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R. Roy (Richard), J.P. Adamczewski, T. Seroz, W. Vermeulen (Wim), J-P. Tassan, L. Schaeffer, E.A. Nigg, J.H.J. Hoeijmakers (Jan) and J-M. Egly (Jean-Marc)

1994

The Mo15 cell cycle kinase is associated with the TFIIH transcription-DNA repair factor.

Publication

Publication

Cell , Volume 79 - Issue 6 p. 1093- 1101

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 important for nucleotide excision repair, most likely through its association with TFIIH, thus providing an unexpected link among three important cellular mechanisms.

Additional Metadata
Keywords *Cyclin-Dependent Kinases, *DNA Repair, *Transcription Factors, TFII, *Transcription, Genetic, 0 (Peptide Fragments), 0 (Taf6 protein, Drosophila), 0 (Transcription Factors), 0 (Transcription Factors, TFII), 148710-81-0 (transcription factor TFIIH), Amino Acid Sequence, Cell Cycle/*physiology, Cell Nucleus/metabolism, Comparative Study, EC 2.7.1.37 (Cyclin-Dependent Kinases), EC 2.7.1.37 (Protein-Serine-Threonine Kinases), EC 2.7.1.37 (cyclin-dependent kinase-activating kinase), EC 2.7.7.- (RNA Polymerase II), Human, Molecular Sequence Data, Peptide Fragments/metabolism, Phosphorylation, Protein Binding, Protein-Serine-Threonine Kinases/immunology/isolation & purification/*metabolism, RNA Polymerase II/metabolism, Support, Non-U.S. Gov't, Transcription Factors/immunology/isolation & purification/*metabolism
Persistent URL doi.org/10.1016/0092-8674(94)90039-6, hdl.handle.net/1765/3075
Journal Cell
Organisation Erasmus MC: University Medical Center Rotterdam
Citation
Roy, R., Adamczewski, J. P., Seroz, T., Vermeulen, W., Tassan, J.-P., Schaeffer, L., … Egly, J.-M. (1994). The Mo15 cell cycle kinase is associated with the TFIIH transcription-DNA repair factor. Cell, 79(6), 1093–1101. doi:10.1016/0092-8674(94)90039-6
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