Polyglutamine expansion in mutant huntingtin disrupts a novel transcription-coupled DNA repair complex, providing an undescribed mechanism of neuronal toxicity and degeneration in Huntington's disease.

Transcription factor proteins play an important role in modulating base damage formation and excision repair at the binding sites in the genome.

Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.

After DNA damage induction, transcription is blocked and XAB2 is released from R-loops allowing a subset of XAB2 molecules to interact with UV-stalled RNAP2 and participating to the TC-NER process.

RNA polymerase recruits the PcrA DNA helicase via a conserved interaction motif in order to remove R-loops and prevent conflicts with replication.

Adult stem cells acquire increased DNA damage as they migrate to a wound site and require active DNA repair mechanisms for normal migration.

Visualization of BRM remodelers engaging their endogenous genomic targets revealed highly transient and dynamic interactions with chromatin, which are fueled by ATP-hydrolysis.

Human genomic DNA contains uracil in the late replicating, constitutive heterochromatic regions, while treatment with drugs perturbing thymidylate biosynthesis shifts the uracil distribution pattern towards the euchromatin in UNG-inhibited cells.

cAMP is identified to play a novel role in regulating DNA demethylation and gene transcription by augmenting the intracellular reactive Fe(II) pool.

HCAR1 knockout mice are unable to initiate brain tissue repair after a hypoxic-ischemic injury.