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Article: Genome-wide analysis of transcription-coupled repair reveals novel transcription events in

Kose, Cansu / Lindsey-Boltz, Laura A / Sancar, Aziz / Jiang, Yuchao

bioRxiv : the preprint server for biology

2024

Abstract: Bulky DNA adducts such as those induced by ultraviolet light are removed from the genomes of multicellular organisms by nucleotide excision repair, which occurs through two distinct mechanisms, global repair, requiring the DNA damage recognition-factor ... ...

Abstract	Bulky DNA adducts such as those induced by ultraviolet light are removed from the genomes of multicellular organisms by nucleotide excision repair, which occurs through two distinct mechanisms, global repair, requiring the DNA damage recognition-factor XPC (xeroderma pigmentosum complementation group C), and transcription-coupled repair (TCR), which does not. TCR is initiated when elongating RNA polymerase II encounters DNA damage, and thus analysis of genome-wide excision repair in XPC-mutants only repairing by TCR provides a unique opportunity to map transcription events missed by methods dependent on capturing RNA transcription products and thus limited by their stability and/or modifications (5'-capping or 3'-polyadenylation). Here, we have performed the eXcision Repair-sequencing (XR-seq) in the model organism
Language	English
Publishing date	2024-03-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.12.562083
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Article ; Online: Molecular Mechanisms of Transcription-Coupled Repair.

Selby, Christopher P / Lindsey-Boltz, Laura A / Li, Wentao / Sancar, Aziz

Annual review of biochemistry

2023 Volume 92, Page(s) 115–144

Abstract: Transcription-coupled repair (TCR), discovered as preferential nucleotide excision repair of UV-induced cyclobutane pyrimidine dimers located in transcribed mammalian genes compared to those in nontranscribed regions of the genome, is defined as faster ... ...

Abstract	Transcription-coupled repair (TCR), discovered as preferential nucleotide excision repair of UV-induced cyclobutane pyrimidine dimers located in transcribed mammalian genes compared to those in nontranscribed regions of the genome, is defined as faster repair of the transcribed strand versus the nontranscribed strand in transcribed genes. The phenomenon, universal in model organisms including
MeSH term(s)	Humans ; Animals ; Mice ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Transcription, Genetic ; Cryoelectron Microscopy ; DNA Repair ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/metabolism ; Mammals/genetics
Chemical Substances	Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-03-31
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	207924-0
ISSN	1545-4509 ; 0066-4154
ISSN (online)	1545-4509
ISSN	0066-4154
DOI	10.1146/annurev-biochem-041522-034232
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Article: The Transcription-Repair Coupling Factor Mfd Prevents and Promotes Mutagenesis in a Context-Dependent Manner.

Lindsey-Boltz, Laura A / Sancar, Aziz

Frontiers in molecular biosciences

2021 Volume 8, Page(s) 668290

Abstract: ... ...

Abstract	The
Language	English
Publishing date	2021-05-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2021.668290
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Article ; Online: Analysis of mammalian circadian clock protein complexes over a circadian cycle.

Cao, Xuemei / Wang, Li / Selby, Christopher P / Lindsey-Boltz, Laura A / Sancar, Aziz

The Journal of biological chemistry

2023 Volume 299, Issue 3, Page(s) 102929

Abstract: Circadian rhythmicity is maintained by a set of core clock proteins including the transcriptional activators CLOCK and BMAL1, and the repressors PER (PER1, PER2, and PER3), CRY (CRY1 and CRY2), and CK1δ. In mice, peak expression of the repressors in the ... ...

