Interplay of the Ubiquitin Proteasome System with Nucleotide Excision Repair
(Samenspel tussen het ubiquitin proteasome systeem en nucleotide excisie herstel)
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Dit proefschrift kwam tot stand binnen de vakgroep Celbiologie en Genetica van de faculteit der Geneeskunde en Gezondheidswetenschappen van de Erasmus Universiteit Rotterdam. De vakgroep maakt deel uit van het Medisch Genetisch Centrum Zuid-West Nederland. Het onderzoek is financieel ondersteund door het Center for Biomedical Genetics, de Koninklijke Nederlandse Akademie van Wetenschappen en de Nederlandse Organisatie voor Wetenschappelijk Onderzoek.
The genetic information stored in the DNA encodes directly or indirectly for all processes important for life. The nucleic acid order of the DNA is (via RNA) translated into proteins. The various proteins have distinct and vital functions that are important for the catalysis of the distinct processes in our cells, furthermore they function in the structures in and outside our cells as well. During the live cycle of every cell a constant challenge from both exogenous as endogenous sources potentially damages both proteins and DNA. Proteins can be easily be replaced by the synthesis of new ones. In contrast however, DNA as the carrier of information itself cannot be replaced and therefore, damage needs to be repaired. Several genome maintenance pathways have evolved that are briefly discussed in chapter2. One of these is the nucleotide excision (NER) repair pathway, which repairs bulky lesions including those induced by the short wave length components of sunlight (UV-C). NER is being discussed in more detail, since this is the main topic of research discussed in this thesis. In NER lesion recognition is either performed by the stalling of the RNA polymerase, leading to the so-called transcription coupled repair subpathway (TC-NER) or by the XPC-complex with the help of the UVDDB complex.
Hoeijmakers, Prof. Dr. J.H.J. (promotor)
- hr 23b
- dna damage
- dna repair
- nucleotide excision repair
- hr 23a