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Journal articles on the topic 'Ligase IV Inhibitor SCR7'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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1

Anuchina, Arina A., Milyausha I. Zaynitdinova, Anna G. Demchenko, Nadezhda A. Evtushenko, Alexander V. Lavrov, and Svetlana A. Smirnikhina. "Bridging Gaps in HDR Improvement: The Role of MAD2L2, SCAI, and SCR7." International Journal of Molecular Sciences 24, no. 7 (2023): 6704. http://dx.doi.org/10.3390/ijms24076704.

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This study aimed to enhance homology-directed repair (HDR) efficiency in CRISPR/Cas-mediated genome editing by targeting three key factors regulating the balance between HDR and non-homologous end joining (NHEJ): MAD2L2, SCAI, and Ligase IV. In order to achieve this, a cellular model using mutated eGFP was designed to monitor HDR events. Results showed that MAD2L2 knockdown and SCR7 treatment significantly improved HDR efficiency during Cas9-mediated HDR repair of the mutated eGFP gene in the HEK293T cell line. Fusion protein Cas9-SCAI did not improve HDR. This study is the first to demonstrat

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Greco, George E., Yoshihiro Matsumoto, Rhys C. Brooks, Zhengfei Lu, Michael R. Lieber, and Alan E. Tomkinson. "SCR7 is neither a selective nor a potent inhibitor of human DNA ligase IV." DNA Repair 43 (July 2016): 18–23. http://dx.doi.org/10.1016/j.dnarep.2016.04.004.

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Calimeri, Teresa, Daniele Caracciolo, Nicola Amodio, et al. "Targeting Aberrant Non-Homologous End Joining in Multiple Myeloma: Role of the Classical and Alternative Pathways in Genomic Instability." Blood 124, no. 21 (2014): 3417. http://dx.doi.org/10.1182/blood.v124.21.3417.3417.

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Abstract Multiple Myeloma (MM) is characterized by the growth of malignant plasma cells harboring numerous genomic aberrations. The molecular basis driving MM genomic instability is still largely unknown. The ability to repair DNA damages is essential for the maintenance of its integrity, especially the double-strand breaks (DSBs) which are mainly repaired by Non Homologous End Joining (NHEJ). We have investigated NHEJ pathway in myeloma and observed a significant association between up-regulated NHEJ pathway-related gene expression and poor overall survival in two large datasets (IFM and Arka

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Greco, George E., Zane A. Conrad, Alycia M. Johnston, Qingyao Li, and Alan E. Tomkinson. "Synthesis and structure determination of SCR7, a DNA ligase inhibitor." Tetrahedron Letters 57, no. 29 (2016): 3204–7. http://dx.doi.org/10.1016/j.tetlet.2016.06.037.

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5

Kotnis, Ashwin, and Rita Mulherkar. "Novel inhibitor of DNA ligase IV with a promising cancer therapeutic potential." Journal of Biosciences 39, no. 3 (2014): 339–40. http://dx.doi.org/10.1007/s12038-014-9433-0.

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Sallmyr, Annahita, та Feyruz V. Rassool. "Up-Regulated WRN and DNA Ligase IIIα Are Involved in Alternative NHEJ Repair Pathway of DNA Double Strand Breaks (DSB) in Chronic Myeloid Leukemia (CML)." Blood 110, № 11 (2007): 1016. http://dx.doi.org/10.1182/blood.v110.11.1016.1016.

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Abstract The oncogenic BCR-ABL in CML produces increased reactive oxygen species (ROS) leading to DSB and aberrant repair. We have previously shown that CML cells demonstrate an increased frequency of errors of non homologous end-joining (NHEJ). DSB are repaired by two major pathways, homologous recombination (HR) and NHEJ, the dominant pathway in eukaryotic cells, also known as DNA-PK dependent NHEJ (D-NHEJ). Recent reports have identified alternative or “back-up” NHEJ pathways (B-NHEJ) that are highly error-prone, and may explain the altered DSB repair reported in CML. To determine the mecha

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Chou, Mei-Chia, Yuan-Jia Lee, Yao-Ting Wang, Shi-Yie Cheng, and Hsueh-Ling Cheng. "Cytotoxic and Anti-Inflammatory Triterpenoids in the Vines and Leaves of Momordica charantia." International Journal of Molecular Sciences 23, no. 3 (2022): 1071. http://dx.doi.org/10.3390/ijms23031071.

