for maintaining cellular differentiation and homeostasis in non-transformed cells. Thus, ARID1A deficiency due to somatic mutations propels tumor progression and dissemination. The recent success of PARP inhibitors in treating homologous recombination DNA repair-deficient tumors has engendered keen interest in developing synthetic lethality-based therapeutic strategies for ARID1A-mutated neoplasms. In this review, we summarize recent advances in understanding the biology of ARID1A in cancer development, with special emphasis on its roles in DNA damage repair. We also discuss strategies to harness synthetic lethal mechanisms for future therapeutics against ARID1A-mutated cancers.
MeSH term(s)	Chromatin ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Histones ; Humans ; Nuclear Proteins/metabolism ; Ovarian Neoplasms/genetics ; Poly(ADP-ribose) Polymerase Inhibitors ; Synthetic Lethal Mutations ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	ARID1A protein, human ; Chromatin ; DNA-Binding Proteins ; Histones ; Nuclear Proteins ; Poly(ADP-ribose) Polymerase Inhibitors ; Transcription Factors
Language	English
Publishing date	2022-09-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-022-00856-5
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Article: Genome-wide mapping of genomic DNA damage: methods and implications

Amente, Stefano / Scala, Giovanni / Majello, Barbara / Azmoun, Somaiyeh / Tempest, Helen G. / Premi, Sanjay / Cooke, Marcus S.

Cellular and molecular life sciences. 2021 Nov., v. 78, no. 21-22

2021

Abstract	Exposures from the external and internal environments lead to the modification of genomic DNA, which is implicated in the cause of numerous diseases, including cancer, cardiovascular, pulmonary and neurodegenerative diseases, together with ageing. However, the precise mechanism(s) linking the presence of damage, to impact upon cellular function and pathogenesis, is far from clear. Genomic location of specific forms of damage is likely to be highly informative in understanding this process, as the impact of downstream events (e.g. mutation, microsatellite instability, altered methylation and gene expression) on cellular function will be positional—events at key locations will have the greatest impact. However, until recently, methods for assessing DNA damage determined the totality of damage in the genomic location, with no positional information. The technique of “mapping DNA adductomics” describes the molecular approaches that map a variety of forms of DNA damage, to specific locations across the nuclear and mitochondrial genomes. We propose that integrated comparison of this information with other genome-wide data, such as mutational hotspots for specific genotoxins, tumour-specific mutation patterns and chromatin organisation and transcriptional activity in non-cancerous lesions (such as nevi), pre-cancerous conditions (such as polyps) and tumours, will improve our understanding of how environmental toxins lead to cancer. Adopting an analogous approach for non-cancer diseases, including the development of genome-wide assays for other cellular outcomes of DNA damage, will improve our understanding of the role of DNA damage in pathogenesis more generally.
Keywords	DNA ; DNA damage ; chromatin ; gene expression ; genomics ; methylation ; microsatellite repeats ; mitochondrial genome ; mutagens ; mutation ; pathogenesis ; transcription (genetics)
Language	English
Dates of publication	2021-11
Size	p. 6745-6762.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03923-6
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Histone methylation and the DNA damage response.

Gong, Fade / Miller, Kyle M

Mutation research. Reviews in mutation research

2017 Volume 780, Page(s) 37–47

Abstract: ... pathways referred to as the DNA damage response (DDR). As nuclear DNA is bound by histone proteins and ... organized into chromatin in eukaryotes, DDR pathways have evolved to sense, signal and repair DNA damage ... involved in the DDR is histone methylation, which is regulated by histone methyltransferase (HMT) and ...

Abstract	Preserving genome function and stability are paramount for ensuring cellular homeostasis, an imbalance in which can promote diseases including cancer. In the presence of DNA lesions, cells activate pathways referred to as the DNA damage response (DDR). As nuclear DNA is bound by histone proteins and organized into chromatin in eukaryotes, DDR pathways have evolved to sense, signal and repair DNA damage within the chromatin environment. Histone proteins, which constitute the building blocks of chromatin, are highly modified by post-translational modifications (PTMs) that regulate chromatin structure and function. An essential histone PTM involved in the DDR is histone methylation, which is regulated by histone methyltransferase (HMT) and histone demethylase (HDM) enzymes that add and remove methyl groups on lysine and arginine residues within proteins respectively. Methylated histones can alter how proteins interact with chromatin, including their ability to be bound by reader proteins that recognize these PTMs. Here, we review histone methylation in the context of the DDR, focusing on DNA double-strand breaks (DSBs), a particularly toxic lesion that can trigger genome instability and cell death. We provide a comprehensive overview of histone methylation changes that occur in response to DNA damage and how the enzymes and reader proteins of these marks orchestrate the DDR. Finally, as many epigenetic pathways including histone methylation are altered in cancer, we discuss the potential involvement of these pathways in the etiology and treatment of this disease.
MeSH term(s)	Animals ; Chromatin/genetics ; DNA Damage/genetics ; Histones/metabolism ; Humans ; Methylation ; Signal Transduction/genetics
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2017-09-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2727833-5
ISSN	1388-2139 ; 1383-5742
ISSN (online)	1388-2139
ISSN	1383-5742
DOI	10.1016/j.mrrev.2017.09.003
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