Relevant bibliographies by topics / Ataxia Telangiectasia and Rad3-related (ATR)

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Ataxia Telangiectasia and Rad3-related (ATR)'

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Published: 9 March 2023

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Journal articles on the topic "Ataxia Telangiectasia and Rad3-related (ATR)"

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Friesner, Joanna D., Bo Liu, Kevin Culligan, and Anne B. Britt. "Ionizing Radiation–dependent γ-H2AX Focus Formation Requires Ataxia Telangiectasia Mutated and Ataxia Telangiectasia Mutated and Rad3-related." Molecular Biology of the Cell 16, no. 5 (May 2005): 2566–76. http://dx.doi.org/10.1091/mbc.e04-10-0890.

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The histone variant H2AX is rapidly phosphorylated at the sites of DNA double-strand breaks (DSBs). This phosphorylated H2AX (γ-H2AX) is involved in the retention of repair and signaling factor complexes at sites of DNA damage. The dependency of this phosphorylation on the various PI3K-related protein kinases (in mammals, ataxia telangiectasia mutated and Rad3-related [ATR], ataxia telangiectasia mutated [ATM], and DNA-PKCs) has been a subject of debate; it has been suggested that ATM is required for the induction of foci at DSBs, whereas ATR is involved in the recognition of stalled replication forks. In this study, using Arabidopsis as a model system, we investigated the ATR and ATM dependency of the formation of γ-H2AX foci in M-phase cells exposed to ionizing radiation (IR). We find that although the majority of these foci are ATM-dependent, ∼10% of IR-induced γ-H2AX foci require, instead, functional ATR. This indicates that even in the absence of DNA replication, a distinct subset of IR-induced damage is recognized by ATR. In addition, we find that in plants, γ-H2AX foci are induced at only one-third the rate observed in yeasts and mammals. This result may partly account for the relatively high radioresistance of plants versus yeast and mammals.
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Kumbhar, Ramhari, Sophie Vidal-Eychenié, Dimitrios-Georgios Kontopoulos, Marion Larroque, Christian Larroque, Jihane Basbous, Sofia Kossida, Cyril Ribeyre, and Angelos Constantinou. "Recruitment of ubiquitin-activating enzyme UBA1 to DNA by poly(ADP-ribose) promotes ATR signalling." Life Science Alliance 1, no. 3 (June 2018): e201800096. http://dx.doi.org/10.26508/lsa.201800096.

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The DNA damage response (DDR) ensures cellular adaptation to genotoxic insults. In the crowded environment of the nucleus, the assembly of productive DDR complexes requires multiple protein modifications. How the apical E1 ubiquitin activation enzyme UBA1 integrates spatially and temporally in the DDR remains elusive. Using a human cell-free system, we show that poly(ADP-ribose) polymerase 1 promotes the recruitment of UBA1 to DNA. We find that the association of UBA1 with poly(ADP-ribosyl)ated protein–DNA complexes is necessary for the phosphorylation replication protein A and checkpoint kinase 1 by the serine/threonine protein kinase ataxia-telangiectasia and RAD3-related, a prototypal response to DNA damage. UBA1 interacts directly with poly(ADP-ribose) via a solvent-accessible and positively charged patch conserved in the Animalia kingdom but not in Fungi. Thus, ubiquitin activation can anchor to poly(ADP-ribose)-seeded protein assemblies, ensuring the formation of functional ataxia-telangiectasia mutated and RAD3-related-signalling complexes.
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Turner, Thomas, and Thomas Caspari. "When heat casts a spell on the DNA damage checkpoints." Open Biology 4, no. 3 (March 2014): 140008. http://dx.doi.org/10.1098/rsob.140008.