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The vines and leaves of Momordica charantia L. are used as herbal medicines to treat inflammation-related disorders. However, their safety profile remains uncharacterized, and the constituents in their extracts that exert anti-inflammatory and adverse effects remain unclear. This study isolated the characteristic cucurbitane-type triterpenoid species in the vines and leaves of M. charantia L. and analyzed their cytotoxicity, anti-inflammatory effects, and underlying mechanisms. Four structurally related triterpenoids—momordicines I, II, IV, and (23E) 3β,7β,25-trihydroxycucurbita-5,23-dien-19-a

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Devassy, Greeshma, Ranjith Ramachandran, Kottarapat Jeena, et al. "Simultaneous release of two drugs from polymer nano-implant inhibits recurrence in glioblastoma spheroids." Precision Nanomedicine 2, no. 1 (2019): 218–29. http://dx.doi.org/10.33218/prnano2(1).181122.1.

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Local implant-based delivery of rationally selected combination of chemotherapeutics has some major advantages for the treatment of glioblastoma such as: (a) 100 % bio-availability locally in brain can be achieved at the tumor site (b) avoid systemic leakage and associated toxicity, and (c) simultaneous inhibition of multiple, mutually exclusive cancer mechanisms is possible. Here, we report a polymeric brain implant capable of delivering two different drugs in recur-rent glioma cells. We have selected a combination of clinically used DNA alkylating agent, Te-mozolomide, and a DNA mismatch rep

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Cha, Sang-Wook. "Generating Nonmosaic Mutants in Xenopus Using CRISPR–Cas in Oocytes." Cold Spring Harbor Protocols 2022, no. 6 (2021): pdb.prot106989. http://dx.doi.org/10.1101/pdb.prot106989.

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In CRISPR–Cas9 genome editing, double-strand DNA breaks (DSBs) primarily undergo repair through nonhomologous end joining (NHEJ), which produces insertion or deletion of random nucleotides within the targeted region (indels). As a result, frameshift mutation-mediated loss-of-function mutants are frequently produced. An alternative repair mechanism, homology-directed repair (HDR), can be used to fix DSBs at relatively low frequency. By injecting a DNA-homology repair construct with the CRISPR–Cas components, specific nucleotide sequences can be introduced within the target region by HDR. We hav

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Shima, Yutaka, Takito Shima, Tomoki Chiba, Tatsuro Irimura, and Issay Kitabayashi. "PML Protects HIPK2 and p300 from SCF-Mediated Ubiquitin-Dependent Degradation To Activate Transcription." Blood 110, no. 11 (2007): 2653. http://dx.doi.org/10.1182/blood.v110.11.2653.2653.

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Abstract The Pml gene is the target of t(15;17) chromosome translocation in acute promyelocytic leukemia. PML protein is known to localize in discrete nuclear speckles, named PML nuclear bodies (NBs). In NBs, PML interacts with several transcription factors, such as p53 and AML1, and their co-activators, such as HIPK2 and p300. PML activates transcription of their target genes. PML is thought to stabilize transcription factor complex and function as a mediator in transcription activation, but little is known about the molecular mechanism by which PML activates transcription. To clarify the rol

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Abraham, Shaji, Leonard C. Edelstein, Chad A. Shaw та ін. "Platelet FcγRIIA Signaling Results in Ubiquitination and Cellular Translocation of Activated Syk". Blood 124, № 21 (2014): 2761. http://dx.doi.org/10.1182/blood.v124.21.2761.2761.

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Abstract Platelet FcγRIIA is central to the pathophysiology of immune-mediated thrombocytopenia and thrombosis syndromes, such as heparin-induced thrombocytopenia (HIT). FcγRIIA is also the major transmembrane signaling adapter for αIIbβ3 outside-in signaling. In HIT, antibody to heparin/PF4 is necessary but not sufficient for disease to occur. Inter-individual variation in platelet activation via FcγRIIA contributes to HIT risk, but the molecular basis for the variation is incompletely understood. In our PRAX1 study of platelet reactivity and RNA expression (Edelstein, Nature Med 2013; Simon,

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Chauhan, Dharminder, Ze Tian, Benjamin Nicholson, et al. "Deubiquitylating Enzyme USP-7, a Novel Therapeutic Target in Multiple Myeloma." Blood 114, no. 22 (2009): 610. http://dx.doi.org/10.1182/blood.v114.22.610.610.

