Relevant bibliographies by topics / Transcription and repair

Academic literature on the topic 'Transcription and repair'

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Published: 11 March 2023

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Journal articles on the topic "Transcription and repair"

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Svejstrup, Jesper Q. "Transcription-coupled DNA repair without the transcription-coupling repair factor." Trends in Biochemical Sciences 26, no. 3 (March 2001): 151. http://dx.doi.org/10.1016/s0968-0004(00)01766-7.

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Osley, Mary Ann. "Transcription RINGs in repair." Nature Cell Biology 7, no. 6 (June 2005): 553–55. http://dx.doi.org/10.1038/ncb0605-553.

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Sweder, K., and P. Hanawalt. "Transcription-coupled DNA repair." Science 262, no. 5132 (October 15, 1993): 439–40. http://dx.doi.org/10.1126/science.8211165.

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Svejstrup, Jesper Q. "Transcription Repair Coupling Factor." Molecular Cell 9, no. 6 (June 2002): 1151–52. http://dx.doi.org/10.1016/s1097-2765(02)00553-1.

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Bhatia, Prakash K., Zhigang Wang, and Errol C. Friedberg. "DNA repair and transcription." Current Opinion in Genetics & Development 6, no. 2 (April 1996): 146–50. http://dx.doi.org/10.1016/s0959-437x(96)80043-8.

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Drapkin, Ronny, Aziz Sancar, and Danny Reinberg. "Where transcription meets repair." Cell 77, no. 1 (April 1994): 9–12. http://dx.doi.org/10.1016/0092-8674(94)90228-3.

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Schaeffer, L., C. P. Selby, and A. Sancar. "Connecting repair and transcription." Trends in Cell Biology 3, no. 7 (July 1993): 229. http://dx.doi.org/10.1016/0962-8924(93)90121-g.

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Deger, Nazli, Yanyan Yang, Laura A. Lindsey-Boltz, Aziz Sancar, and Christopher P. Selby. "Drosophila, which lacks canonical transcription-coupled repair proteins, performs transcription-coupled repair." Journal of Biological Chemistry 294, no. 48 (October 17, 2019): 18092–98. http://dx.doi.org/10.1074/jbc.ac119.011448.

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Verhage, R. A., A. J. van Gool, N. de Groot, J. H. Hoeijmakers, P. van de Putte, and J. Brouwer. "Double mutants of Saccharomyces cerevisiae with alterations in global genome and transcription-coupled repair." Molecular and Cellular Biology 16, no. 2 (February 1996): 496–502. http://dx.doi.org/10.1128/mcb.16.2.496.

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The nucleotide excision repair (NER) pathway is thought to consist of two subpathways: transcription-coupled repair, limited to the transcribed strand of active genes, and global genome repair for nontranscribed DNA strands. Recently we cloned the RAD26 gene, the Saccharomyces cerevisiae homolog of human CSB/ERCC6, a gene involved in transcription-coupled repair and the disorder Cockayne syndrome. This paper describes the analysis of yeast double mutants selectively affected in each NER subpathway. Although rad26 disruption mutants are defective in transcription-coupled repair, they are not UV sensitive. However, double mutants of RAD26 with the global genome repair determinants RAD7 and RAD16 appeared more UV sensitive than the single rad7 or rad16 mutants but not as sensitive as completely NER-deficient mutants. These findings unmask a role of RAD26 and transcription-coupled repair in UV survival, indicate that transcription-coupled repair and global genome repair are partially overlapping, and provide evidence for a residual NER modality in the double mutants. Analysis of dimer removal from the active RPB2 gene in the rad7/16 rad26 double mutants revealed (i) a contribution of the global genome repair factors Rad7p and Rad16p to repair of the transcribed strand, confirming the partial overlap between both NER subpathways, and (ii) residual repair specifically of the transcribed strand. To investigate the transcription dependence of this repair activity, strand-specific repair of the inducible GAL7 gene was investigated. The template strand of this gene was repaired only under induced conditions, pointing to a role for transcription in the residual repair in the double mutants and suggesting that transcription-coupled repair can to some extent operate independently from Rad26p. Our findings also indicate locus heterogeneity for the dependence of transcription-coupled repair on RAD26.
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Nouspikel, Thierry P., Nevila Hyka-Nouspikel, and Philip C. Hanawalt. "Transcription Domain-Associated Repair in Human Cells." Molecular and Cellular Biology 26, no. 23 (October 2, 2006): 8722–30. http://dx.doi.org/10.1128/mcb.01263-06.