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Peregrine Laziosi (1265–1345), an Italian priest, became the patron saint of cancer patients when the tumour in his left leg miraculously disappeared after he developed a fever. Elevated body temperature can cause tumours to regress and sensitizes cancer cells to agents that break DNA. Why hyperthermia blocks the repair of broken chromosomes by changing the way that the DNA damage checkpoint kinases ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) are activated is an unanswered question. This review discusses the current knowledge of how heat affects the ATR–Chk1 and ATM–Chk2 kinase networks, and provides a possible explanation of why homeothermal organisms such as humans still possess this ancient heat response.
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DeHart, Jason L., Joshua L. Andersen, Erik S. Zimmerman, Orly Ardon, Dong Sung An, Jana Blackett, Baek Kim, and Vicente Planelles. "The Ataxia Telangiectasia-Mutated and Rad3-Related Protein Is Dispensable for Retroviral Integration." Journal of Virology 79, no. 3 (February 1, 2005): 1389–96. http://dx.doi.org/10.1128/jvi.79.3.1389-1396.2005.

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ABSTRACT Integration into the host cell DNA is an essential part of the retroviral life cycle and is required for the productive replication of a retrovirus. Retroviral integration involves cleavage of the host DNA and insertion of the viral DNA, forming an integration intermediate that contains two gaps, each with a viral 5′ flap. The flaps are then removed, and the gap is filled by as yet unidentified nuclease and polymerase activities. It is thought that repair of these gaps flanking the site of retroviral integration is achieved by host DNA repair machinery. The ATM and Rad3-related protein (ATR) is a member of the phosphatidylinositol 3 kinase-related family of protein kinases that play a major role in sensing and triggering repair of DNA lesions in mammalian cells. In an effort to examine the role of ATR in retroviral integration, we used RNA interference to selectively downregulate ATR and measured integration efficiency. In addition, we examined the possible role that Vpr may play in enhancing integration and, in particular, whether activation of ATR by Vpr (Roshal et al., J. Biol. Chem. 278:25879-25886, 2003) will favor human immunodeficiency virus type 1 integration. We conclude that cells in which ATR has been depleted are competent for retroviral integration. We also conclude that the presence of Vpr as a virion-bound protein does not enhance integration of a lentivirus vector in dividing cells.
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Vidal-Eychenié, Sophie, Chantal Décaillet, Jihane Basbous, and Angelos Constantinou. "DNA structure-specific priming of ATR activation by DNA-PKcs." Journal of Cell Biology 202, no. 3 (July 29, 2013): 421–29. http://dx.doi.org/10.1083/jcb.201304139.

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Three phosphatidylinositol-3-kinase–related protein kinases implement cellular responses to DNA damage. DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia-telangiectasia mutated respond primarily to DNA double-strand breaks (DSBs). Ataxia-telangiectasia and RAD3-related (ATR) signals the accumulation of replication protein A (RPA)–covered single-stranded DNA (ssDNA), which is caused by replication obstacles. Stalled replication intermediates can further degenerate and yield replication-associated DSBs. In this paper, we show that the juxtaposition of a double-stranded DNA end and a short ssDNA gap triggered robust activation of endogenous ATR and Chk1 in human cell-free extracts. This DNA damage signal depended on DNA-PKcs and ATR, which congregated onto gapped linear duplex DNA. DNA-PKcs primed ATR/Chk1 activation through DNA structure-specific phosphorylation of RPA32 and TopBP1. The synergistic activation of DNA-PKcs and ATR suggests that the two kinases combine to mount a prompt and specific response to replication-born DSBs.
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Asmal, M., E. Dean, J. Evans, M. Middleton, and R. Plummer. "VX-970, selective inhibitor of ataxia telangiectasia and Rad3-related (ATR) protein." Annals of Oncology 26 (March 2015): ii8. http://dx.doi.org/10.1093/annonc/mdv084.4.

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Takeuchi, Makoto, Michihiro Tanikawa, Kazunori Nagasaka, Katsutoshi Oda, Yoshiko Kawata, Shinya Oki, Chuwa Agapiti, et al. "Anti-Tumor Effect of Inhibition of DNA Damage Response Proteins, ATM and ATR, in Endometrial Cancer Cells." Cancers 11, no. 12 (December 1, 2019): 1913. http://dx.doi.org/10.3390/cancers11121913.

