DNA–protein crosslinks (DPCs) induced by aldehydes interfere with replication and
transcription. Hereditary deficiencies in DPC repair and aldehyde clearance processes …

DNA–protein crosslinks (DPCs) arise from enzymatic intermediates, metabolism or
chemicals like chemotherapeutics. DPCs are highly cytotoxic as they impede DNA-based …

Covalent DNA–protein cross-links (DPCs) are pervasive DNA lesions that challenge
genome stability and can be induced by metabolic or chemotherapeutic cross-linking agents …

The transcription‐coupled repair (TCR) pathway resolves transcription‐blocking DNA
lesions to maintain cellular function and prevent transcriptional arrest. Stalled RNA …

Transcription-coupled nucleotide excision repair (TC-NER) efficiently eliminates DNA
damage that impedes gene transcription by RNA polymerase II (RNA Pol II). TC-NER is …

DNA damage severely impedes gene transcription by RNA polymerase II (Pol II), causing
cellular dysfunction. Transcription-Coupled Nucleotide Excision Repair (TC-NER) …

Transcription-coupled repair (TCR) is the major pathway to remove transcription-blocking
lesions. Although discovered for nearly 40 years, the mechanism and critical players of …

Transcription-coupled DNA repair (TCR) removes bulky DNA lesions impeding RNA
polymerase II (RNAPII) transcription. Recent studies have outlined the stepwise assembly of …

DNA–protein crosslinks (DPCs) are highly toxic DNA lesions that are relevant to multiple
human diseases. They are caused by various endogenous and environmental agents, and …

The nucleoside analogue decitabine (or 5-aza-dC) is used to treat several haematological
cancers. Upon its triphosphorylation and incorporation into DNA, 5-aza-dC induces covalent …