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Article ; Online: Active mRNA degradation by EXD2 nuclease elicits recovery of transcription after genotoxic stress.

Sandoz, Jérémy / Cigrang, Max / Zachayus, Amélie / Catez, Philippe / Donnio, Lise-Marie / Elly, Clèmence / Nieminuszczy, Jadwiga / Berico, Pietro / Braun, Cathy / Alekseev, Sergey / Egly, Jean-Marc / Niedzwiedz, Wojciech / Giglia-Mari, Giuseppina / Compe, Emmanuel / Coin, Frédéric

Nature communications

2023 Volume 14, Issue 1, Page(s) 341

Abstract: The transcriptional response to genotoxic stress involves gene expression arrest, followed by recovery of mRNA synthesis (RRS) after DNA repair. We find that the lack of the EXD2 nuclease impairs RRS and decreases cell survival after UV irradiation, ... ...

Abstract	The transcriptional response to genotoxic stress involves gene expression arrest, followed by recovery of mRNA synthesis (RRS) after DNA repair. We find that the lack of the EXD2 nuclease impairs RRS and decreases cell survival after UV irradiation, without affecting DNA repair. Overexpression of wild-type, but not nuclease-dead EXD2, restores RRS and cell survival. We observe that UV irradiation triggers the relocation of EXD2 from mitochondria to the nucleus. There, EXD2 is recruited to chromatin where it transiently interacts with RNA Polymerase II (RNAPII) to promote the degradation of nascent mRNAs synthesized at the time of genotoxic attack. Reconstitution of the EXD2-RNAPII partnership on a transcribed DNA template in vitro shows that EXD2 primarily interacts with an elongation-blocked RNAPII and efficiently digests mRNA. Overall, our data highlight a crucial step in the transcriptional response to genotoxic attack in which EXD2 interacts with elongation-stalled RNAPII on chromatin to potentially degrade the associated nascent mRNA, allowing transcription restart after DNA repair.
MeSH term(s)	DNA Damage ; DNA Repair ; Chromatin/genetics ; Transcription, Genetic ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; RNA, Messenger/genetics
Chemical Substances	Chromatin ; RNA Polymerase II (EC 2.7.7.-) ; RNA, Messenger
Language	English
Publishing date	2023-01-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-35922-5
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Article ; Online: Easy Ruthenium-Catalysed Oxidation of Primary Amines to Nitriles under Oxidant-Free Conditions.

Achard, Thierry / Egly, Julien / Sigrist, Michel / Maisse-François, Aline / Bellemin-Laponnaz, Stéphane

Chemistry (Weinheim an der Bergstrasse, Germany)

2019 Volume 25, Issue 58, Page(s) 13271–13274

Abstract: A dehydrogenation of primary amine to give the corresponding nitrile under oxidant- and base-free conditions catalysed by simple [Ru(p-cym) ... ...

Abstract	A dehydrogenation of primary amine to give the corresponding nitrile under oxidant- and base-free conditions catalysed by simple [Ru(p-cym)Cl
Language	English
Publishing date	2019-09-24
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1478547-X
ISSN	1521-3765 ; 0947-6539
ISSN (online)	1521-3765
ISSN	0947-6539
DOI	10.1002/chem.201902557
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Article ; Online: RYR2 Channel Inhibition Is the Principal Mechanism of Flecainide Action in CPVT.

Kryshtal, Dmytro O / Blackwell, Daniel J / Egly, Christian L / Smith, Abigail N / Batiste, Suzanne M / Johnston, Jeffrey N / Laver, Derek R / Knollmann, Bjorn C

Circulation research

2020 Volume 128, Issue 3, Page(s) 321–331

Abstract: Rationale: The class Ic antiarrhythmic drug flecainide prevents ventricular tachyarrhythmia in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), a disease caused by hyperactive RyR2 (cardiac ryanodine receptor) mediated calcium ...

