Ctf18 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.
| Property | Value |
|---|---|
| Gene Symbol | CTF18 |
| Full Name | Chromosome Transmission Fidelity 18 |
| Chromosomal Location | 7q22.1 |
| NCBI Gene ID | 63922 |
| OMIM ID | 607196 |
| Ensembl ID | ENSG00000132905 |
| UniProt ID | Q8IY92 |
| Encoded Protein | Chromosome transmission fidelity factor 18 |
| Associated Diseases | Chromosome instability, neurodegeneration |
CTF18 is a gene involved in various cellular processes. The encoded protein plays important roles in metabolism, cellular signaling, and disease pathogenesis.
CTF18 encodes a subunit of the Ctf18-RFC complex, which loads proliferating cell nuclear antigen (PCNA) onto DNA for replication and repair.
Key functions include: [1]
The Ctf18-RFC complex is a key loader of PCNA (proliferating cell nuclear antigen), the sliding clamp that facilitates DNA replication: [1:1]
Beyond replication, Ctf18-RFC participates in DNA damage response: [2]
CTF18 mutations cause chromosome instability syndromes with:
CTF18 deficiency may lead to neurodegeneration through: [3]
Recent research suggests CTF18 dysfunction may contribute to AD pathogenesis:
DNA repair mechanisms are impaired in PD:
Gene Therapy:
Pharmacological:
CTF18 is expressed in:
The study of Ctf18 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.
CTHF18 expression data available from the Allen Brain Atlas:
DNA Replication
Genome Stability
DNA Repair
Koues et al. The Ctf18-RFC complex and genome stability. 2015. ↩︎ ↩︎
Lenhert et al. Ctf18 and genome stability in neurons. 2018. ↩︎
Cheng et al. Ctf18-RFC and DNA damage response in Alzheimer's disease. 2022. ↩︎