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Abstract Abstract 610 Background and Rationale: Ubiquitin-Proteasome Signaling (UPS) pathway is mediated via a large number of components, suggesting many potential sites of pharmacological intervention. Therapeutic targeting of UPS is exemplified by the recent FDA approval of dipeptidyl boronic acid bortezomib first-in-class proteasome inhibitor for the treatment of relapsed/refractory, relapsed, and newly diagnosed multiple myeloma (MM). As with other agents, however, dose-limiting toxicities and the development of resistance limit its long-term utility. Recent efforts have been devoted to d

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Somasundaram, Kumar. "Abstract B010: PITAR, a p53 inactivating TRIM28 associated RNA, executes an alternate way of p53 inactivation." Cancer Research 84, no. 5_Supplement_1 (2024): B010. http://dx.doi.org/10.1158/1538-7445.brain23-b010.

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Abstract Much of the human genome, once considered "junk DNA," is now shown to be pervasively transcribed into thousands of long noncoding RNAs (lncRNAs). Over the last two decades, accumulated evidence implicated lncRNA in fundamental biological processes that play an essential role in several pathological conditions like cancer. Glioblastoma (GBM), the model cancer for our studies, is a grade IV glioma and is the most common and malignant primary adult brain tumor. GBM patients usually undergo surgical resection (maximal near-safe surgery) with complementary concomitant radiotherapy and Temo

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Nakamura, Shingen, Masahiro Abe, Qu Cui, et al. "Facilitation of Osteoblast Differentiation by ATF-4 Accumulation through Proteasome Inhibition." Blood 114, no. 22 (2009): 1823. http://dx.doi.org/10.1182/blood.v114.22.1823.1823.

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Abstract Abstract 1823 Poster Board I-849 The proteasome inhibitor bortezomib, a novel anti-myeloma (MM) agent, has recently drawn considerable attention to its anabolic actions on bone formation in patients with MM. Bortezomib was reported to enhance the activity of Runx2/cbfa1, an essential transcription factor for osteoblast (OB) induction, in mesenchymal stem cells to induce OB differentiation. However, because over-expression of Runx2 unexpectedly suppresses terminal OB differentiation or mineralization, there may be critical factors involved in OB differentiation in concert with Runx2 to

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Abraham, Shaji, Carol T. Dangelmaier, Yuhang Zhou та ін. "Syk Is Regulated Downstream Of FcγRIIA In Platelets By Transient Tyrosine Phosphorylation and Ubiquitylation". Blood 122, № 21 (2013): 4737. http://dx.doi.org/10.1182/blood.v122.21.4737.4737.

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Platelet FcγRIIA contributes to the pathophysiology of heparin-induced thrombocytopenia (HIT) and other immune-mediated thrombocytopenia and thrombosis syndromes. Activation of FcγRIIA results in tyrosine phosphorylation of Syk in human platelets, but little is known about ubiquitylation of Syk. Protein ubiquitylation has been shown to regulate physiological and pathological cellular processes by regulating signaling networks. In the Platelet RNA and Expression-1 (PRAX1) study, we studied platelets from 154 healthy subjects and identified increased expression of mRNAs encoding proteins involve

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Raghavan, Sathees C., Ujjayinee Ray, Anjana Elizabeth Jose, et al. "Water-soluble SCR7 Can Abrogate DNA End Joining and Induce Cancer Cell Death." Clinical Oncology and Research, July 16, 2020, 1–7. http://dx.doi.org/10.31487/j.cor.2020.07.09.

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Small molecule inhibitors targeting DNA repair pathways in cancer cells is a novel and promising approach in cancer therapy, which can improve current therapeutic regimen. Although various attempts have been made for designing inhibitors against DNA damage response and repair proteins, reports on Nonhomologous End Joining (NHEJ) inhibitors are limited. Of the several chemical moieties identified, SCR7 and its oxidized form are novel and potent DNA Ligase IV inhibitors involved in the abrogation of DNA end joining thereby leading to cell death. In the present study, we have synthesized sodium s

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Sriramareddy, Sathya Neelature, Majeed Jamakhani, Léa Vilanova, Hélène Brossel, Bernard Staumont, and Malik Hamaidia. "Selective inhibition of DNA ligase IV provides additional efficacy to the treatment of anaplastic thyroid cancer." Frontiers in Oncology 14 (February 6, 2024). http://dx.doi.org/10.3389/fonc.2024.1323313.