Abstract	Rationale: The class Ic antiarrhythmic drug flecainide prevents ventricular tachyarrhythmia in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), a disease caused by hyperactive RyR2 (cardiac ryanodine receptor) mediated calcium (Ca) release. Although flecainide inhibits single RyR2 channels in vitro, reports have claimed that RyR2 inhibition by flecainide is not relevant for its mechanism of antiarrhythmic action and concluded that sodium channel block alone is responsible for flecainide's efficacy in CPVT. Objective: To determine whether RyR2 block independently contributes to flecainide's efficacy for suppressing spontaneous sarcoplasmic reticulum Ca release and for preventing ventricular tachycardia in vivo. Methods and results: We synthesized N-methylated flecainide analogues (QX-flecainide and Conclusions: Flecainide remains an effective inhibitor of RyR2-mediated arrhythmogenic Ca release even when cardiac sodium channels are blocked. In mice with CPVT, sodium channel block alone did not prevent ventricular tachycardia. Hence, RyR2 channel inhibition likely constitutes the principal mechanism of antiarrhythmic action of flecainide in CPVT.
MeSH term(s)	Action Potentials ; Animals ; Anti-Arrhythmia Agents/pharmacology ; Calcium Channel Blockers/pharmacology ; Calcium Signaling ; Calsequestrin/genetics ; Calsequestrin/metabolism ; Disease Models, Animal ; Female ; Flecainide/pharmacology ; HEK293 Cells ; Heart Rate/drug effects ; Humans ; Male ; Mice, Knockout ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Phosphorylation ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism ; Sheep, Domestic ; Tachycardia, Ventricular/genetics ; Tachycardia, Ventricular/metabolism ; Tachycardia, Ventricular/physiopathology ; Tachycardia, Ventricular/prevention & control ; Voltage-Gated Sodium Channel Blockers/pharmacology ; Mice
Chemical Substances	Anti-Arrhythmia Agents ; Calcium Channel Blockers ; Calsequestrin ; Ryanodine Receptor Calcium Release Channel ; Voltage-Gated Sodium Channel Blockers ; casq2 protein, mouse ; ryanodine receptor 2. mouse ; Flecainide (K94FTS1806)
Language	English
Publishing date	2020-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.120.316819
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Article ; Online: Eicosanoid-Regulated Myeloid ENaC and Isolevuglandin Formation in Human Salt-Sensitive Hypertension.

Ertuglu, Lale A / Pitzer Mutchler, Ashley / Jamison, Sydney / Laffer, Cheryl L / Elijovich, Fernando / Saleem, Mohammad / Blackwell, Daniel J / Kryshtal, Dmytro O / Egly, Christian L / Sahinoz, Melis / Sheng, Quanhu / Wanjalla, Celestine N / Pakala, Suman / Yu, Justin / Gutierrez, Orlando M / Kleyman, Thomas R / Knollmann, Björn C / Ikizler, T Alp / Kirabo, Annet

Hypertension (Dallas, Tex. : 1979)

2023 Volume 81, Issue 3, Page(s) 516–529

Abstract: Background: The mechanisms by which salt increases blood pressure in people with salt sensitivity remain unclear. Our previous studies found that high sodium enters antigen-presenting cells (APCs) via the epithelial sodium channel and leads to the ... ...

Abstract	Background: The mechanisms by which salt increases blood pressure in people with salt sensitivity remain unclear. Our previous studies found that high sodium enters antigen-presenting cells (APCs) via the epithelial sodium channel and leads to the production of isolevuglandins and hypertension. In the current mechanistic clinical study, we hypothesized that epithelial sodium channel-dependent isolevuglandin-adduct formation in APCs is regulated by epoxyeicosatrienoic acids (EETs) and leads to salt-sensitive hypertension in humans. Methods: Salt sensitivity was assessed in 19 hypertensive subjects using an inpatient salt loading and depletion protocol. Isolevuglandin-adduct accumulation in APCs was analyzed using flow cytometry. Gene expression in APCs was analyzed using cellular indexing of transcriptomes and epitopes by sequencing analysis of blood mononuclear cells. Plasma and urine EETs were measured using liquid chromatography-mass spectrometry. Results: Baseline isolevuglandin Conclusions: Isolevuglandin formation in APCs responds to acute changes in salt intake in salt-sensitive but not salt-resistant people with hypertension, and this may be regulated by renal 14,15 EET. Baseline levels of isolevuglandin
MeSH term(s)	Humans ; Sodium Chloride, Dietary/metabolism ; Epithelial Sodium Channels/metabolism ; Hypertension ; Sodium Chloride/metabolism ; Eicosanoids ; Blood Pressure/physiology ; Lipids
Chemical Substances	Sodium Chloride, Dietary ; isolevuglandin ; Epithelial Sodium Channels ; Sodium Chloride (451W47IQ8X) ; Eicosanoids ; Lipids
Language	English
Publishing date	2023-09-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.123.21285
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Zs.A 1488: Show issues

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Article ; Online: DNA repair complex licenses acetylation of H2A.Z.1 by KAT2A during transcription.