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While the incidence of endometrial cancer continues to rise, the therapeutic options remain limited for advanced or recurrent cases, and most cases are resistant to therapy. The anti-tumor effect of many chemotherapeutic drugs and radiotherapy depends on the induction of DNA damage in cancer cells; thus, activation of DNA damage response (DDR) pathways is considered an important factor affecting resistance to therapy. When some DDR pathways are inactivated, inhibition of other DDR pathways can induce cancer-specific synthetic lethality. Therefore, DDR pathways are considered as promising candidates for molecular-targeted therapy for cancer. The crosstalking ataxia telangiectasia mutated and Rad3 related and checkpoint kinase 1 (ATR-Chk1) and ataxia telangiectasia mutated and Rad3 related and checkpoint kinase 2 (ATM-Chk2) pathways are the main pathways of DNA damage response. In this study, we investigated the anti-tumor effect of inhibitors of these pathways in vitro by assessing the effect of the combination of ATM or ATR inhibitors and conventional DNA-damaging therapy (doxorubicin (DXR), cisplatin (CDDP), and irradiation) on endometrial cancer cells. Both the inhibitors enhanced the sensitivity of cells to DXR, CDDP, and irradiation. Moreover, the combination of ATR and Chk1 inhibitors induced DNA damage in endometrial cancer cells and inhibited cell proliferation synergistically. Therefore, these molecular therapies targeting DNA damage response pathways are promising new treatment strategies for endometrial cancer.
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Ward, Irene M., Kay Minn, and Junjie Chen. "UV-induced Ataxia-telangiectasia-mutated and Rad3-related (ATR) Activation Requires Replication Stress." Journal of Biological Chemistry 279, no. 11 (January 23, 2004): 9677–80. http://dx.doi.org/10.1074/jbc.c300554200.

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Tibelius, Alexandra, Joachim Marhold, Hanswalter Zentgraf, Christoph E. Heilig, Heidemarie Neitzel, Bernard Ducommun, Anita Rauch, Anthony D. Ho, Jiri Bartek, and Alwin Krämer. "Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1." Journal of Cell Biology 185, no. 7 (June 22, 2009): 1149–57. http://dx.doi.org/10.1083/jcb.200810159.

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Primary microcephaly, Seckel syndrome, and microcephalic osteodysplastic primordial dwarfism type II (MOPD II) are disorders exhibiting marked microcephaly, with small brain sizes reflecting reduced neuron production during fetal life. Although primary microcephaly can be caused by mutations in microcephalin (MCPH1), cells from patients with Seckel syndrome and MOPD II harbor mutations in ataxia telangiectasia and Rad3 related (ATR) or pericentrin (PCNT), leading to disturbed ATR signaling. In this study, we show that a lack of MCPH1 or PCNT results in a loss of Chk1 from centrosomes with subsequently deregulated activation of centrosomal cyclin B–Cdk1.
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Pancholi, Neha J., Alexander M. Price, and Matthew D. Weitzman. "Take your PIKK: tumour viruses and DNA damage response pathways." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1732 (September 11, 2017): 20160269. http://dx.doi.org/10.1098/rstb.2016.0269.

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Viruses regulate cellular processes to facilitate viral replication. Manipulation of nuclear proteins and pathways by nuclear replicating viruses often causes cellular genome instability that contributes to transformation. The cellular DNA damage response (DDR) safeguards the host to maintain genome integrity, but DNA tumour viruses can manipulate the DDR to promote viral propagation. In this review, we describe the interactions of DNA tumour viruses with the phosphatidylinositol 3-kinase-like protein kinase (PIKK) pathways, which are central regulatory arms of the DDR. We review how signalling through the ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3 related (ATR), and DNA-dependent protein kinases (DNA-PK) influences viral life cycles, and how their manipulation by viral proteins may contribute to tumour formation. This article is part of the themed issue ‘Human oncogenic viruses’.
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Dissertations / Theses on the topic "Ataxia Telangiectasia and Rad3-related (ATR)"

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Alsubhi, Nouf. "Targeting ataxia telangiectasia-mutated and Rad3-related kinase (ATR) in PTEN-deficient breast cancers for personalized cancer therapy." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/52080/.

