L67 is a potent and specific inhibitor of DNA ligase IIIα (LigIIIα) that preferentially targets mitochondrial LigIIIα resulting in mitochondrial dysfunction.
L67 is a potent and specific inhibitor of DNA ligase IIIα (LigIIIα) that preferentially targets mitochondrial LigIIIα resulting in mitochondrial dysfunction. L67 preferentially targets cancer cell mitochondria resulting in enhanced ROS production and caspase 1-dependent apoptosis. L67 in combination with PARP inhibitors decreases survival rate of therapy resistant breast cancer and leukemia cells.
Based on the crystal structure of human DNA ligase I complexed with nicked DNA, computer-aided drug design was used to identify compounds in a database of 1.5 million commercially available low molecular weight chemicals that were predicted to bind to
Resistance to imatinib (IM) and other tyrosine kinase inhibitors (TKI)s is an increasing problem in leukemias caused by expression of BCR-ABL1. As chronic myeloid leukemia (CML) cell lines expressing BCR-ABL1 utilize an alternative non-homologous end-joining pathway (ALT NHEJ) to repair
Elevated levels of DNA ligase IIIα (LigIIIα) have been identified as a biomarker of an alteration in DNA repair in cancer cells that confers hypersensitivity to a LigIIIα inhibitor, L67, in combination with a poly (ADP-ribose) polymerase inhibitor. Because LigIIIα
Journal of molecular biology, 431(1), 102-110 (2018-05-12)
The efficient site-specific DNA double-strand breaks (DSB) created by CRISPR/Cas9 has revolutionized genome engineering and has great potential for editing hematopoietic stem/progenitor cells (HSPCs). However, detailed understanding of the variables that influence choice of DNA-DSB repair (DDR) pathways by HSPC
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