Relevant bibliographies by topics / Ligase IV Inhibitor SCR7

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  1. Journal articles
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  3. Conference papers

Academic literature on the topic 'Ligase IV Inhibitor SCR7'

Author: Grafiati
Published: 6 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "Ligase IV Inhibitor SCR7"

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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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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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Dissertations / Theses on the topic "Ligase IV Inhibitor SCR7"

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Menchon, Grégory. "Criblage virtuel et fonctionnel sur le complexe XRCC4/ADN ligase IV/Cer-XLF de ligature des cassures double-brin de l'ADN : application en radiosensibilisation tumorale." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30395.

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En cancérologie, la radiothérapie est une des armes essentielles pour éradiquer les cellules tumorales. Les cassures des deux brins de l'ADN dites "double-brin" qu'elle induit sont particulièrement toxiques et constituent la principale cause de mort cellulaire. La NHEJ (Jonction d'Extrémités Non-Homologues) est la voie métabolique majeure de réparation de ces cassures double-brin de l'ADN et par ce mécanisme, les cellules humaines adoptent une résistance à la radiothérapie. Ce mécanisme de réparation constitue donc une cible de choix pour un traitement anticancéreux combiné en vue d'augmenter
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Pandey, Monica. "Understanding the Sequence Dependence of NHEJ Mediated Double-strand Break Repair, and Identification of Novel DNA Ligase Inhibitors and their Potential Use as Cancer Therapeutics." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4146.

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Repair of DNA breaks is essential for maintenance of genomic integrity. DNA double-strand breaks (DSBs) are considered as the most harmful DNA lesions within the cells which if left unrepaired or are misrepaired, can lead to a wide variety of genetic alterations, chromosomal rearrangements either culminating in oncogenic transformation or apoptosis. Therefore, the cell adopts two major pathways, Homologous recombination (HR) and nonhomologous end joining (NHEJ), in order to repair these DSBs thereby maintaining genome stability. HR mediated DSB repair is error-free and is functional during the
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Conference papers on the topic "Ligase IV Inhibitor SCR7"

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Lin, Tingting, Zhilian Zhou, Lifeng Zhu, Yandan Fan, Xiaofen Ding, and Yingming Sun. "Abstract 3066: DNA ligase IV inhibitor and X-ray exert a synthetic lethal in loss-of-function p53 cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3066.

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