Abstract
Human Tousled kinase 1 (TLK1) plays an important role in chromatin remodeling, replication, and DNA damage response and repair. TLK1 activity is immediately, but transiently, downregulated after genotoxic insult, and its recovery is important for exit from checkpoint arrest and cell survival after radiation. The data in this article compliments research presented in the paper titled, “Tousled kinase activator, gallic acid, promotes DNA repair and suppresses radiation cytotoxicity in salivary gland cells” [1]. The identification of small molecule activators and inhibitors of TLK1 provided an opportunity to pharmacologically alter the protein׳s activity to elucidate its role in DNA damage response pathways. TLK1 effectors, gallic acid (GA) and thioridazine (THD) activate and inhibit the kinase, respectively, and the data report on the impact of these compounds and the significance of TLK1 to DNA break repair and the survival of human salivary acinar cells.
Highlights
Human Tousled kinase 1 (TLK1) plays an important role in chromatin remodeling, replication, and DNA damage response and repair
The data in this article compliments research presented in the paper titled, “Tousled kinase activator, gallic acid, promotes DNA repair and suppresses radiation cytotoxicity in salivary gland cells” [1]
The repair of DNA double-strand breaks predominantly occurs by nonhomologous end joining (NHEJ), and using a cell-based reporter assay we reported the effect of TLK1 function on NHEJ repair of I-SceI-induced chromosomal breaks
Summary
Graph, figure Olympus Provis AX70 microscope, BD LSR II flow cytometer, BioTek Synergy 4 hybrid microplate reader. Repair of restriction enzyme (I SceI)- induced double strand break was studied in HEK293-PC222 cells. Influence of small molecule TLK1 effectors on cell survival highlight their clinical utility in altering tissue response to radiation. Enhanced TLK1 activity leads to improved DNA break repair kinetics, and an examination of TLK1-. The data in the article demonstrate the effects of small molecule modulators of TLK1 activity in DNA damage response to and repair of radiation-induced DNA breaks. Unrepaired DNA breaks activate apoptosis, and the consequential effect of TLK1 function on cell survival and programmed cell death was demonstrated. The repair of DNA double-strand breaks predominantly occurs by nonhomologous end joining (NHEJ), and using a cell-based reporter assay we reported the effect of TLK1 function on NHEJ repair of I-SceI-induced chromosomal breaks
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