Abstract	Circadian rhythmicity is maintained by a set of core clock proteins including the transcriptional activators CLOCK and BMAL1, and the repressors PER (PER1, PER2, and PER3), CRY (CRY1 and CRY2), and CK1δ. In mice, peak expression of the repressors in the early morning reduces CLOCK- and BMAL1-mediated transcription/translation of the repressors themselves. By late afternoon the repressors are largely depleted by degradation, and thereby their expression is reactivated in a cycle repeated every 24 h. Studies have characterized a variety of possible protein interactions and complexes associated with the function of this transcription-translation feedback loop. Our prior investigation suggested there were two circadian complexes responsible for rhythmicity, one containing CLOCK-BMAL and the other containing PER2, CRY1, and CK1δ. In this investigation, we acquired data from glycerol gradient centrifugation and gel filtration chromatography of mouse liver extracts obtained at different circadian times to further characterize circadian complexes. In addition, anti-PER2 and anti-CRY1 immunoprecipitates obtained from the same extracts were analyzed by liquid chromatography-tandem mass spectrometry to identify components of circadian complexes. Our results confirm the presence of discrete CLOCK-BMAL1 and PER-CRY-CK1δ complexes at the different circadian time points, provide masses of 255 and 707 kDa, respectively, for these complexes, and indicate that these complexes are composed principally of the core circadian proteins.
MeSH term(s)	Animals ; Mice ; ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Circadian Clocks/genetics ; Circadian Rhythm/genetics ; CLOCK Proteins/genetics ; CLOCK Proteins/metabolism ; Liver/metabolism ; Multiprotein Complexes/metabolism ; Gene Expression Profiling ; Feedback, Physiological
Chemical Substances	ARNTL Transcription Factors ; CLOCK Proteins (EC 2.3.1.48) ; Multiprotein Complexes
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.102929
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Article ; Online: Bringing It All Together: Coupling Excision Repair to the DNA Damage Checkpoint.

Lindsey-Boltz, Laura A

Photochemistry and photobiology

2016 Volume 93, Issue 1, Page(s) 238–244

Abstract: Nucleotide excision repair and the ATR-mediated DNA damage checkpoint are two critical cellular responses to the genotoxic stress induced by ultraviolet (UV) light and are important for cancer prevention. In vivo genetic data indicate that these global ... ...

Abstract	Nucleotide excision repair and the ATR-mediated DNA damage checkpoint are two critical cellular responses to the genotoxic stress induced by ultraviolet (UV) light and are important for cancer prevention. In vivo genetic data indicate that these global responses are coupled. Aziz Sancar et al. developed an in vitro coupled repair-checkpoint system to analyze the basic steps of these DNA damage stress responses in a biochemically defined system. The minimum set of factors essential for repair-checkpoint coupling include damaged DNA, the excision repair factors (XPA, XPC, XPF-ERCC1, XPG, TFIIH, RPA), the 5'-3' exonuclease EXO1, and the damage checkpoint proteins ATR-ATRIP and TopBP1. This coupled repair-checkpoint system was used to demonstrate that the ~30 nucleotide single-stranded DNA (ssDNA) gap generated by nucleotide excision repair is enlarged by EXO1 and bound by RPA to generate the signal that activates ATR.
MeSH term(s)	DNA Damage ; DNA Repair ; DNA, Single-Stranded/radiation effects ; DNA-Binding Proteins/metabolism ; Humans ; Ultraviolet Rays
Chemical Substances	DNA, Single-Stranded ; DNA-Binding Proteins
Language	English
Publishing date	2016-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	123540-0
ISSN	1751-1097 ; 0031-8655
ISSN (online)	1751-1097
ISSN	0031-8655
DOI	10.1111/php.12667
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Article ; Online: Cross-species investigation into the requirement of XPA for nucleotide excision repair.

Kose, Cansu / Cao, Xuemei / Dewey, Evan B / Malkoç, Mustafa / Adebali, Ogün / Sekelsky, Jeff / Lindsey-Boltz, Laura A / Sancar, Aziz

Nucleic acids research

2023 Volume 52, Issue 2, Page(s) 677–689

Abstract: After reconstitution of nucleotide excision repair (excision repair) with XPA, RPA, XPC, TFIIH, XPF-ERCC1 and XPG, it was concluded that these six factors are the minimal essential components of the excision repair machinery. All six factors are highly ... ...

