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Target intelligence / Profile preview
HIV-1 Tat specific factor 1 (HTATSF1)
- Target
- HTATSF1
- Molecular classification
- Transcription cofactor, Splicing factor, Component of the spliceosome (17S U2 snRNP complex), RNA-binding protein, DNA repair factor
01
Overview
HIV-1 Tat specific factor 1 (HTATSF1) is a human protein acting as a multifunctional RNA-binding cofactor. It is essential for efficient HIV-1 transcription, acting by interacting with the viral Tat protein to stimulate transcriptional elongation from the HIV-1 promoter (TAR element). HTATSF1 is also a component of the 17S U2 snRNP complex, where it participates in early spliceosome assembly, intron retention, and branch site recognition during pre-mRNA splicing. In addition, HTATSF1 plays a role in the repair of double-strand DNA breaks via homologous recombination. It is considered an HIV dependency factor but is not currently a direct therapeutic target, likely due to its critical cellular functions in gene expression and maintenance.
- Other names
- Tat-SF1TAT-SF1TATSF1dJ196E23.217S U2 SnRNP complex component HTATSF1HIV Tat-specific factor 1
02
Mechanism of action
No clinically established direct-acting drugs; in principle, inhibition would impair HIV-1 transcription and replication by blocking Tat-dependent elongation
03
Biological functions
Regulation of transcriptional elongation (as a cofactor for HIV-1 Tat; also generally in RNA polymerase II–mediated transcription)Splicing of pre-mRNA, specifically in spliceosome assembly and intron retentionCoupling of transcription and splicingDouble-strand break repair via homologous recombinationRegulation of branch site selection in pre-mRNA splicing
04
Disease associations
Infection (essential host cofactor for HIV-1 replication and gene expression)Potentially implicated in cancers or other diseases tied to transcription/splicing dysregulation (not directly established in available results)
05
Safety considerations
Potential toxicity due to essential roles in cellular transcription and splicing—systemic inhibition could disrupt normal cell gene expression and mRNA processingPotential effects on DNA repair
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