ATP-dependent 5'-3' DNA helicase, component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. The ATP-dependent helicase activity of XPD/repD is required for DNA opening. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. XPD/repD acts by forming a bridge between CAK and the core-TFIIH complex. ATP + H2O = ADP + H(+) + phosphate Binds 1 [4Fe-4S] cluster. Component of the 7-subunit TFIIH core complex composed of XPB/repB, XPD/repD, gtf2h1, gtf2h2, gtf2h3, gtf2h4 and gtf2h5, which is active in NER. The core complex associates with the 3-subunit CDK-activating kinase (CAK) module composed of cycH/cyclin H, cdk7 and mnat1 to form the 10-subunit holoenzyme (holo-TFIIH) active in transcription. Levels accumulate after the removal of the food source and increase with the onset of development (expression peaks at 3-4 hours of development and decreases to a low baseline level by 7 hours). Expression remain elevated during chemotaxis and formation of multicellular assemblies, and then return to baseline levels for the rest of the development. Up-regulated in response to DNA damage due to UV light or exposure to cisplatin. Unaffected by exposure to hydrogen peroxide. Belongs to the helicase family. RAD3/XPD subfamily.