Abstract	After reconstitution of nucleotide excision repair (excision repair) with XPA, RPA, XPC, TFIIH, XPF-ERCC1 and XPG, it was concluded that these six factors are the minimal essential components of the excision repair machinery. All six factors are highly conserved across diverse organisms spanning yeast to humans, yet no identifiable homolog of the XPA gene exists in many eukaryotes including green plants. Nevertheless, excision repair is reported to be robust in the XPA-lacking organism, Arabidopsis thaliana, which raises a fundamental question of whether excision repair could occur without XPA in other organisms. Here, we performed a phylogenetic analysis of XPA across all species with annotated genomes and then quantitatively measured excision repair in the absence of XPA using the sensitive whole-genome qXR-Seq method in human cell lines and two model organisms, Caenorhabditis elegans and Drosophila melanogaster. We find that although the absence of XPA results in inefficient excision repair and UV-sensitivity in humans, flies, and worms, excision repair of UV-induced DNA damage is detectable over background. These studies have yielded a significant discovery regarding the evolution of XPA protein and its mechanistic role in nucleotide excision repair.
MeSH term(s)	Animals ; Humans ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Drosophila melanogaster/metabolism ; Excision Repair ; Nucleotides/metabolism ; Phylogeny ; Xeroderma Pigmentosum Group A Protein/genetics ; Xeroderma Pigmentosum Group A Protein/metabolism ; Plants/metabolism ; Evolution, Molecular
Chemical Substances	DNA-Binding Proteins ; Nucleotides ; Xeroderma Pigmentosum Group A Protein ; XPA protein, human
Language	English
Publishing date	2023-12-05
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad1104
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Article ; Online: Nucleotide excision repair in Human cell lines lacking both XPC and CSB proteins.

Lindsey-Boltz, Laura A / Yang, Yanyan / Kose, Cansu / Deger, Nazli / Eynullazada, Khagani / Kawara, Hiroaki / Sancar, Aziz

Nucleic acids research

2023 Volume 51, Issue 12, Page(s) 6238–6245

Abstract: Nucleotide excision repair removes UV-induced DNA damage through two distinct sub-pathways, global repair and transcription-coupled repair (TCR). Numerous studies have shown that in human and other mammalian cell lines that the XPC protein is required ... ...

Abstract	Nucleotide excision repair removes UV-induced DNA damage through two distinct sub-pathways, global repair and transcription-coupled repair (TCR). Numerous studies have shown that in human and other mammalian cell lines that the XPC protein is required for repair of DNA damage from nontranscribed DNA via global repair and the CSB protein is required for repair of lesions from transcribed DNA via TCR. Therefore, it is generally assumed that abrogating both sub-pathways with an XPC-/-/CSB-/- double mutant would eliminate all nucleotide excision repair. Here we describe the construction of three different XPC-/-/CSB-/- human cell lines that, contrary to expectations, perform TCR. The XPC and CSB genes were mutated in cell lines derived from Xeroderma Pigmentosum patients as well as from normal human fibroblasts and repair was analyzed at the whole genome level using the very sensitive XR-seq method. As predicted, XPC-/- cells exhibited only TCR and CSB-/- cells exhibited only global repair. However, the XPC-/-/CSB-/- double mutant cell lines, although having greatly reduced repair, exhibited TCR. Mutating the CSA gene to generate a triple mutant XPC-/-/CSB-/-/CSA-/- cell line eliminated all residual TCR activity. Together, these findings provide new insights into the mechanistic features of mammalian nucleotide excision repair.
MeSH term(s)	Animals ; Humans ; DNA Repair/genetics ; DNA Damage ; Xeroderma Pigmentosum/genetics ; Cell Line ; Receptors, Antigen, T-Cell/genetics ; Ultraviolet Rays ; Mammals/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism
Chemical Substances	Receptors, Antigen, T-Cell ; XPC protein, human (156533-34-5) ; DNA-Binding Proteins
Language	English
Publishing date	2023-04-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad334
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Article ; Online: Mycobacteria excise DNA damage in 12- or 13-nucleotide-long oligomers by prokaryotic-type dual incisions and performs transcription-coupled repair.

Selby, Christopher P / Lindsey-Boltz, Laura A / Yang, Yanyan / Sancar, Aziz

The Journal of biological chemistry

2020 Volume 295, Issue 50, Page(s) 17374–17380

Abstract: In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concerted dual incisions bracketing the lesion, followed by gap filling and ligation. So far, two dual-incision patterns have ...

Abstract	In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concerted dual incisions bracketing the lesion, followed by gap filling and ligation. So far, two dual-incision patterns have been discovered: the prokaryotic type, which removes the damage in 11-13-nucleotide-long oligomers, and the eukaryotic type, which removes the damage in 24-32-nucleotide-long oligomers. However, a recent study reported that the UvrC protein of
MeSH term(s)	Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; DNA Damage ; DNA Repair ; Endodeoxyribonucleases/genetics ; Endodeoxyribonucleases/metabolism ; Escherichia coli Proteins/genetics ; Escherichia coli Proteins/metabolism ; Mycobacterium smegmatis/genetics ; Mycobacterium smegmatis/metabolism ; Oligonucleotides/genetics ; Oligonucleotides/metabolism ; Transcription, Genetic
Chemical Substances	Bacterial Proteins ; Escherichia coli Proteins ; Oligonucleotides ; Endodeoxyribonucleases (EC 3.1.-) ; endodeoxyribonuclease uvrABC (EC 3.1.25.-)
Language	English
Publishing date	2020-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.AC120.016325
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Article ; Online: Super hotspots and super coldspots in the repair of UV-induced DNA damage in the human genome.