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Background: Phosphatase and tensin homolog (PTEN) is a multifunctional gene which acts as a tumour suppressor gene and is involved in DND damage response (DDR) mechanisms. PTEN has been found to be mutated in different types of human cancers including breast cancer. Ataxia-telangiectasia mutated (ATM) and RAD3- related (ATR) are involved in DDR and they have roles in cell cycle regulation and apoptosis. Previously ATM inhibition caused synthetic lethality in prostate and colorectal cancer cells with PTEN deficiency. In this study we hypothesize that PTEN plays key roles in breast carcinogenesis and that inhibition of ATR in the context of PTEN deficiency can provide a novel therapeutic approach through a synthetic lethality mechanism. Methods: In this study a large, well-characterised and molecularly annotated series of breast cancer (n=1954) was utilized to evaluate the clinicopathological and biological role of PTEN protein expression assessed using immunohistochemistry (IHC) and tissue microarrays technology. Several breast cancer cell lines (n=4) representing various molecular classes and PTEN status were studied in vitro using functional assays. Cellular consequences of ATR inhibitor (VE-821) treatment were investigated in a panel of PTEN-proficient including MCF7 and MDA-MB-231, and PTEN-deficient including BT-549 and MDA-MB-468 breast cancer cell lines. DNA repair expression profiling, MTS cell-proliferation assay, FACS for cell cycle, γH2AX and FITC-annexin V flow cytometry analysis were performed on PTEN-deficient and PTEN-proficient cells to study the functional consequences of PTEN deficiency on breast cancer cells. Results: PTEN was expressed in the nucleus and cytoplasm of malignant cells. The negative nuclear expression was detected in 62.6%, whilst negative/low cytoplasmic expression was found in 40.2% cases of breast cancer. The negative nuclear PTEN IHC expression was associated with features of aggressive behavior including higher grade, nuclear pleomorphism, higher mitotic index, larger tumour size, oestrogen receptor (ER) negativity, high risk Nottingham prognostic index (NPI≥3.4) and shorter breast cancer specific survival (BCSS) (pvalue < 0.05). Interestingly, in tumours with low nuclear PTEN, high ATR and/or high pChk1 (pCHK1Ser345) expression was also linked to poor BCSS (P-values < 0.05). Preclinical study demonstrated that PTEN-deficient breast cancer cells feature altered transcriptional expression of several genes involved in DNA repair pathways. Compared with ATR inhibitor (VE-821) in PTEN-proficient breast cancer cells, ATR inhibition in PTEN-deficient cells was associated with accumulation of double strand DNA breaks, cell cycle arrest at G2/M phases, and increased apoptosis. Conclusions: PTEN deficiency has prognostic significance in breast cancer, and selective targeting of ATR in PTEN-deficient cells with ATR inhibitor (VE-821) can serve as a potential avenue for development of personalized therapy for breast cancer patients.
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Ichisima, Jose. "Verification and rectification of cell type-specific splicing of a Seckel syndrome-associated ATR mutation using iPS cell model." Kyoto University, 2019. http://hdl.handle.net/2433/243306.

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Cartwright, Brian. "Exploration of Ataxia Telangiectasia and Rad3-Related’s (ATR’s) Role in Cell Death Regulation: Implications in Development, Cancer, and Stroke." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3664.