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ABSTRACT Nucleotide excision repair (NER), which is arguably the most versatile DNA repair system, is strongly attenuated in human cells of the monocytic lineage when they differentiate into macrophages. Within active genes, however, both DNA strands continue to be proficiently repaired. The proficient repair of the nontranscribed strand cannot be explained by the dedicated subpathway of transcription-coupled repair (TCR), which is targeted to the transcribed strand in expressed genes. We now report that the previously termed differentiation-associated repair (DAR) depends upon transcription, but not simply upon RNA polymerase II (RNAPII) encountering a lesion: proficient repair of both DNA strands can occur in a part of a gene that the polymerase never reaches, and even if the translocation of RNAPII is blocked with transcription inhibitors. This suggests that DAR may be a subset of global NER, restricted to the subnuclear compartments or chromatin domains within which transcription occurs. Downregulation of selected NER genes with small interfering RNA has confirmed that DAR relies upon the same genes as global genome repair, rather than upon TCR-specific genes. Our findings support the general view that the genomic domains within which transcription is active are more accessible than the bulk of the genome to the recognition and repair of lesions through the global pathway and that TCR is superimposed upon that pathway of NER.
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Dissertations / Theses on the topic "Transcription and repair"

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Chambers, Anna Louise. "Transcription termination by a transcription-repair coupling factor." Thesis, University of Bristol, 2005. http://hdl.handle.net/1983/b95a2024-73ae-460d-89bf-3c064a780c78.

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Lainé, Jean-Philippe. "TFIIH and transcription coupled repair." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. http://www.theses.fr/2005STR13195.

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La bonne coordination des différents évènements qui participent au maintien de l’intégrité du génome et régulent son expression est un pré-requis pour la différentiation, la prolifération et le vie de la cellule. L’interconnection de ces divers phénomènes est illustrée par l’existence d’un complex aux multiples fonctions, le facteur TFIIH. Identifié à l’origine comme un facteur de transcription associé à l’ARN polymérase II, TFIIH participe également à la réparation de l’AND soumis à diverses attaques génotoxiques. Je me suis interessé à le contribution fonctionelle et structurale de la sous-unité p52, une des dix sous-unités de TFIIH, au sein du complex, ainsi qu’au lien reliant les mecanismes de transcription et de réparation, dans lesquelles TFIIH joue un role prépondérent. Premièrement, j’ai démontré que l’extrémité carboxyl terminale de p52 était importante pour stabiliser l’ancrage de XPB, une des sous-unité de TFIIH, au sein du complex. Cette interaction est primordiale pour permettre à XPB d’exercer son role dans l’ouverture de l’ADN au cours de l’initiation de la transcription. Puis, je me suis attaché aux mécanismes couplant la réparation à la transcription. J’ai montré qu’une ARN polymérase arretée sur une lésion est capable de recruter les différents facteurs de réparation et d’induire le relarguage d’un fragment d’ADN contenant le dommage
Accurate coordination of the various events that maintain the integrity of the genome and regulate its expression is a prerequisite for differentiation, proliferation and cell life. The interconnection of such cellular processes is highlighted by the multi-functional complex TFIIH. Originally identified as a RNA polymerase II transcription factor, TFIIH also participates in the DNA nucleotide excision repair (NER) reaction. Ve focused my work on the functional/structural contribution within the complex of p52, one of the ten subunits of TFIIH, the link between transcription and NER, and the role of TFIIH in both. I first demonstrated that the carboxy-terminal of p52 is important for stabilizing the anchoring of XPB, another subunit of TFIIH, within the complex. This interaction is important for the role of XPB in the DNA opening step during transcription initiation. Then I focused my attention on the mechanism linking transcription to NER. I was able to show that a stalled elongating RNA polymerase II is able to recruit the repair factors at the site of the lesion and promote the removal of the DNA patch containing the lesion
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Kim, Young-In Timothy. "Determinants of bacterial transcription-coupled repair." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521101.