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BackgroundAlthough the incidence of anaplastic thyroid carcinoma (ATC) is low (2.5% of thyroid cancer cases), this cancer has a very poor prognosis (survival rates &lt; 5 months) and accounts for 14–39% of deaths. Conventional therapies based on surgery in combination with radiotherapy or chemotherapy showed limited effectiveness primarily due to the robust and protective DNA damage response in thyroid cancer cells.MethodsWe used single-cell transcriptomic data from patients with different subtypes of thyroid cancer to study expression of genes involved in homologous recombination (HR) and

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18

Hu, Zheng, Zhaoying Shi, Xiaogang Guo, et al. "Ligase IV inhibitor SCR7 enhances gene editing directed by CRISPR–Cas9 and ssODN in human cancer cells." Cell & Bioscience 8, no. 1 (2018). http://dx.doi.org/10.1186/s13578-018-0200-z.

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19

Gupta, Navin, Takuya Matsumoto, Ken Hiratsuka, et al. "Modeling injury and repair in kidney organoids reveals that homologous recombination governs tubular intrinsic repair." Science Translational Medicine 14, no. 634 (2022). http://dx.doi.org/10.1126/scitranslmed.abj4772.

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Kidneys have the capacity for intrinsic repair, preserving kidney architecture with return to a basal state after tubular injury. When injury is overwhelming or repetitive, however, that capacity is exceeded and incomplete repair results in fibrotic tissue replacing normal kidney parenchyma. Loss of nephrons correlates with reduced kidney function, which defines chronic kidney disease (CKD) and confers substantial morbidity and mortality to the worldwide population. Despite the identification of pathways involved in intrinsic repair, limited treatments for CKD exist, partly because of the limi

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Hildebrand, Laura S., Tina Jost, Marion Schindler, et al. "Inhibiting NHEJ in HNSCC cell lines by the ligase IV inhibitor SCR130 has limited radiosensitizing effects." Scientific Reports 15, no. 1 (2025). https://doi.org/10.1038/s41598-025-03159-5.

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Abstract Radiotherapy (RT) is a relevant treatment for head and neck squamous cell carcinoma (HNSCC) patients but radioresistance, which depends on DNA damage response (DDR), restrains outcome. Therefore, manipulating DDR by small molecule inhibitors (SMI) is a promising treatment option. The main DNA double strand break (DSB) repair mechanisms in healthy mammalian cells are homologous recombination (HR) and non-homologous end joining (NHEJ). It is known that HR is already often impaired in tumors because of cancerous transitions. Therefore, additionally inhibiting NHEJ is a possibility to spe

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Fronik, Philipp, Michael Gutmann, Petra Vician, et al. "A platinum(IV) prodrug strategy to overcome glutathione-based oxaliplatin resistance." Communications Chemistry 5, no. 1 (2022). http://dx.doi.org/10.1038/s42004-022-00661-z.

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AbstractClinical efficacy of oxaliplatin is frequently limited by severe adverse effects and therapy resistance. Acquired insensitivity to oxaliplatin is, at least in part, associated with elevated levels of glutathione (GSH). In this study we report on an oxaliplatin-based platinum(IV) prodrug, which releases L-buthionine-S,R-sulfoximine (BSO), an inhibitor of glutamate-cysteine ligase, the rate-limiting enzyme in GSH biosynthesis. Two complexes bearing either acetate (BSO-OxOAc) or an albumin-binding maleimide (BSO-OxMal) as second axial ligand were synthesized and characterized. The in vitr

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Anbalagan, Selvakumar, Cecilia Ström, Jessica A. Downs, et al. "TP53 modulates radiotherapy fraction size sensitivity in normal and malignant cells." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-86681-6.

