Ask about this productRelated genes to: Lig3 antibody
- Gene:
- LIG3 NIH gene
- Name:
- DNA ligase 3
- Previous symbol:
- LIG2
- Synonyms:
- LIG3alpha
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2018-08-14
Related products to: Lig3 antibody
Related articles to: Lig3 antibody
- The main protease (MPro) of coronaviruses (CoVs) is an essential enzyme involved in viral replication and represents an attractive target for antiviral drug discovery. Based on the similar binding pocket residues within the MPro of different CoVs, this study aimed to identify potential inhibitors of SARS-CoV-2 MPro from PDB ID 6M2N using integrated computational approaches. Interaction-based pharmacophore modeling, virtual screening, molecular docking, MM-GBSA binding energy calculation, and molecular dynamics simulation (MDS) were performed using BIOVIA Discovery Studio. The validated pharmacophore model was utilized to screen the ZINC database, followed by docking and 100 ns MDS analyses of the top-ranked compounds. The pharmacophore model 01 demonstrated favorable predictive performance (AUC = 0.781). Virtual screening identified 483 compounds, from which 15 compounds were selected for docking studies. Among them, ZINC95473654 (Lig-1), ZINC95473725 (Lig-2), and ZINC08792368 (Lig-3) exhibited strong binding affinity toward MPro. Lig-1 demonstrated the best docking score and binding free energy, along with stable interactions with key catalytic residues HIS41, CYS145, and GLU166. MDS analyses further confirmed that Lig-1, Lig-2 and Lig-3 maintained stable conformations. The hydrogen bond distance monitoring and post MDS-MM-GBSA results suggest Lig-1 followed by Lig-3 as an inhibitor for MPro and persistent intermolecular interactions throughout the 100 ns simulation period. The findings suggest that Lig-1, followed by Lig-3, may serve as promising computational lead compounds targeting SARS-CoV-2 MPro, representing promising candidates for further experimental validation. - Source: PubMed
Publication date: 2026/08/27
Khan Mohd YasirMaarfi FarahShah Abid UllahDuraisamy NithyadeviCherkaoui MohammedHemida Maged Gomaa - Oestrogen receptor alpha (ERα) is a driver of hormone-dependent breast cancer, yet current therapies are often hindered by drug resistance and adverse effects. In this study, we developed a structure-based virtual screening workflow to identify novel quinoxaline derivatives as computationally prioritized potential ERα modulators. The quinoxaline analogues obtained from PubChem are screened through validated docking model of ERα. The top-ranked candidates were further refined by MD simulations in GROMACS for 300 ns to assess complex stability and interaction persistence, followed by MM-PBSA binding free energy calculations to quantify binding energetics. The prioritized quinoxaline hits exhibited more favourable predicted docking scores than reference ligand, tamoxifen, while MD trajectory analyses indicated stable complex formation with sustained predicted interactions involving key ERα binding site residues. MM-PBSA highlights LIG3 as the most promising lead with a favourable energy (ΔG = -34.15 kcal/mol). Complementary ADMET profiling predicted favourable pharmacokinetic behaviour and low toxicity for the prioritized compounds. This integrated in silico strategy demonstrates that quinoxaline scaffolds, specifically LIG3, represent promising computationally prioritized templates for the further development and experimental evaluation of ERα targeted ligands. These findings provide a reliable computational framework for the prioritization and structural optimization of next-generation anti-breast cancer agents. - Source: PubMed
Publication date: 2026/09/07
Sharma AKumar DNarasimhan BMarwaha R K - The potential functional Single Nucleotide Polymorphism (SNPs) of DNA Damage Response (DDR)-related genes may influence AML aggressiveness and clinical outcomes through regulating genomic stability. However, systematic evaluation of functionally relevant SNPs across the entire DDR cascade in AML remains limited. In our study, significant associations were identified across multiple DDR modules. In the damage sensing module, rs2155209 TC/CC genotypes were protective against hyperleukocytosis and associated with longer OS, while rs1805794 CG/GG genotypes increased hyperleukocytosis risk. In the signal transduction module, rs521102 AA genotype was a risk factor for thrombocytopenia but unexpectedly associated with prolonged OS; rs738722 TT genotype increased hyperleukocytosis risk; rs1045051 GT/GG genotype conferred a higher relapse risk; and rs1799949 GA/AA genotype as a protective factor for high BM blast percentage. In the DNA repair module, rs3744356 TT genotypes predicted higher WBC counts and lower complete remission rate. Both rs3744356 TT genotype and rs2296675 GA genotype were associated with shorter OS (HR = 1.719, 95% CI = 1.082 -2.741, = 0.022; HR = 1.511, 95% CI = 1.046 - 2.182, = 0.028). SNPs in effector genes and showed no significant associations. In summary, SNPs across the DDR pathway-particularly in damage sensing, signal transduction, and DNA repair modules-are significantly associated with AML clinical features, treatment response, and survival. Our findings provide a foundation for developing DDR-based polygenic risk models and support the potential integration of germline SNP profiling into precision medicine strategies for AML. - Source: PubMed
Publication date: 2026/07/01
Zhang AminWu HanyangLiu WanchengMa Daoxin - Colorectal cancers (CRCs) with deficient DNA mismatch repair (dMMR) and microsatellite instability (MSI) are believed to be intrinsically immunogenic and respond more favorably to immune checkpoint inhibitor (ICI) therapy. However, a significant fraction of dMMR/MSI CRCs do not respond or eventually develop resistance to ICIs. The mechanisms underlying dMMR/MSI-associated immunogenicity is unclear. The aim of this study was to investigate the role and mechanism of MSI-induced antitumor immunity in CRCs. - Source: PubMed
Publication date: 2026/07/16
Hao SuisuiSato YoshiakiBattaglin FrancescaXiu JoanneWang Yi-JunAshouri KaramLizardo DarlenyLiu ZhaojinLu XinyanOberley MatthewSchoen Robert ELenz Heinz-JosefYu JianZhang Lin - Colorectal cancer (CRC) with microsatellite instability (MSI) is often treated with immune checkpoint inhibitors (ICIs), such as anti-PD-1 antibodies. However, a substantial fraction of MSI CRCs do not respond to ICIs. Recent studies have identified the DNA helicase WRN as a synthetic lethal target in MSI cancer cells, leading to the development of several small-molecule WRN inhibitors that are currently in clinical trials. In this study, we found that targeting WRN in MSI CRC cells triggered a robust antitumor immune response. Cell death induced by WRN inhibition was selective in MSI CRC cells and led to the release of extrachromosomal circular DNA (eccDNA), which directly stimulated immune cell activation and cytokine production. The deletion of nuclear ligase LIG3, a key mediator of eccDNA biogenesis, abolished the antitumor and immunogenic effects of WRN inhibition in MSI CRC cells and tumors. Furthermore, WRN inhibition potentiated anti-PD-1 therapy in MSI CRC models, including syngeneic mouse tumors and patient-derived tumor organoids. Together, these results reveal eccDNA-mediated immunogenic effects of WRN inhibition in MSI CRC, further strengthening the rationale for combining WRN inhibitors with ICIs. - Source: PubMed
Publication date: 2026/07/16
Hao SuisuiSato YoshiakiLiu ZhaojinLizardo DarlenyLu XinyanLenz Heinz-JosefSchoen Robert EYu JianZhang Lin