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Trautinger, Brigitte W. "Interplay between DNA replication, transcription and repair." Thesis, University of Nottingham, 2002. http://eprints.nottingham.ac.uk/14281/.

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The Ruv ABC and RecBCD protein complexes together can collapse and repair arrested replication forks. With their help a fork structure can be re-established on which replication can be restarted. ruv and recB mutants are therefore quite sensitive to UV light. Their survival is greatly decreased in the absence of the signalling molecules (p)ppGpp and increased when excess (p)ppGpp is present. (p)ppGpp are the effector molecules of the stringent response, regulating adaptation to starvation and other stressful environmental changes. Absence of (p)ppGpp can be compensated for by mutations in RNA polymerase that are called stringent mutations. Some of those, called rpo *, also - like excess (p)ppGpp - increase the survival of UV irradiated ruv and recB cells. A model proposed by McGlynn and Lloyd (Cell, Vol. 101, pp35-45, March 31, 2000) suggests that this is achieved by modulation of RNA polymerase, which decreases the incidence of replication fork blocks. In this work twenty-seven rpo * mutants were isolated, sequenced and mapped on the 3D structure of Thermus aquatic us RNA polymerase. I have found mutants in the ~ and ~' subunits of RNA polymerase. They lie mostly on the inner surface of the protein, well placed to make contact with the DNA substrate or the RNA product. A large number of rifampicin resistant mutations among rpo* mutations is explained by an overlap between the so-called Rif pocket and the "rpo* pocket". rpo * mutations, like stringent mutations, lead to a decrease in cell size, suppress filamentation and increase viability. For in vitro studies I purified wild type and two mutant RNA polymerases with help of a his-tagged a subunit. The experiments confirmed that rpo* mutant RNA polymerases form less stable open complexes than wild type, just like previously investigated stringent RNA polymerases. In addition I have shown here that (p)ppGpp leads to the destabilisation of RNA polymerase complexes stalled by nucleotide starvation or UV-induced lesions, though there is as yet no indication that rpo * mutations act in the same way.
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Fan, Jun. "Single-molecule basis of transcription-coupled DNA repair." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC213.