Semer, M / Bidon, B / Larnicol, A / Caliskan, G / Catez, P / Egly, J M / Coin, F / Le May, N

Nature chemical biology

2019 Volume 15, Issue 10, Page(s) 992–1000

Abstract: Post-translational modifications of histone variant H2A.Z accompany gene transactivation, but its modifying enzymes still remain elusive. Here, we reveal a hitherto unknown function of human KAT2A (GCN5) as a histone acetyltransferase (HAT) of H2A.Z at ... ...

Abstract	Post-translational modifications of histone variant H2A.Z accompany gene transactivation, but its modifying enzymes still remain elusive. Here, we reveal a hitherto unknown function of human KAT2A (GCN5) as a histone acetyltransferase (HAT) of H2A.Z at the promoters of a set of transactivated genes. Expression of these genes also depends on the DNA repair complex XPC-RAD23-CEN2. We established that XPC-RAD23-CEN2 interacts both with H2A.Z and KAT2A to drive the recruitment of the HAT at promoters and license H2A.Z acetylation. KAT2A selectively acetylates H2A.Z.1 versus H2A.Z.2 in vitro on several well-defined lysines and we unveiled that alanine-14 in H2A.Z.2 is responsible for inhibiting the activity of KAT2A. Notably, the use of a nonacetylable H2A.Z.1 mutant shows that H2A.Z.1ac recruits the epigenetic reader BRD2 to promote RNA polymerase II recruitment. Our studies identify KAT2A as an H2A.Z.1 HAT in mammals and implicate XPC-RAD23-CEN2 as a transcriptional co-activator licensing the reshaping of the promoter epigenetic landscape.
MeSH term(s)	Acetylation ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line ; DNA Repair/physiology ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Fibroblasts ; Gene Expression Regulation ; Histone Acetyltransferases/metabolism ; Histones/metabolism ; Humans ; Lysine Acetyltransferase 5
Chemical Substances	CETN2 protein, human ; Calcium-Binding Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Histones ; histone H2A.F-Z ; RAD23A protein, human (156533-33-4) ; XPC protein, human (156533-34-5) ; Histone Acetyltransferases (EC 2.3.1.48) ; KAT2A protein, human (EC 2.3.1.48) ; KAT5 protein, human (EC 2.3.1.48) ; Lysine Acetyltransferase 5 (EC 2.3.1.48) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2019-09-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2202962-X
ISSN	1552-4469 ; 1552-4450
ISSN (online)	1552-4469
ISSN	1552-4450
DOI	10.1038/s41589-019-0354-y
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Zs.A 6251: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: The 14th Datta Lecture. TFIIH: from transcription to clinic.

Egly, J M

FEBS letters

2001 Volume 498, Issue 2-3, Page(s) 124–128

Abstract: Once a large proportion of the genes responsible for genetic disorders are identified in the post-genome era, the fundamental challenge is to establish a genotype/phenotype relationship. Our aim is to explain how mutations in a given gene affect its ... ...

Abstract	Once a large proportion of the genes responsible for genetic disorders are identified in the post-genome era, the fundamental challenge is to establish a genotype/phenotype relationship. Our aim is to explain how mutations in a given gene affect its enzymatic function and, in consequence, disturb the life of the cell. Genome integrity is continuously threatened by the occurrence of DNA damage arising from cellular exposure to irradiation and genotoxic chemicals. This mutagenic or potentially lethal DNA damage induces various cellular responses including cell cycle arrest, transcription alteration and processing by DNA repair mechanisms, such as the nucleotide excision repair (NER) pathway. Disruption of NER in response to genotoxic injuries results in autosomal recessive hereditary diseases such as Xeroderma pigmentosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD). One of the most immediate consequences of the induction of strand-distorting lesions is the arrest of transcription in which TFIIH plays a role in addition to its role in DNA repair. The observations made by clinicians close to XP, TTD and CS patients, suggested that transcription defects responsible for brittle hair and nails for TTD, or developmental abnormalities for CS, resulted from TFIIH mutations. Here a story will be related which could be called 'a multi-faceted factor named TFIIH'. As biochemists, we have characterized each component of TFIIH, three of which are XPB and XPD helicases and cdk7, a cyclin-dependent kinase. With the help of structural biologists, we have characterized most of the specific three-dimensional structures of TFIIH subunits and obtained its electron microscopy image. Together these approaches help us to propose a number of structure-function relationships for TFIIH. Through transfection and microinjection assays, cell biology allows us to determine the role of TFIIH in transcription and NER. We are thus in a position to explain, at least in part, transcription initiation mechanisms and their coupling to DNA repair. We now know how the XPB helicase opens the promoter region for RNA synthesis and that one of the roles of XPD helicase is to anchor the cdk7 kinase to the core-TFIIH. In XP and CS associated patients, we have demonstrated that some XPD mutations prevent an optimal phosphorylation of nuclear receptors by cdk7 with, as a consequence, a drop in the expression of genes sensitive to hormone action. We have thus shown that hormonal responses operate through TFIIH. Careful analysis of each TFIIH subunit also shows how the p44 Ring finger participates in certain promoter escape reactions. We are also able to localize the action of TFIIH in the sequence of events that lead to the elimination of DNA lesions. Thanks to the combination of these different approaches we are obtaining a much clearer picture of the TFIIH complex and its integration into the life of the cell.
MeSH term(s)	Cell Cycle/physiology ; DNA Repair/genetics ; DNA Repair/physiology ; Humans ; Models, Biological ; RNA, Messenger/metabolism ; Transcription Factor TFIIH ; Transcription Factors/chemistry ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription Factors, TFII ; Transcription, Genetic/genetics ; Transcription, Genetic/physiology ; Xeroderma Pigmentosum/genetics ; Xeroderma Pigmentosum/physiopathology
Chemical Substances	RNA, Messenger ; Transcription Factors ; Transcription Factors, TFII ; Transcription Factor TFIIH (148710-81-0)
Language	English
Publishing date	2001-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/s0014-5793(01)02458-9
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Article ; Online: Promoters of ASCL1- and NEUROD1-dependent genes are specific targets of lurbinectedin in SCLC cells.

