Nuclear nucleic acid-binding protein C1D (C1D)

C1D is a small, ubiquitously expressed nuclear protein encoded by the C1D gene that binds both DNA and RNA, serving multiple cellular functions crucial for maintaining genomic stability. It participates in DNA double-strand break repair—acting as an activator and substrate for DNA-dependent protein kinase, and regulates RNA processing through association with RNA exosome subunits. C1D functions additionally as a transcriptional corepressor for nuclear hormone receptors, most notably the thyroid hormone receptor, modulating gene expression. In response to DNA damage that exceeds repair capacity, C1D induces apoptosis, most notably through p53-dependent pathways, supporting its characterization as a tumor suppressor candidate. Its diverse interactions make C1D integral to cellular survival, quality control of nucleic acids, and safeguarding genomic integrity. While not currently a direct drug target, its regulatory roles in apoptosis and DNA repair are being explored for cancer therapy, highlighting its potential as a biomarker for DNA repair proficiency and therapeutic response.

Other names

C1D nuclear receptor corepressorSUN-CoRSUNCORhC1Dnuclear DNA-binding protein C1DC1D DNA-binding proteinsmall unique nuclear receptor corepressor

Indirect: Drugs that modulate DNA damage response (e.g. DNA-PK inhibitors) may alter C1D-mediated apoptosis and repair. Indirect: Proteasome inhibitors may affect C1D protein levels, increasing apoptotic cell death in tumor models. There is no evidence of direct pharmacological targeting.