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Les cellules vivantes sont constamment soumises à des agents, endogènes et exogènes, qui peuvent induire des lésions sur l'ADN. Ces agents peuvent menacer l'intégrité du génome, bloquer les processus de réplication, transcription et traduction, ou encore avoir des effets génotoxiques. Les organismes ont alors développé des systèmes de surveillance qui coordonnent la réparation de l'ADN et la progression du cycle cellulaire afin de lutter contre l'accumulation de dommages sur leur ADN. Les mécanismes de réparation de l'ADN, découverts à la fois dans les organismes procaryotes et eucaryotes, ont pour rôle le maintien de l'intégrité du matériel génétique. Ces mécanismes comprennent la réparation par excision de nucléotides (NER), la réparation par excision de bases (BER), la réparation des mésappariements (MMR) et la réparation des cassures double-brin (DSBR). La réparation couplée à la transcription (RCT) est une sous-voie de la réparation par excision de nucléotides qui permet une réparation rapide des lésions uniquement localisées sur le brin transcrit et affectant des gènes en cours de transcription. Elle se différencie de la sous-voie de la réparation du génome global (GGR) qui opère sur l'ensemble du génome sans distinction entre les brins transcrits et non transcrits. L'implication dans la RCT de l'ARN Polymérase (ARNP) et de la protéine Mfd (Mutation Frequency Decline), aussi connue sous le nom TRCF (Transcription Repair Coupling Factor), est ce qui permet la réparation préférentielle du brin transcrit. Le blocage de l'ARNP par une lésion sur le brin transcrit agit comme un senseur de dommage et déclenche la RCT. En effet, l'ARNP bloquée doit être déplacée afin de rendre la lésion accessible aux facteurs de réparation avals. Chez E. Coli c'est la translocase Mfd qui joue ce rôle : elle déplace l'ARNP bloquée et coordonne l'assemblage des facteurs UvrAB(C) au site de la lésion. Des études récentes ont montré que, après s'être lié à l'ARNP et l'avoir déplacée, Mfd reste sur l'ADN sous la forme d'un complexe de translocation stable impliquant l'ARNP même si cette dernière n'est plus directement liée à l'ADN. La technique de nanomanipulation par pince magnétique de molécules uniques d'ADN portant une lésion a été utilisée afin de comprendre comment UvrAB(C) sont recrutés via le complexe Mfd-ARNP. Cette technique a permis d'observer en temps réel jusqu'à l'incision par UvrC la RCT, qui comporte un grand nombre d'étapes et implique de nombreuses protéines. Il a été observé que le recrutement d'UvrA et d'UvrAB par le complexe Mfd-ARNP stoppe la translocation du complexe sur l'ADN et entraine la dissolution du complexe avec un passage de relais moléculaire dans une cinétique lente. La combinaison de la nanomanipulation de molécule-unique avec la fluorescence montre en outre que la dissolution du complexe entraine non seulement la perte de l'ARNP mais aussi celle de Mfd. Ce passage de témoin moléculaire permet d'avoir une réaction d'incision du brin endommagé par UvrC plus rapide par rapport à ce qui se produit lors de la réaction sur une molécule unique dans le cadre de la réparation globale du génome. Un modèle global intégrant les protéines impliquées dans la RCT et la GGR et donnant les caractéristiques cinétiques des différentes réactions se produisant en parallèle dans les deux sous-voies a été proposé
The DNA in living cells is constantly threatened by damages from both endogenous and exogenous agents, which can threaten genomic integrity, block processes of replication, transcription and translation and have also genotoxic effects. In response to the DNA damage challenge, organisms have evolved diverse surveillance mechanisms to coordinate DNA repair and cell-cycle progression. Multiple DNA repair mechanisms, discovered in both prokaryotic and eukaryotic organisms, bear the responsibility of maintaining genomic integrity; these mechanisms include nucleotide excision repair (NER), base excision repair (BER), mismatch repair (MMR) and double strand break repair (DSBR). Transcription-coupled DNA repair (TCR) is a specialized NER subpathway characterized by enhanced repair of the template strand of actively transcribed genes as compared to the classical global genome repair (GGR) subpathway of NER which does not distinguish between template and non-template strands. TCR achieves specialization via the involvement of RNA polymerase (RNAP) and the Mfd (Mutation Frequency Decline) protein, also known as TRCF (transcription repair coupling factor). TCR repair initiates when RNAP stalls at a DNA lesion on the transcribed strand and serves as the da mage sensor. The stalled RNAP must be displaced so as to make the lesion accessible to downstream repair components. E. Coli Mfd translocase participates in this process by displacing stalled RNAP from the lesion and then coordinating assembly of the UvrAB(C) components at th( damage site. Recent studies have shown that after binding to and displacing stalled RNAP, Mfd remains on the DNA in the form of a stable, translocating complex with evicted RNAP. So as to understand how UvrAB(C) are recruited via the Mfd-RNAP complex, magnetic trapping of individual, damaged DNA molecules was employed to observe-in real-time this multi¬component, multi-step reaction, up to and including the DNA incision reaction by UvrC. It was found that the recruitment of UvrA and UvrAB to the Mfd-RNAP complex halts the translocating complex and then causes dissolution of the complex in a molecular "hand-off" with slow kinetics Correlative single-molecule nanomanipulation and fluorescence further show that dissolution of the complex leads to loss of not only RNAP but also Mfd. Hand-off then allows for enhanced incision of damaged DNA by the UvrC component as compared to the equivalent single-moleculE GGR incision reaction. A global model integrating TCR and GGR components in repair was proposed, with the overall timescales for the parallel reactions provided
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Malik, Shivani. "REGULATORY MECHANISMS OF TRANSCRIPTION AND ASSOCIATED DNA REPAIR." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/626.