Costanzo, Federico / Martínez Diez, Marta / Santamaría Nuñez, Gema / Díaz-Hernandéz, Juan Ignacio / Genes Robles, Carlos Mario / Díez Pérez, Javier / Compe, Emmanuel / Ricci, Romeo / Li, Tsai-Kun / Coin, Frédéric / Martínez Leal, Juan Fernando / Garrido-Martin, Eva Maria / Egly, Jean Marc

EMBO molecular medicine

2022 Volume 14, Issue 4, Page(s) e14841

Abstract: Small-Cell Lung Cancer (SCLC) is an aggressive neuroendocrine malignancy with a poor prognosis. Here, we focus on the neuroendocrine SCLC subtypes, SCLC-A and SCLC-N, whose transcription addiction was driven by ASCL1 and NEUROD1 transcription factors ... ...

Abstract	Small-Cell Lung Cancer (SCLC) is an aggressive neuroendocrine malignancy with a poor prognosis. Here, we focus on the neuroendocrine SCLC subtypes, SCLC-A and SCLC-N, whose transcription addiction was driven by ASCL1 and NEUROD1 transcription factors which target E-box motifs to activate up to 40% of total genes, the promoters of which are maintained in a steadily open chromatin environment according to ATAC and H3K27Ac signatures. This leverage is used by the marine agent lurbinectedin, which preferentially targets the CpG islands located downstream of the transcription start site, thus arresting elongating RNAPII and promoting its degradation. This abrogates the expression of ASCL1 and NEUROD1 and of their dependent genes, such as BCL2, INSM1, MYC, and AURKA, which are responsible for relevant SCLC tumorigenic properties such as inhibition of apoptosis and cell survival, as well as for a part of its neuroendocrine features. In summary, we show how the transcription addiction of these cells becomes their Achilles's heel, and how this is effectively exploited by lurbinectedin as a novel SCLC therapeutic endeavor.
MeSH term(s)	Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Carbolines/pharmacology ; Cell Line, Tumor ; Heterocyclic Compounds, 4 or More Rings/pharmacology ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Promoter Regions, Genetic/drug effects ; Repressor Proteins/metabolism ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/metabolism
Chemical Substances	ASCL1 protein, human ; Basic Helix-Loop-Helix Transcription Factors ; Carbolines ; Heterocyclic Compounds, 4 or More Rings ; NEUROD1 protein, human ; PM 01183 ; Repressor Proteins ; INSM1 protein, human (147955-03-1)
Language	English
Publishing date	2022-03-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202114841
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Zs.A 6784: Show issues

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Article ; Online: CDK7 and MITF repress a transcription program involved in survival and drug tolerance in melanoma.

Berico, Pietro / Cigrang, Max / Davidson, Guillaume / Braun, Cathy / Sandoz, Jeremy / Legras, Stephanie / Vokshi, Bujamin Hektor / Slovic, Nevena / Peyresaubes, François / Gene Robles, Carlos Mario / Egly, Jean-Marc / Compe, Emmanuel / Davidson, Irwin / Coin, Frederic

EMBO reports

2021 Volume 22, Issue 9, Page(s) e51683

Abstract: Melanoma cell phenotype switching between differentiated melanocytic and undifferentiated mesenchymal-like states drives metastasis and drug resistance. CDK7 is the serine/threonine kinase of the basal transcription factor TFIIH. We show that ... ...

