Genome and disease : 14 tables by Jean-Nicolas Volff

By Jean-Nicolas Volff

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Prof. David N. Cooper Institute of Medical Genetics, Cardiff University Heath Park, Cardiff CF14 4XN (UK) Tel. uk Abeysinghe/Chuzhanova/Cooper 34 Volff J-N (ed): Genome and Disease. Genome Dyn. Basel, Karger, 2006, vol 1, pp 35–52 Nucleotide Excision Repair and Related Human Diseases V. Bergoglio, T. Magnaldo Laboratory of Genetic Instability and Cancer, CNRS, Institut Gustave Roussy, Villejuif, France Abstract Nucleotide excision repair (NER) of DNA-lesions is the most versatile DNA repair mechanism involved in genome maintenance, cell and organismal preservation.

The full NER capacity of XP-V cells explains their nearly normal level of UV-survival and the delayed onset of photo-induced epithelioma in most XP-V patients compared to classical XP patients. Frequency and geographic distribution of XP complementation groups is not uniform worldwide. In Europe and in North Africa the incidence of XP newborns is about 1:250,000 whereas in Japan incidence is 1:40 000 with a prevalence for XP-A complementation group (table 1). Common hallmarks: Clinically, very high skin photosensitivity and a range of cutaneous afflictions of variable extent characterize all xeroderma pigmentosum patients.

Entry of DNA resynthesis factors (DNA polymerases ␦ and ␧, PCNA and RFC) promotes unloading of XPG and ERCC1-XPF from the DNA while RPA remains associated as part of DNA resynthesis apparatus. Finally, DNA ligase I carries out the ligation of the 5Ј-3Ј ends of the synthesized DNA patch [17]. NER Deficiency Syndromes Xeroderma Pigmentosum Genetic heterogeneity: Xeroderma pigmentosum syndrome has been first described by Hebra and Kaposi in 1874. The clinical heterogeneity of XP patients has been suspected to result from genetic heterogeneity for a long time.

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