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Transcription is a crucial regulatory step in gene regulation modulated by several proteins. Any misregulation during transcription can lead to many diseases including cancer, neurodegenerative disorders and aging making it imperative to have a detailed mechanistic view of the process. Over the recent years, 26S proteasome has been implicated in transcriptional regulation through its proteolytic and non-proteolytic activities. While, the proteolytic role of proteasome in transcription has been extensively studied, its non-proteolytic function is poorly understood. Thus, one of my thesis aims had been to analyze the non-proteolytic role of proteasome in transcription. My results have revealed the non-proteolytic role of 26S proteasome in establishing a specific protein interaction network at the promoter for stimulated transcriptional initiation in vivo . In addition to its roles in transcription, 26S proteasome also plays an important role in the degradation of RNA polymerase II stalled at DNA lesion facilitating the rapid repair of transcriptionally active genes through a process of transcription coupled repair (TCR). My studies have addressed the key question of the fate of RNA polymerase II stalled at a lesion. My findings show that RNA polymerase II interacts with an elongation and TCR-specific factor, Rad26p. Upon encountering a lesion, RNA polymerase II stalls and unloads Rad26p on the site of DNA damage. Subsequently, the elongating RNA polymerase II is disassembled through the degradation of its largest subunit, Rpb1p. Further; our studies have also uncovered a novel role of Rad26p in chromatin disassembly, which facilitates transcriptional elongation and hence TCR. This work provides valuable insights into interplay of chromatin structure, transcriptional elongation and TCR. Finally, extending the regulatory knowledge of sense transcriptional initiation to antisense, my work has revealed the extensive participation of GTFs in the process. Collectively, results of above studies provide a comprehensive view of transcription and associated process of active genome repair.
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Cerutti, Elena. "Nucleotide Excision Repair at the crossroad with transcription." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1057.

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L’intégrité de l’ADN est continuellement remise en question par divers agents endogènes et exogènes (p. ex., la lumière ultraviolette, la fumée de cigarette, la pollution de l’environnement, les dommages oxydatifs, etc.) qui causent des lésions de l’ADN qui interfèrent avec les fonctions cellulaires correctes. Le mécanisme de réparation par excision de nucléotides (NER) supprime les adduits d’ADN déformantes l’hélice tels que les lésions induites par les UV et il existe dans deux sous voies distinctes selon l’endroit où les lésions de l’ADN sont situées dans le génome. L’une de ces sous voies est directement liée à la transcription de l’ADN (TCR) par l’ARN Polymérase 2 (ARNP2). Dans la première partie de ce travail, nous avons démontré qu’un mécanisme NER entièrement compétent est également nécessaire pour la réparation de l’ADN ribosomique (ADNr), transcrite par ARN Polymérase 1 (ARNP1) et représentant 60 % de la transcription cellulaire totale. De plus, nous avons identifié et clarifié le mécanisme de deux protéines responsables du repositionnement nucléolaire dépendant des UV de l’ARNP1 et de l’ADNr observé pendant la réparation. Dans la deuxième partie de ce travail, nous avons étudié la fonctionne moléculaire de la protéine XAB2 lors de la réparation NER et nous avons démontré son implication dans le processus TCR. De plus, nous avons également montré la présence de XAB2 dans un complexe d’épissage du pré-ARNm. Enfin, nous avons décrit l’impact de XAB2 sur la mobilité de l’ARNP2 lors des premières étapes de la réparation TCR, suggérant ainsi un rôle de XAB2 dans le processus de reconnaissance des lésions
The integrity of DNA is continuously challenged by a variety of endogenous and exogenous agents (e.g. ultraviolet light, cigarette smoke, environmental pollution, oxidative damage, etc.) that cause DNA lesions which interfere with proper cellular functions. Nucleotide Excision Repair (NER) mechanism removes helix-distorting DNA adducts such as UV-induced lesions and it exists in two distinct sub-pathways depending where DNA lesions are located within the genome. One of these sub pathways is directly linked to the DNA transcription by RNA Polymerase 2 (TCR). In the first part of this work, we demonstrated that a fully proficient NER mechanism is also necessary for repair of ribosomal DNA, transcribed by RNA polymerase 1 and accounting for the 60 % of the total cellular transcription. Furthermore, we identified and clarified the mechanism of two proteins responsible for the UV-dependent nucleolar repositioning of RNAP1 and rDNA observed during repair. In the second part of this work, we studied the molecular function of the XAB2 protein during NER repair and we demonstrated its involvement in the TCR process. In addition, we also shown the presence of XAB2 in a pre-mRNA splicing complex. Finally, we described the impact of XAB2 on RNAP2 mobility during the first steps of TCR repair, thus suggesting a role of XAB2 in the lesion recognition process
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MacKinnon-Roy, Christine. "The role of transcription elongation factor IIS in transcription-coupled nucleotide excision repair." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28454.

