Tag: DNA repair

Protein ADP-ribosylation is an important post-translational modification that uses NAD+ to regulate proteins and cellular pathways. Explore mono- and poly-ADP-ribosylation, PARP enzymes, DNA repair, chromatin regulation, cancer, metabolism, inflammation, and cell death.

Protein SUMOylation is an important post-translational modification that regulates protein activity, localization, stability, molecular interactions, gene expression, DNA repair, and cellular stress responses. Learn about SUMO proteins, Ubc9, SUMO ligases, SENPs, SUMO–ubiquitin crosstalk, and SUMO proteomics.

The DNA damage response is a cellular defense system that detects DNA damage, coordinates repair, regulates cell-cycle checkpoints, and protects the stability of the genome.

ATM is a key protein kinase in the DNA damage response. Discover how it detects DNA double-strand breaks, activates signaling pathways, regulates the cell cycle, and helps maintain genome stability.

ATR is a key protein kinase that protects cells from replication stress and DNA damage. Explore how ATR detects single-stranded DNA, stabilizes replication forks, activates CHK1, and maintains genome stability.

BRCA1 is a central tumour‑suppressor protein that regulates homologous recombination, DNA end resection and checkpoint signalling. By coordinating high‑fidelity DNA repair and protecting replication forks, BRCA1 maintains genome stability and prevents oncogenic transformation.

NBS1, also known as nibrin or NBN, is the regulatory subunit of the MRN complex, the master sensor of DNA…

RAD50 is the structural architect of the MRN complex and an essential stabiliser of DNA double‑strand breaks. Through ATP‑dependent conformational changes and zinc‑hook‑mediated DNA tethering, RAD50 coordinates MRE11 and NBS1 to ensure accurate DNA repair and maintain genome stability.

MRE11 is the core nuclease of the MRN complex and a master regulator of DNA double‑strand break repair. By initiating DNA end resection, activating ATM signalling and stabilising damaged chromosomes, MRE11 plays a central role in maintaining genome stability and preventing chromosomal instability.

The MRN complex, composed of MRE11, RAD50 and NBS1, is the primary sensor of DNA double‑strand breaks and a central regulator of genome stability. By activating ATM, initiating homologous recombination and stabilising damaged chromosomes, MRN safeguards cells against genomic instability and disease.

ATM, ATR, DNA-PK, and p53 are key regulators of the DNA damage response. Learn how these pathways detect DNA damage, coordinate repair, control the cell cycle, and protect genome stability.

DNA-PK is a key component of the DNA damage response that helps repair DNA double-strand breaks through the non-homologous end joining pathway and supports genome stability.

Single‑chain RING finger ubiquitin ligases form an important subgroup of E3 enzymes within the ubiquitin–proteasome system. Unlike multi‑subunit Cullin–RING ligases,…

Genomic instability describes the increased tendency of cells to accumulate genetic alterations due to failures in DNA repair, replication fidelity, and chromosome segregation. It plays a central role in cancer development, ageing, and hereditary disorders.

RING finger ubiquitin ligases are the largest class of E3 enzymes in the ubiquitin–proteasome system, defined by a zinc‑binding cross‑brace RING domain that positions E2~Ub for direct ubiquitin transfer. They regulate essential cellular processes including cell cycle progression, DNA repair, immunity, and neuronal function. Dysregulation of RING and RBR ligases such as MDM2 and Parkin contributes to cancer and neurodegeneration, while modern PROTAC therapeutics harness CRL4^CRBN and CRL2^VHL complexes to redirect ubiquitination toward disease‑associated proteins.