Thymidine glycol Antibody, Clone B29: HRP

Thymidine glycol (TG) is a prominent oxidative DNA lesion formed when deoxythymidine undergoes oxidation, either directly or via reactive intermediates such as thymidine chlorohydrin. As a stable and abundant product of oxidative stress, TG serves as a critical biomarker of DNA damage in both nuclear and mitochondrial genomes. In the context of neuroscience, TG accumulation is increasingly recognized as a contributor to genomic instability in post-mitotic neurons, which are particularly vulnerable to oxidative damage due to high metabolic activity and limited DNA repair capacity. Elevated levels of TG have been detected in aging brain tissue and in neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), where oxidative stress and impaired DNA repair are central pathological features. TG lesions can interfere with DNA replication and transcription, leading to mutations, transcriptional arrest, and activation of DNA damage response pathways. If unrepaired, these lesions may trigger neuronal dysfunction, apoptosis, or chronic inflammation—key drivers of neurodegeneration. Understanding the formation, repair, and biological consequences of thymidine glycol is essential for elucidating the molecular mechanisms underlying neuronal aging and degeneration. As a sensitive indicator of oxidative DNA damage, TG also holds promise as a diagnostic and prognostic biomarker in neurodegenerative disease research.

Cancer | Cell Signaling | DNA Damage and Repair | DNA/RNA | Epigenetics and Nuclear Signaling | Oxidation | Oxidative Stress | Post-translational Modifications

A 1:100 dilution of SMC-611 was sufficient to detect thymidine glycol in human renal cancer tissue by IHC analysis using Goat anti-rabbit IgG:HRP as a secondary antibody.