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Transcription-coupled nucleotide excision repair (TC-NER) removes bulky DNA lesions from the template strand at actively transcribed genes. The RNA polymerase II (RNAPII) holoenzyme complex forms a stable ternary complex at the site of DNA damage which may block access of DNA repair proteins to the site of DNA lesions. Therefore, there is considerable interest in understanding how repair is coupled to transcription. Based on elegant in vitro studies, it has been hypothesized that transcription elongation factor IIS (TFIIS), by catalyzing the reverse translocation of RNAPII, may allow access of DNA repair proteins to sites of DNA damage. Here, we tested this hypothesis by assessing TC-NER capacity in cells in which TFIIS expression has been reduced by RNA interference. Surprisingly, we found that decreased TFIIS levels did not affect the repair of transcription-blocking DNA lesions and did not affect the sensitivity of targeted cells to UV light or cisplatin. These results do not support a role for TFIIS in TC-NER. We conclude conservatively that TFIIS levels are not limiting for TC-NER.
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Abdullah, Mohamad Faiz Foong. "Transcription factors and mismatch repair proteins in meiotic recombination." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249637.

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Riedl, Thilo. "Tfiih : A factor between DNA repair and transcriptional activation." Université Louis Pasteur (Strasbourg) (1971-2008), 2003. http://www.theses.fr/2003STR13059.

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Books on the topic "Transcription and repair"

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Naegeli, Hanspeter. Mechanisms of DNA damage recognition in mammalian cells. Heidelberg: Springer-Verlag, 1997.

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Mechanisms of DNA damage recognition in mammalian cells. New York: Chapman & Hall, 1997.

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Hardy, Robert George. Alterations in cadherin and catenin expression in colonic neoplasia, injury and repair: Regulation of p-cadherin transcription in the colon. Birmingham: University of Birmingham, 2003.

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Fritz, Lucie. Differential DNA repair in mammalian ribosomal genes. 1994.

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Book chapters on the topic "Transcription and repair"

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Hanawalt, Philip C., and Graciela Spivak. "Transcription-Coupled DNA Repair." In Advances in DNA Damage and Repair, 169–79. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4865-2_14.

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Westwick, J. K., and D. A. Brenner. "Proto-oncogenes/ transcription factors." In Liver Growth and Repair, 297–310. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_12.

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Verhage, R. A., M. Tijsterman, P. van de Putte, and J. Brouwer. "Transcription-Coupled and Global Genome Nucleotide Excision Repair." In DNA Repair, 157–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-48770-5_8.

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van der Horst, Gijsbertus T. J., Harry van Steeg, Rob J. W. Berg, Kiyoji Tanaka, Errol Friedberg, Dirk Bootsma, and Jan H. J. Hoeijmakers. "Transcription-coupled Repair as a Biodefence Mechanism." In Biodefence Mechanisms Against Environmental Stress, 181–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72082-6_19.

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Pramanik, Suravi, Shrabasti Roychoudhury, and Kishor K. Bhakat. "Oxidized DNA Base Damage Repair and Transcription." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 1–17. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-4501-6_156-1.

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Pramanik, Suravi, Shrabasti Roychoudhury, and Kishor K. Bhakat. "Oxidized DNA Base Damage Repair and Transcription." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 1621–37. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-15-9411-3_156.

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Bohr, Vilhelm A., Adabalayam Balajee, Robert Brosh, Jan Nehlin, Amrita Machwe, Michele Evans, Grigory Dianov, and David Orren. "DNA Repair and Transcription in Premature Aging Syndromes." In Advances in DNA Damage and Repair, 27–34. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4865-2_3.

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Gaillard, Hélène, Ralf Erik Wellinger, and Andrés Aguilera. "Methods to Study Transcription-Coupled Repair in Chromatin." In Methods in Molecular Biology, 141–59. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-190-1_10.

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Shanbhag, Niraj M., and Roger A. Greenberg. "The Dynamics of DNA Damage Repair and Transcription." In Imaging Gene Expression, 227–35. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-526-2_16.

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Gaillard, Hélène, Ralf Erik Wellinger, and Andrés Aguilera. "Methods to Study Transcription-Coupled Repair in Chromatin." In Methods in Molecular Biology, 273–88. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2474-5_15.

