Rad23A Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Rad23A Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
RAD23A (RAD23 Homolog A) is a DNA damage repair gene that encodes a protein involved in nucleotide excision repair (NER) and the [ubiquitin-proteasome system](/mechanisms/ubiquitin-proteasome-system). Located on chromosome 19p13.13, RAD23A encodes a 362-amino acid protein that serves as a molecular adaptor in both DNA repair and protein degradation pathways. The gene is constitutively expressed in all tissues, with particularly high expression in the brain, reflecting the importance of DNA repair and protein quality control in neuronal cells.
Function
RAD23A is a protein involved in nucleotide excision repair (NER) and the ubiquitin-proteasome system. It serves as a receptor for XPC and helps recruit the TFIIH complex to DNA damage sites. RAD23A also interacts with proteasomes and helps deliver ubiquitinated substrates for degradation.
In [neurons](/entities/neurons), RAD23A plays a dual role in DNA repair and protein quality control. Both functions are critical for maintaining neuronal health, as neurons are long-lived cells that must manage accumulated damage over decades.
Disease Associations
Alzheimer's Disease
RAD23A is involved in clearing damaged proteins through the proteasome. Impaired function may contribute to protein aggregation in AD.
Parkinson's Disease
RAD23A-mediated DNA repair and protein quality control are both relevant to PD pathogenesis. [Alpha-synuclein](/proteins/alpha-synuclein) aggregation may be influenced by RAD23A function.
Xeroderma Pigmentosum
While primarily associated with NER genes, RAD23A variants can modify XP severity and neurological manifestations.
Expression
RAD23A is expressed in all brain regions, with high expression in the [hippocampus](/brain-regions/hippocampus) and cerebral [cortex](/brain-regions/cortex). Expression is constitutive and upregulated by DNA damage.
Key Publications
[RAD23A in NER and proteasome (2002)](https://doi.org/10.1016/s0092-8674(02)00710-9)
[DNA repair and protein quality control in AD (2019)](https://doi.org/10.1016/j.neurobiolaging.2019.06.012)
Background
The study of Rad23A Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
External Links
[PubMed](https://pubmed.ncbi.nlm.nih.gov/) - Biomedical literature
[Alzheimer's Disease Neuroimaging Initiative](https://adni.loni.usc.edu/) - Research data
[Allen Brain Atlas](https://brain-map.org/) - Brain gene expression data