Abstract	Melanoma cell phenotype switching between differentiated melanocytic and undifferentiated mesenchymal-like states drives metastasis and drug resistance. CDK7 is the serine/threonine kinase of the basal transcription factor TFIIH. We show that dedifferentiation of melanocytic-type melanoma cells into mesenchymal-like cells and acquisition of tolerance to targeted therapies is achieved through chronic inhibition of CDK7. In addition to emergence of a mesenchymal-type signature, we identify a GATA6-dependent gene expression program comprising genes such as AMIGO2 or ABCG2 involved in melanoma survival or targeted drug tolerance, respectively. Mechanistically, we show that CDK7 drives expression of the melanocyte lineage transcription factor MITF that in turn binds to an intronic region of GATA6 to repress its expression in melanocytic-type cells. We show that GATA6 expression is activated in MITF-low melanoma cells of patient-derived xenografts. Taken together, our data show how the poorly characterized repressive function of MITF in melanoma participates in a molecular cascade regulating activation of a transcriptional program involved in survival and drug resistance in melanoma.
MeSH term(s)	Cell Line, Tumor ; Drug Tolerance ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism
Chemical Substances	MITF protein, human ; Microphthalmia-Associated Transcription Factor
Language	English
Publishing date	2021-07-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202051683
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: XPC is an RNA polymerase II cofactor recruiting ATAC to promoters by interacting with E2F1.

Bidon, B / Iltis, I / Semer, M / Nagy, Z / Larnicol, A / Cribier, A / Benkirane, M / Coin, F / Egly, J-M / Le May, N

Nature communications

2018 Volume 9, Issue 1, Page(s) 2610

Abstract: The DNA damage sensor XPC is involved in nucleotide excision repair. Here we show that in the absence of damage, XPC co-localizes with RNA polymerase II (Pol II) and active post-translational histone modifications marks on a subset of class II promoters ... ...

Abstract	The DNA damage sensor XPC is involved in nucleotide excision repair. Here we show that in the absence of damage, XPC co-localizes with RNA polymerase II (Pol II) and active post-translational histone modifications marks on a subset of class II promoters in human fibroblasts. XPC depletion triggers specific gene down-expression due to a drop in the deposition of histone H3K9 acetylation mark and pre-initiation complex formation. XPC interacts with the histone acetyltransferase KAT2A and specifically triggers the recruitment of the KAT2A-containing ATAC complex to the promoters of down-expressed genes. We show that a strong E2F1 signature characterizes the XPC/KAT2A-bound promoters and that XPC interacts with E2F1 and promotes its binding to its DNA element. Our data reveal that the DNA repair factor XPC is also an RNA polymerase II cofactor recruiting the ATAC coactivator complex to promoters by interacting with the DNA binding transcription factor E2F1.
MeSH term(s)	Acetylation ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; E2F1 Transcription Factor/genetics ; E2F1 Transcription Factor/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; HeLa Cells ; Histone Acetyltransferases/genetics ; Histone Acetyltransferases/metabolism ; Histones/genetics ; Histones/metabolism ; Humans ; Primary Cell Culture ; Promoter Regions, Genetic ; Protein Binding ; Protein Processing, Post-Translational ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; Xeroderma Pigmentosum/genetics ; Xeroderma Pigmentosum/metabolism ; Xeroderma Pigmentosum/pathology
Chemical Substances	DNA-Binding Proteins ; E2F1 Transcription Factor ; E2F1 protein, human ; Histones ; XPC protein, human (156533-34-5) ; Histone Acetyltransferases (EC 2.3.1.48) ; KAT2A protein, human (EC 2.3.1.48) ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2018-07-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-05010-0
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Article: Cockayne syndrome, between transcription and DNA repair defects.

Dubaele, S / Egly, J M

Journal of the European Academy of Dermatology and Venereology : JEADV

2003 Volume 16, Issue 3, Page(s) 220–226

MeSH term(s)	Cockayne Syndrome/genetics ; DNA Repair ; Humans ; Mutation ; Transcription Factors/metabolism ; Transcription, Genetic
Chemical Substances	Transcription Factors
Language	English
Publishing date	2003-03-06
Publishing country	England
Document type	Comment ; Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	1128828-0
ISSN	1468-3083 ; 0926-9959
ISSN (online)	1468-3083
ISSN	0926-9959
DOI	10.1046/j.1468-3083.2002.00453.x
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