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DTL facilitates the Fanconi anemia pathway for ultraviolet-induced DNA repair in retinal pigment epithelial cells

JIUCHUN GUO1, JIE PAN2,*, QIANQIAN GUO2
1 Binzhou Second People’s Hospital, Binzhou, 256800, China
2 Department of Ophthalmology, Zibo Central Hospital, Zibo, 255000, China
* Corresponding Author:JIE PAN,
(This article belongs to this Special Issue: Cellular Biomechanics in Health and Diseases)

BIOCELL 2022, 46(2), 505-510. https://doi.org/10.32604/biocell.2021.015785

Received 13 January 2021; Accepted 07 February 2021; Issue published 20 October 2021

Abstract

The excessive energy of light, especially the invisible rays with lower wavelength, is basically absorbed by retinal pigment epithelium (RPE) and usually causes DNA damage. The molecular mechanism behind DNA damage repair response to this frequent stress in RPE is not clearly understood. In this study, we determined that the Fanconi anemia (FA) pathway was activated in human RPE ARPE-19 cells after ultraviolet (UV) B and C treatment. Moreover, immunoprecipitation (IP) of FANCD2 indicated that denticleless E3 ubiquitin protein ligase homolog (DTL) closely interacted with FANCD2. Knockdown of DTL weakened the activity of the FA pathway in ARPE-19 cells responding to UV treatment. Finally, the DTL promoter was incubated with a biotin-labeled probe and pulled down by streptavidin beads followed by the genomic DNA sonication. p53 was indicated by mass spectrum and further determined by chromatin IP assay. Taken together, our results demonstrated that DTL regulated by p53 could activate the FA pathway for UV-induced DNA damage repair in retinal pigment epithelial cells.

Keywords

DTL, Fanconi anemia pathway, Retinal pigment epithelial, p53

Cite This Article

GUO, J., PAN, J., GUO, Q. (2022). DTL facilitates the Fanconi anemia pathway for ultraviolet-induced DNA repair in retinal pigment epithelial cells. BIOCELL, 46(2), 505–510.



This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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