Ribosomal protein S3 (rpS3) has endonuclease activity for DNA repair. In particular, rpS3 cleaves the phosphodiester bonds of damaged DNA. In this study, we show that the repair domain of rpS3 spans amino acids 144-189. We fused rpS3 with the transactivator of transcription (TAT) sequence to introduce the rpS3 repair domain into cells. We find that the TAT-rpS3 (aa: 144-189) peptide cleaves UV-induced cyclobutane pyrimidine dimers (CPDs) in cells. We also reveal that the TAT-rpS3 peptide reduces matrix metalloproteinase-1 (MMP-1) induction in UV-irradiated fibroblasts and increases cell migration activity. Taken together, our study suggests that penetration of the rpS3 repair domain into cells can cleave UV-induced CPDs and reduce MMP-1 expression induced by UV.
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http://dx.doi.org/10.1002/1873-3468.13479 | DOI Listing |
Eur Heart J
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai Heart Failure Research Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Background And Aims: Members of the CCN matricellular protein family are crucial in various biological processes. This study aimed to characterize vascular cell-specific effects of CCN5 on neointimal formation and its role in preventing in-stent restenosis (ISR) after percutaneous coronary intervention (PCI).
Methods: Stent-implanted porcine coronary artery RNA-seq and mouse injury-induced femoral artery neointima single-cell RNA sequencing were performed.
EMBO Rep
January 2025
Department of Biochemistry, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Homologous recombination is a largely error-free DNA repair mechanism conserved across all domains of life and is essential for the maintenance of genome integrity. Not only are the mutations in homologous recombination repair genes probable cancer drivers, some also cause genetic disorders. In particular, mutations in the Bloom (BLM) helicase cause Bloom Syndrome, a rare autosomal recessive disorder characterized by increased sister chromatid exchanges and predisposition to a variety of cancers.
View Article and Find Full Text PDFNat Commun
January 2025
Mechanisms, Biomarkers and Models Section - Genome Stability Group, Department of Environment and Health, Istituto Superiore di Sanità, Viale Regina Elena, 299 - 00161, Rome, Italy.
The WRN protein is vital for managing perturbed replication forks. Replication Protein A strongly enhances WRN helicase activity in specific in vitro assays. However, the in vivo significance of RPA binding to WRN has largely remained unexplored.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Area of Bioscience and Biotechnology, School of Materials Science, Japan Advanced Institute of Science and Technology, Asahidai, Nomicity, Ishikawa, Japan. Electronic address:
Site-directed RNA editing (SDRE) holds significant promise for treating genetic disorders resulting from point mutations. Gene therapy, for common genetic illnesses is becoming more popular and, although viable treatments for genetic disorders are scarce, stop codon mutation-related conditions may benefit from gene editing. Effective SDRE generally depends on introducing many guideRNA molecules relative to the target gene; however, large ratios cannot be achieved in the context of gene therapy applications.
View Article and Find Full Text PDFDNA double strand breaks (DSBs) are widely considered the most cytotoxic DNA lesions occurring in cells because they physically disrupt the connectivity of the DNA double helix. Homologous recombination (HR) is a high-fidelity DSB repair pathway that copies the sequence spanning the DNA break from a homologous template, most commonly the sister chromatid. How both DNA ends, and the sister chromatid are held in close proximity during HR is unknown.
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