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From gametogenesis until death an organism’s genome is under constant bombardment from endogenous and exogenous sources of DNA damage. To maintain genomic integrity amid this damage, cells have evolved responses which allow them to either preserve viability for recovery or initiate self-destructive pathways depending on the severity of DNA damage. One protein involved in initiating and carrying out these responses is the protein kinase ataxia telangiectasia and Rad3-related (ATR). ATR is known primarily for its regulatory role in initiating the checkpoint-signaling cascade following DNA damage and replicative stress. These signaling events lead to cell cycle arrest, DNA repair, or apoptosis when damage is too extreme. In addition to these kinase-dependent roles, ATR also is capable of directly blocking the intrinsic apoptotic pathway through structural sequestration of the proapoptotic protein tBid. The sum of these regulatory events is a delicate balancing act resulting in either cell death or cell survival depending on the severity of the damage and the differentiation state of the cell in question. In the following studies, we sought to investigate the complex interplay of ATR’s kinase and structural roles in determining cellular fate. First, we investigated the structural role of prolyl isomerization of ATR across development by using mouse models of two isomerically locked forms of ATR which were previously shown to lock cytoplasmic ATR into a single isomer. Studies showed that ATR which is locked in ATR-L (trans-ATR, hATR-P429A/mATR-P432A) is embryonically lethal and that heterozygotes tend to have neurological and other developmental abnormalities. This contrasts with ATR-H (cis-ATR, hATR-S428A/mATR-S431A), which is viable, but naturally prone to cancer development. Next, we used various in vitro stroke-like conditions to test if ATR inhibition could serve as a therapeutic target for stroke. We found that ATR inhibition is protective in non-dividing neuron-like cells; whereas, it potentiates death in cycling glial and immune-like cycling cells. Thus, ATR inhibition could likely be a target for both neuron sparing and immunosuppressive anti-stroke therapeutic strategies. Taken together, these studies provide insightful information into the structural and pathological roles of ATR in development and disease.
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KIDIYOOR, GURURAJ RAO. "ATR MEDIATED REGULATION OF CELLULAR AND NUCLEAR PLASTICITY." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/561090.

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Protein kinase ATR (Ataxia Telangiectasia and Rad3-related) is a key regulator of genomic integrity. In addition to its vital, well-understood role in maintaining replication fork stability, ATR is also involved in mediating mechanical stress response at the nuclear envelope preventing potential threats to the genome. Our data from sub-cellular distribution and interactome analysis of ATR suggests that ATR contributes to several cellular processes in multiple organelles such as mitochondria, actin cytoskeleton, Golgi and nuclear envelope. At the nuclear envelope ATR is present on both inner and outer nuclear membranes, on the nuclear pores and bound to perinuclear chromatin and to perinuclear actin fibers. In this study we show that ATR regulates nuclear membrane integrity by maintaining nuclear morphology and optimal membrane tension, by counteracting mechanical force imbalances at the NE and by coordinating nuclear events with nuclear and cell migration. We report a novel role of ATR in preventing and protecting nuclear envelope damage and DNA damage caused by mechanical constrains acting on the nucleus. Further we show that by maintaining nuclear envelope integrity ATR facilitates cell migration on 2D surfaces and by regulating nuclear membrane components and by limiting nuclear envelope damage it aids cell survival during confined 3D migrations. Loss of ATR dampens neuronal migration during development and cancer cells lacking ATR are inefficient in extravasation, do not survive circulation and fail to successfully metastasize into the host environment. Therefore, by promoting cell survival in altering mechanical microenvironment and during metastasis and invasion, ATR assists tumor development, suggesting a dual role for this kinase in tumorigenisis
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Abu, Sanad Atlal. "Dual inhibition of Ataxia-telangiectasia and Rad3-related (ATR) and Poly-ADP polymerase (PAPR) pathways enhances Topoisomerase l cytotoxicity in colon cancer cell lines:pre- clinical assessment of pathway-specific novel therapeutics." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=123053.