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Conference papers on the topic "Transcription and repair"

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CHIBA, NATSUKO, and LEIZHEN WEI. "BRCA1 IS INVOLVED IN THE TRANSCRIPTION-COUPLED REPAIR OF UV LESIONS." In Proceedings of the Tohoku University Global Centre of Excellence Programme. IMPERIAL COLLEGE PRESS, 2012. http://dx.doi.org/10.1142/9781848169067_0061.

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Casey, J. L., L. Gu, D. Davis, G. Q. Cai, Q. Ding, and A. B. B. Carter. "Oxidant-Mediated Transcription and Post-Translational Modification of PGC-1α Is Required for Fibrotic Repair." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7874.

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Seoane, Marcos, Laia Pagerols Raluy, Karoline Kaufmann, Julia Strauss, Kevin Dierck, Jüergen Thomale, Johanna M. Brandner, et al. "Abstract 2950: Regulation of the functional interface between nucleotide excision repair and transcription by MITF modulates melanoma growth." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2950.

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Tanikawa, Michihiro. "Abstract 1430: The spliceosome U2 snRNP factors promote genome stability through distinct mechanisms; transcription of repair factors and R-loop processing." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1430.

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Moneo, Victoria, Patricia Martínez, Beatriz de Castro, Sofía Cascajares, Sonia Avila, Luis F. Garcia-Fernandez, and Carlos M. Galmarini. "Abstract A174: Comparison of the antitumor activity of Trabectedin, Lurbinectedin, Zalypsis and PM00128 in a panel of human cells deficient in transcription/NER repair factors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a174.

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Venkataraman, Anand, Andreas Stolcke, Wen Wang, Dimitra Vergyri, Jing Zheng, and Venkata Ramana Rao Gadde. "An efficient repair procedure for quick transcriptions." In Interspeech 2004. ISCA: ISCA, 2004. http://dx.doi.org/10.21437/interspeech.2004-193.

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"Transcriptional mutagenesis-based reporter system for the analysis of DNA repair." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-582.

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Zhou, Wenhui, Jian Ouyang, Kathryn Huber, and Charlotte Kuperwasser. "Abstract PR17: The transcriptional repressor Slug promotes the DNA damage response." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-pr17.

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Di, Li-Jun, Madeline M. Wong, Clay T. Wakano, Jung Byun, Lyuba Varticovski, Kent Hunter, Olufunmilayo I. Olopade, and Kevin Gardner. "Abstract B33: Transcriptional control of genome surveillance and repair by a metabolic switch." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b33.

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Shikata, Tetsuo, Toshihiko Shiraishi, Kumiko Tanaka, Shin Morishita, and Ryohei Takeuchi. "Effects of Amplitude and Frequency of Vibration Stimulation on Cultured Osteoblasts." In ASME 2007 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/detc2007-34949.

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Mechanical stimulation to bones affects osteogenesis such as decrease of bone mass of astronauts under zero gravity, walking rehabilitation to bone fracture and fracture repair with ultrasound devices. Bone cells have been reported to sense and response to mechanical stimulation at cellular level morphologically and metabolically. In the view of mechanical vibrations, bone cells are deformed according to mechanical stimulation and their mechanical characteristics. Recently, it was reported that viscoelasticity of cells was measured using tensile and creep tests and that there was likely natural frequency and nonlinearity of cells in the sense of structural dynamics. It suggests that there is effective frequency and amplitude of mechanical stimulation on osteogenesis by bone cells. In this study, sinusoidal inertia force was applied to cultured osteoblasts, MC3T3-E1, and effects of frequency and acceleration amplitude of mechanical vibration on the cells were investigated in respect of cell proliferation, cell morphology, bone matrix generation and alkaline phosphatase (ALP) gene expression. After the cells were cultured in culture plates in a CO2 incubator for one day and adhered on the cultured plane, vibrating groups of the culture plates were set on an aluminum plate attached to a exciter and cultured under sinusoidal excitation in another incubator separated from non-vibrating groups of the culture plates. Acceleration amplitude and frequency were set to several kinds of conditions. The time evolution of cell density was obtained by counting the number of cells with a hemocytometer. The cell morphology was observed with a phase contrast microscope. Calcium salts generated by the cells were observed by being stained with alizarin red S solution and their images were captured with a CCD camera. The vibrating groups for the cell proliferation and the calcium salts staining were sinusoidally excited for 24 hours a day during 28-day cultivation. Gene expression of ALP was measured by a real-time RT-PCR method. After the vibrating groups for the PCR were excited for 6 hours, the total RNAs were extracted. After reverse transcription, real-time RT-PCR was performed. Gene expression for ALP and a housekeeping gene were determined simultaneously for each sample. Gene levels in each sample were normalized to the measured housekeeping gene levels. As a result, it is shown that saturate cell density becomes high and bone matrix generation is promoted by applying mechanical vibration and that there may be some peaks to frequency and a certain threshold value to acceleration amplitude of mechanical vibration for saturation cell density and bone matrix generation.
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Reports on the topic "Transcription and repair"

