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Protein-DNA damage interactions are critical for understanding the mechanism of DNA repair and damage response. However, due to the relatively random distributions of UV-induced damage and other DNA bulky adducts, it is challenging to measure the interactions between proteins and these lesions across the genome. To address this issue, we developed a new method named Protein-Associated DNA Damage Sequencing (PADD-seq) that uses Damage-seq to detect damage distribution in chromatin immunoprecipitation-enriched DNA fragments. It is possible to delineate genome-wide protein-DNA damage interactions at base resolution with this strategy. Using PADD-seq, we observed that RNA polymerase II (Pol II) was blocked by UV-induced damage on template strands, and the interaction declined within 2 h in transcription-coupled repair-proficient cells. On the other hand, Pol II was clearly restrained at damage sites in the absence of the transcription-repair coupling factor CSB during the same time course. Furthermore, we used PADD-seq to examine local changes in H3 acetylation at lysine 9 (H3K9ac) around cisplatin-induced damage, demonstrating the method's broad utility. In conclusion, this new method provides a powerful tool for monitoring the dynamics of protein-DNA damage interaction at the genomic level, and it encourages comprehensive research into DNA repair and damage response.
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http://dx.doi.org/10.1093/nar/gkad008 | DOI Listing |
Inflamm Res
September 2025
Department of Cardiology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Cardiovascular diseases (CVDs) are a group of conditions that significantly affect human health and are among the leading causes of death and disability worldwide. Clinical trials and basic research have demonstrated that inflammation plays a pivotal role in the development of CVDs. The inflammasome is a critical component of the innate immune system, involved in various inflammatory responses to pathogens and tissue damage.
View Article and Find Full Text PDFResearch (Wash D C)
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, characterized by a high propensity for metastasis, poor prognosis, and limited treatment options. Research has demonstrated a substantial correlation between the expression of protein arginine N-methyltransferase 1 (PRMT1) and enhanced proliferation, metastasis, and poor outcomes in TNBC. However, the specific role of PRMT1 in lung metastasis and chemoresistance remains unclear.
View Article and Find Full Text PDFExp Neurobiol
August 2025
Institute of Medical Science, Ajou University School of Medicine, Suwon 16499, Korea.
Neural tumors represent diverse malignancies with distinct molecular profiles and present particular challenges due to the blood-brain barrier, heterogeneous molecular etiology including epigenetic dysregulation, and the affected organ's critical nature. KCC-07, a selective and blood-brain barrier penetrable MBD2 (methyl CpG binding domain protein 2) inhibitor, can suppress tumor development by inducing p53 signaling, proven only in medulloblastoma. Here we demonstrate KCC-07 treatment's application to other neural tumors.
View Article and Find Full Text PDFNucleic Acids Res
September 2025
Department of Biosciences & Bioengineering, IIT Bombay, Mumbai 400076, India.
Embryonic stem cells (ESCs), which are susceptible to DNA damage, depend on a robust and highly efficient DNA damage response (DDR) mechanism for their survival. However, the implications of physical force-mediated DNA damage on ESC fate remain unclear. We show that stiffness-dependent spreading of mouse ESCs (mESCs) induces DNA damage through nuclear compression, with DNA damage causing differentiation through Lamin A/C.
View Article and Find Full Text PDFSci China Life Sci
September 2025
The Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Hutchinson-Gilford progeria syndrome (HGPS) is a rare progeroid disorder, and approximately 90% of cases are caused by LMNA mutation that yields the lamin A/C variant progerin. Progerin is toxic, and its clearance and disruption have positive benefits on HGPS cells and mice and even HGPS patients. However, accelerating progerin clearance is still an unaddressed issue.
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