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Manipulating the DNA repair mechanisms involved in the repair of Topoisomerase-I (Top I) mediated DNA damage may enhance the therapeutic benefits of Top I poisons. Poly-ADP ribose polymerase (PARP) inhibitors can increase the cytotoxicity of several anticancer agents by inhibiting various DNA repair pathways including homologous recombinational repair (HRR)(1). However, inhibition of PARP may result in compensatory activation of the ATR pathway partially limiting the sensitization of chemotherapeutic agents seen with PARP inhibitors. Recently, a specific ATR inhibitor, VE-821 has demonstrated excellent sensitization to various chemotherapeutic agents with preferential antitumor activity in tumor cells as compared to normal cells(2).Colon cancer cell lines: HCT116, Lovo (p53 wild type) and HT29 (p53 mutated) were treated with SN38 (the active metabolite of irinotecan, a topoisomerase I inhibitor), the PARP inhibitor (ABT-888) and/or the ATR inhibitor (VE821) at different concentrations. The SRB cytotoxicity assay was used to determine the IC50 of each drug separately and in combination. DNA damage caused by these agents was quantified by phosphorylated-H2AX. Cell cycle alterations and protein levels (western analysis) were determined after drug treatment.
Manipuler les mécanismes de réparation de l'ADN impliquées dans la réparation de dommage de l'ADN médiatisé de la topoisomérase-1 (Top I) peut renforcer les bienfaits thérapeutiques des poisons Top I. Les inhibiteurs de polymérase poly-ADP ribose (PARP) peuvent augmenter la cytotoxicité de plusieurs agents anticancéreux en inhibant différentes voies de réparation de l'ADN comprenant la réparation par recombinaison homologue (HRR)(1). Cependant, l'inhibition de la PARP peut entraîner une activation compensatoire de la voie ATR, limitant partiellement la sensibilisation des agents chimiothérapiques observés avec les inhibiteurs de PARP. Récemment, un inhibiteur de l'ATR spécifique, VE-821 a démontré une excellente sensibilisation à divers agents chimiothérapiques avec une activité antitumorale préférentielle dans les cellules tumorales par rapport aux cellules normales (2).Lignes cellulaires du cancer du côlon : HCT 116, Lovo (type sauvage de p53) et HT29 (p53 muté) ont été traités avec SN38, l'inhibiteur de la PARP (ABT-888) et/ou l'inhibiteur de l'ATR (VE821) à différentes concentrations. Le dosage de cytotoxicité SRB a été utilisé pour déterminer IC50 de chaque médicament séparément ou en combinaison. Les dommages DNA causés par ces agents ont été quantifiés par phosphorylée-H2AX. Les altérations du cycle cellulaire et des protéines (analyse de l'ouest) ont été déterminées après un traitement médicamenteux.
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Shaj, Kavya. "Differing functions of ATR kinase in human epidermal keratinocytes exposed to Ultraviolet B Radiation." Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright156704699234269.

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Wolf, Horrell Erin M. "Regulation of UV-Protective Pathways Downstream of the Melanocortin 1 Receptor in Melanocytes." UKnowledge, 2016. http://uknowledge.uky.edu/physiology_etds/29.

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Malignant cutaneous melanoma is the deadliest form of skin cancer, and a majority of melanoma diagnoses are a result of exposure to ultraviolet (UV) radiation. UV radiation causes DNA damage, which if not repaired correctly via nucleotide excision repair (NER) can result in mutations and melanomagenesis. The melanocortin 1 receptor (MC1R) is a Gs protein coupled receptor located on melanocyte plasma membranes and is involved in protecting the skin from UV induced damage. MC1R signaling results in the activation of two protective pathways: 1) induction of eumelanin synthesis downstream of micropthalmia-associated transcription factor (MITF) and 2) acceleration of NER downstream of ataxia telangiectaseia mutated and Rad3 related (ATR). MC1R signaling, however, also promotes melanocyte proliferation, therefore, the activation of the MC1R pathway must be regulated. The overall hypothesis of this dissertation is that the pathways downstream of MC1R can be manipulated to protect against UV induced damage. Chapter 2 investigates the regulation of the MC1R neutral antagonist human β-defensin 3 (βD3). UV damage did not induce βD3 mRNA expression in ex vivo human skin explants. The induction of βD3 expression instead correlated with inflammatory cytokines including TNF. Chapter 3 investigates the interdependence and cross talk between the two protective pathways downstream of MC1R. We directly tested the effect of MITF on the acceleration of NER and the effect of ATR on the induction of eumelanin synthesis following MC1R activation. MITF was not required for the acceleration of NER as mediated by ATR, however, the induction of transcription of enzymes involved in eumelanin synthesis was dependent upon ATR kinase activity. Finally, Chapter 4 investigates the mechanism by which MC1R promoted proliferation and whether the two UV protective pathways downstream of MC1R could be selectively activated without the risk of melanocyte proliferation. MC1R signaling resulted in activation of the mechanistic target of rapamycin complex 1 (mTORC1), a major regulator of cell growth and proliferation. Inhibition of mTORC1 signaling via rapamycin prevented MC1R induced proliferation in vitro. Rapamycin, however, did not prevent MC1R induced eumelanin synthesis or the acceleration of NER in vitro or in vivo suggesting it is possible to selectively activate the beneficial signaling pathways without the risk of melanocyte proliferation. The results of this dissertation suggest that MC1R signaling could be augmented in individuals to prevent UV induced damage.
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Tayeh, Zainab. "Centrosome integrity as a determinant of replication stress." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-1300-5.