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Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada400021.

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Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada417977.

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Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada391167.

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Wright, Adam, Marija Milacic, Karen Rothfels, Joel Weiser, Quang Trinh, Bijay Jassal, Robin Haw, and Lincoln Stein. Evaluating the Predictive Accuracy of Reactome's Curated Biological Pathways. Reactome, November 2022. http://dx.doi.org/10.3180/poster/20221109wright.

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Reactome is a database of human biological pathways manually curated from the primary literature and peer-reviewed by experts. To evaluate the utility of Reactome pathways for predicting functional consequences of genetic perturbations, we compared predictions of perturbation effects based on Reactome pathways against published empirical observations. Ten cancer-relevant Reactome pathways, representing diverse biological processes such as signal transduction, cell division, DNA repair, and transcriptional regulation, were selected for testing. For each pathway, root input nodes and key pathway outputs were defined. We then used pathway-diagram-derived logic graphs to predict, either by inspection by biocurators or using a novel algorithm MP-BioPath, the effects of bidirectional perturbations (upregulation/activation or downregulation/inhibition) of single root inputs on the status of key outputs. These predictions were then compared to published empirical tests.
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Grafi, Gideon, and Brian Larkins. Endoreduplication in Maize Endosperm: An Approach for Increasing Crop Productivity. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575285.bard.

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The focus of this research project is to investigate the role of endoreduplication in maize endosperm development and the extent to which this process contributes to high levels of starch and storage protein synthesis. Although endoreduplication has been widely observed in many cells and tissues, especially those with high levels of metabolic activity, the molecular mechanisms through which the cell cycle is altered to produce consecutive cycles of S-phase without an intervening M-phase are unknown. Our previous research has shown that changes in the expression of several cell cycle regulatory genes coincide with the onset of endoreduplication. During this process, there is a sharp reduction in the activity of the mitotic cyclin-dependent kinase (CDK) and activation of the S-phase CDK. It appears the M-phase CDK is stable, but its activity is blocked by a proteinaceous inhibitor. Coincidentally, the S-phase checkpoint protein, retinoblastoma (ZmRb), becomes phosphorylated, presumably releasing an E2F-type transcriptional regulator which promotes the expression of genes responsible for DNA synthesis. To investigate the role of these cell cycle proteins in endoreduplication, we have created transgenic maize plants that express various genes in an endosperm-specific manner using a storage protein (g-zein) promoter. During the first year of the grant, we constructed point mutations of the maize M-phase kinase, p34cdc2. One alteration replaced aspartic acid at position 146 with asparagine (p3630-CdcD146N), while another changed threonine 161 to alanine (p3630-CdcT161A). These mutations abolish the activity of the CDK. We hypothesized that expression of the mutant forms of p34cdc2 in endoreduplicating endosperm, compared to a control p34cdc2, would lead to extra cycles of DNA synthesis. We also fused the gene encoding the regulatory subunit of the M- phase kinase, cyclin B, under the g-zein promoter. Normally, cyclin B is expected to be destroyed prior to the onset of endoreduplication. By producing high levels of this protein in developing endosperm, we hypothesized that the M-phase would be extended, potentially reducing the number of cycles of endoreduplication. Finally, we genetically engineered the wheat dwarf virus RepA protein for endosperm-specific expression. RepA binds to the maize retinoblastoma protein and presumably releases E2F-like transcription factors that activate DNA synthesis. We anticipated that inactivation of ZmRb by RepA would lead to additional cycles of DNA synthesis.
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