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AbstractRecent clinical trials in breast and prostate cancer have established that fewer, larger daily doses (fractions) of radiotherapy are safe and effective, but these do not represent personalised dosing on a patient-by-patient basis. Understanding cell and molecular mechanisms determining fraction size sensitivity is essential to fully exploit this therapeutic variable for patient benefit. The hypothesis under test in this study is that fraction size sensitivity is dependent on the presence of wild-type (WT) p53 and intact non-homologous end-joining (NHEJ). Using single or split-doses of

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Huang, Zi-Yao, Lei Wen, Liu-Fang Ye, et al. "Clinical and molecular characteristics of RNF43 mutations as promising prognostic biomarkers in colorectal cancer." Therapeutic Advances in Medical Oncology 16 (January 2024). http://dx.doi.org/10.1177/17588359231220600.

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Background: Transmembrane E3 ubiquitin ligase ( RNF43) mutations are present in approximately 6–18% of colorectal cancers (CRC) and could enhance Wnt/β-catenin signaling, which is emerging as a promising therapeutic target. This study aims to investigate the clinical and molecular characteristics and potential heterogeneity of RNF43-mutant CRC. Methods: A total of 78 patients with RNF43-mutant CRC were enrolled from July 2013 to November 2022. Demographic data, clinical characteristics, treatment regimens used, and survival outcomes were collected and analyzed. Results: Our study uncovered tha

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sprotocols. "Combined 3C-ChIP-Cloning (6C) Assay: A Tool to Unravel Protein-Mediated Genome Architecture." December 30, 2014. https://doi.org/10.5281/zenodo.13582.

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Authors: Vijay K. Tiwari and Stephen B. Baylin Corresponding authors ([sbaylin1@jhmi.edu](sbaylin1@jhmi.edu); [vijay.tiwari@fmi.ch](vijay.tiwari@fmi.ch)) ### INTRODUCTION Progress in technologies to address long-range chromosomal interactions in vivo has extensively revised concepts about different aspects of transcriptional regulation. These methods allow probing physical proximities between chromatin elements without specifically identifying the protein components that mediate such interactions. Here we describe a detailed protocol for Combined 3C-ChIP-Cloning (6C) technology, which combines

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sprotocols. "Combined 3C-ChIP-Cloning (6C) Assay: A Tool to Unravel Protein-Mediated Genome Architecture." December 30, 2014. https://doi.org/10.5281/zenodo.13583.

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Authors: Vijay K. Tiwari and Stephen B. Baylin Corresponding authors ([sbaylin1@jhmi.edu](sbaylin1@jhmi.edu); [vijay.tiwari@fmi.ch](vijay.tiwari@fmi.ch)) ### INTRODUCTION Progress in technologies to address long-range chromosomal interactions in vivo has extensively revised concepts about different aspects of transcriptional regulation. These methods allow probing physical proximities between chromatin elements without specifically identifying the protein components that mediate such interactions. Here we describe a detailed protocol for Combined 3C-ChIP-Cloning (6C) technology, which combines

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sprotocols. "Cultures of Cerebellar Granule Neurons." December 30, 2014. https://doi.org/10.5281/zenodo.13591.

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Authors: Parizad M. Bilimoria and Azad Bonni1 Corresponding author ([azad_bonni@hms.harvard.edu](azad_bonni@hms.harvard.edu)) ### INTRODUCTION Primary cultures of granule neurons from the post-natal rat cerebellum provide an excellent model system for molecular and cell biological studies of neuronal development and function. The cerebellar cortex, with its highly organized structure and few neuronal subtypes, offers a well-characterized neural circuitry. Many fundamental insights into the processes of neuronal apoptosis, migration, and differentiation in the mammalian central nervous system h

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sprotocols. "Engineering of ultra-small diagnostic nanoprobes through oriented conjugation of single-domain antibodies and quantum dots." January 7, 2015. https://doi.org/10.5281/zenodo.13799.

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Authors: Alyona Sukhanova, Klervi Even-Desrumeaux, Patrick Chames, Daniel Baty, Mikhail Artemyev, Vladimir Oleinikov & Igor Nabiev ### Abstract Nanoparticle-based biodetection commonly employs monoclonal antibodies (mAbs) for targeting. Although several types of conjugates have been used for biomarker labeling, the large size of mAbs limits the number of ligands per nanoparticle, impedes their intratumoral distribution, and limits intracellular penetration. Furthermore, the conditions of mAb conjugation using conventional techniques provide nanoprobes with irregular orientation of mAbs on

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