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Book chapters on the topic "Ataxia Telangiectasia and Rad3-related (ATR)"

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Awasthi, Poorwa, Vipin Kumar Yadav, Manisha Dixit, and Amit Kumar. "Ataxia Telangiectasia and Rad3-Related (ATR)." In Encyclopedia of Signaling Molecules, 452–59. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101789.

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Awasthi, Poorwa, Vipin Kumar Yadav, Manisha Dixit, and Amit Kumar. "Ataxia Telangiectasia and Rad3-Related (ATR)." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101789-1.

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Conference papers on the topic "Ataxia Telangiectasia and Rad3-related (ATR)"

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Wilsker, Deborah, Allison M. Marrero, Angie Dull, Thomas D. Pfister, Scott M. Lawrence, John Carter, Michelle Gottholm-Ahalt, et al. "Abstract B24: Ataxia-telangiectasia and Rad3-related (ATR) phosphorylation as a pharmacodynamic biomarker of ATR activation in solid tumor tissue models." In Abstracts: AACR Precision Medicine Series: Cancer Cell Cycle - Tumor Progression and Therapeutic Response; February 28 - March 2, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.cellcycle16-b24.

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Bateman, Nicholas, Pang-ing Teng, Kelly Conrads, Chad Hamilton, George Maxwell, Christopher Bakkenist, and Thomas Conrads. "Abstract 2747: Pharmacological inhibition of the DNA damage response kinases, ATR (Ataxia telangiectasia and Rad3 related) and ATM (Ataxia telangiectasia mutated), broadly sensitizes diverse subtypes of gynecological cancer cells to ionizing radiation." 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.am2014-2747.

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Yang, Qingyuan, Ruiqing Yang, Ming Zhan, Narasimharao Nalabothula, and France Carrier. "Abstract 1312: Functional significance for an hnRNP A18 signature RNA motif in the 3'UTR of Ataxia Telangiectasia and RAD3 related (ATR) transcript." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1312.

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Krebs, Matthew G., Juanita Lopez, Anthony El-Khoueiry, Yung-Jue Bang, Sophie Postel-Vinay, Wassim Abida, Louise Carter, et al. "Abstract CT026: Phase I study of AZD6738, an inhibitor of ataxia telangiectasia Rad3-related (ATR), in combination with olaparib or durvalumab in patients (pts) with advanced solid cancers." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-ct026.

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Yap, Timothy A., Maria J. de Miguel Luken, Brent O'Carrigan, Desam Roda, Dionysis Papadatos-Pastos, David Lorente, Nina Tunariu, et al. "Abstract PR14: Phase I trial of first-in-class ataxia telangiectasia-mutated and Rad3-related (ATR) inhibitor VX-970 as monotherapy (mono) or in combination with carboplatin (CP) in advanced cancer patients (pts) with preliminary evidence of target modulation and antitumor activity." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-pr14.

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Tan, David S., Vincent Castonguay, Gregory Cote, Johann S. De Bono, Bassel El-Rayes, Nashat Gabrail, Satoru Iwasa, et al. "EP294/#883 Elimusertib, an oral ataxia telangiectasia and RAD3-related inhibitor, in advanced gynecologic cancers with DNA damage response defects." In IGCS 2022 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-igcs.385.

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Yap, Timothy, Elizabeth Lee, David Spigel, Elisa Fontana, Martin Højgaard, Stephanie Lheureux, Niharika B. Mettu, et al. "Abstract CC04-01: First-in-human biomarker-driven phase I TRESR trial of ataxia telangiectasia and Rad3-related inhibitor (ATRi) RP-3500 in patients (pts) with advanced solid tumors harboring synthetic lethal (SL) genomic alterations." In Abstracts: AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; October 7-10, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1535-7163.targ-21-cc04-01.

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