THO complex subunit 1 (THOC1)

THO complex subunit 1 (THOC1) is a core component of the evolutionarily conserved THO/TREX complex that couples transcription elongation with mRNA processing and nuclear export[1][3]. THOC1 physically interacts with RNA polymerase II during transcription and with factors needed for splicing and mRNA export, ensuring that only fully processed mRNAs are exported from the nucleus[3]. Depletion of THOC1 disrupts transcriptional elongation and mRNA export and leads to the formation of R-loops (DNA-RNA hybrids), contributing to DNA damage and genome instability[1]. THOC1 is implicated in apoptosis regulation via a caspase-6- and BAK1/BCL2L1-dependent pathway (independently of p53) and may play a role in cell cycle checkpoint activation prior to apoptosis[3]. Overexpression of THOC1 is frequently found in cancers, including ovarian, lung, breast, and colon, correlating with tumor invasiveness and progression[5]. Mutations in THOC1 also cause autosomal dominant nonsyndromic deafness DFNA86[1][3]. THOC1 has no known direct drug interactions or specific small-molecule inhibitors currently in clinical use. **Note:** - THOC1 is **not** a classic druggable receptor or enzyme but is increasingly studied due to its central roles in gene expression, genome maintenance, and disease[3][5]. - There is no evidence of any approved drugs targeting THOC1, nor well-established mechanisms of drug action specific to THOC1 inhibition or modulation as of this date[3][5].

Other names

HPR1p84N5P84Nuclear matrix protein p84hTREX84DFNA86tho1