Jiang, Yuchao / Li, Wentao / Lindsey-Boltz, Laura A / Yang, Yuchen / Li, Yun / Sancar, Aziz

The Journal of biological chemistry

2021 Volume 296, Page(s) 100581

Abstract: The formation of UV-induced DNA damage and its repair are influenced by many factors that modulate lesion formation and the accessibility of repair machinery. However, it remains unknown which genomic sites are prioritized for immediate repair after UV ... ...

Abstract	The formation of UV-induced DNA damage and its repair are influenced by many factors that modulate lesion formation and the accessibility of repair machinery. However, it remains unknown which genomic sites are prioritized for immediate repair after UV damage induction, and whether these prioritized sites overlap with hotspots of UV damage. We identified the super hotspots subject to the earliest repair for (6-4) pyrimidine-pyrimidone photoproduct by using the eXcision Repair-sequencing (XR-seq) method. We further identified super coldspots for (6-4) pyrimidine-pyrimidone photoproduct repair and super hotspots for cyclobutane pyrimidine dimer repair by analyzing available XR-seq time-course data. By integrating datasets of XR-seq, Damage-seq, adductSeq, and cyclobutane pyrimidine dimer-seq, we show that neither repair super hotspots nor repair super coldspots overlap hotspots of UV damage. Furthermore, we demonstrate that repair super hotspots are significantly enriched in frequently interacting regions and superenhancers. Finally, we report our discovery of an enrichment of cytosine in repair super hotspots and super coldspots. These findings suggest that local DNA features together with large-scale chromatin features contribute to the orders of magnitude variability in the rates of UV damage repair.
MeSH term(s)	DNA Damage ; DNA Repair/genetics ; Genome, Human/genetics ; Genome, Human/radiation effects ; Humans ; Pyrimidine Dimers/metabolism ; Ultraviolet Rays/adverse effects
Chemical Substances	Pyrimidine Dimers ; pyrimidine-pyrimidone dimer
Language	English
Publishing date	2021-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.100581
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Article ; Online: Effects of replication domains on genome-wide UV-induced DNA damage and repair.

Huang, Yanchao / Azgari, Cem / Yin, Mengdie / Chiou, Yi-Ying / Lindsey-Boltz, Laura A / Sancar, Aziz / Hu, Jinchuan / Adebali, Ogun

PLoS genetics

2022 Volume 18, Issue 9, Page(s) e1010426

Abstract: Nucleotide excision repair is the primary repair mechanism that removes UV-induced DNA lesions in placentals. Unrepaired UV-induced lesions could result in mutations during DNA replication. Although the mutagenesis of pyrimidine dimers is reasonably well ...

Abstract	Nucleotide excision repair is the primary repair mechanism that removes UV-induced DNA lesions in placentals. Unrepaired UV-induced lesions could result in mutations during DNA replication. Although the mutagenesis of pyrimidine dimers is reasonably well understood, the direct effects of replication fork progression on nucleotide excision repair are yet to be clarified. Here, we applied Damage-seq and XR-seq techniques and generated replication maps in synchronized UV-treated HeLa cells. The results suggest that ongoing replication stimulates local repair in both early and late replication domains. Additionally, it was revealed that lesions on lagging strand templates are repaired slower in late replication domains, which is probably due to the imbalanced sequence context. Asymmetric relative repair is in line with the strand bias of melanoma mutations, suggesting a role of exogenous damage, repair, and replication in mutational strand asymmetry.
MeSH term(s)	DNA/genetics ; DNA Damage/genetics ; DNA Repair/genetics ; DNA Replication/genetics ; HeLa Cells ; Humans ; Pyrimidine Dimers/genetics ; Ultraviolet Rays/adverse effects
Chemical Substances	Pyrimidine Dimers ; DNA (9007-49-2)
Language	English
Publishing date	2022-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010426
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