Thierry Seroz

Learn More
A protein kinase activity that phosphorylates the C-terminal domain (CTD) of RNA polymerase II and is associated with the basal transcription-repair factor TFIIH (also called BTF2) resides with MO15, a cyclin-dependent protein kinase that was first found to be involved in cell cycle regulation. Using in vivo and in vitro repair assays, we show that MO15 is(More)
In order to unravel the mechanism that regulates transcription of protein-coding genes, we investigated the function of the p44 subunit of TFIIH, a basal transcription factor that is also involved in DNA repair. We have shown previously that mutations in the C terminus of the XPD helicase, another subunit of TFIIH, prevent its regulation by p44 (Coin, F.,(More)
Nucleotide excision repair (NER) removes UV-induced photoproducts and numerous other DNA lesions in a highly conserved 'cut-and-paste' reaction that involves approximately 25 core components. In addition, several other proteins have been identified which are dispensable for NER in vitro but have an undefined role in vivo and may act at the interface of NER(More)
Mutations of the survival motor neurone gene (SMN) are associated with spinal muscular atrophy (SMA), a frequent lethal autosomal recessive disorder. In spite of this, no phenotype-genotype correlation was observed, since the SMN gene is lacking in the majority of patients affected with either the severe form (type I) or the milder forms (types II and III).(More)
TFIIH is a basal transcription factor for protein-coding genes. It contains ERCC2, ERCC3, MO15 and cyclin H, polypeptides implicated in nucleotide excision repair or cell cycle regulation. The dysfunction of TFIIH could result in a large panel of genetic disorders, such as xeroderma pigmentosum, Cockayne's syndrome and trichothiodystrophy. This link between(More)
The localized transcription of several muscle genes at the motor endplate is controlled by the Ets transcription factor GABP. To evaluate directly its contribution to the formation of the neuromuscular junction, we generated transgenic mice expressing a general Ets dominant-negative mutant specifically in skeletal muscle. Quantitative RT-PCR analysis(More)
,* t d&g P. Adamczewski,*t Thierry Seroz,” Wim Vermeulen,* Jean-Pierre Tassan,§ Laurent Schaeffer, * Erich A. Nigg,§ Jan H. J. Hoeijmakers,* and Jean-Marc Egly* *Institut de Gbnetique et de Biologie Mol&ulaire et Cellulaire Centre National de la Recherche Scientifique lnstitut National de la Sante et de la Recherche M6dicale I, rue Laurent Fries 67404(More)
TFIIH is a multiprotein factor involved in transcription and DNA repair and is implicated in DNA repair/transcription deficiency disorders such as xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy. Eight out of the nine genes encoding the subunits forming TFIIH have already been cloned. We report here the identification, cDNA cloning and gene(More)
XPB is a subunit of the basal transcription factor TFIIH, which is also involved in nucleotide excision repair (NER) and potentially in cell cycle regulation. A frameshift mutation in the 3'-end of the XPB gene is responsible for a concurrence of two disorders: xeroderma pigmentosum (XP) and Cockayne's syndrome (CS). We have isolated TFIIH from cells(More)
TFIIH, a multisubunit complex was shown to be involved in several biological fundamental mechanisms of the cell: transcription, nucleotide excision repair and cell cycle regulation. p62 is one of the six subunits that constitutes the core of TFIIH versus the holoenzyme, which contains, in addition, the ternary kinase CAK complex. To gain an insight into the(More)
  • 1