Inhaltszusammenfassung

Hereditary defects in the transcription-coupled nucleotide excision repair (TC-NER) pathway of damaged DNA cause severe neurodegenerative disease Cockayne syndrome (CS), however the origin and chemical nature of the underlying DNA damage had remained unknown. To find out, to which degree the structural properties of DNA lesions determine the extent of transcription arrest in human CS cells, we performed quantitative host cell reactivation analyses of expression vectors containing various synt...Hereditary defects in the transcription-coupled nucleotide excision repair (TC-NER) pathway of damaged DNA cause severe neurodegenerative disease Cockayne syndrome (CS), however the origin and chemical nature of the underlying DNA damage had remained unknown. To find out, to which degree the structural properties of DNA lesions determine the extent of transcription arrest in human CS cells, we performed quantitative host cell reactivation analyses of expression vectors containing various synthetic adducts. We found that a single 3-(deoxyguanosin-N2-yl)-2-acetylaminofluorene adduct (dG(N2)-AAF) constitutes an unsurmountable obstacle to transcription in both CS-A and CS-B cells and is» weiterlesen» einklappen

Autoren

Klassifikation

DFG Fachgebiet:
Grundlagen der Biologie und Medizin

DDC Sachgruppe:
Biowissenschaften, Biologie