ArticleScientific reports2025
Inhibition of scheggia/SLC25A1 citrate transporter alleviates XPD deficits.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
XPD is an evolutionarily conserved protein critical for DNA repair, transcription, cell cycle, and chromosome segregation. XPD mutations result in complex genetic diseases, including xeroderma pigmentosum (XP). XPD is also implicated in protecting cells from oxidative stress but has not been linked to specific metabolic gene functions. Here, we report an intriguing genetic interaction between Drosophila Xpd and the scheggia (sea) gene encoding the mitochondrial citrate transporter. We show that the reduced eye size by Xpd RNAi in Drosophila is partially restored by the knockdown of sea. sea RNAi suppresses ectopic cell death and DNA damages resulting from Xpd knockdown. To test whether this negative relationship between Xpd and sea can be recapitulated in human cells, we examined the effects of CTPI-2, an inhibitor of the human citrate transporter SLC25A1, on the survival of XPD mutant cells (HD2) carrying the R683W point mutation (XPD
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