Nucleotide excision repair (NER) is a multistep process capable to remove a 
variety of DNA distorting lesions from prokaryotic and eukaryotic genomes. In 
eukaryotic cells, the process requires more than 30 proteins to perform the 
different steps, i.e. recognition of DNA damage, single strand incisions and 
excision of the lesion-containing DNA fragment and DNA repair 
synthesis/ligation. NER can operate via two subpathways: global genome repair 
(GGR) and a specialized pathway coupled to active transcription 
(transcription-coupled repair, TCR) and directed to DNA lesions in the 
transcribed strand of active genes. Both in vivo as well as in cultured cells 
the fast removal of transcription blocking lesions by TCR is crucial to escape 
from lethal effects of inhibited transcription inhibition The most delicate step 
in NER is the recognition of the DNA lesions in their different chromatin 
context and the mechanism of damage recognition in GGR and TCR is principally 
different and requires specific proteins. In GGR, the XPC-HR23B is essential for 
the formation of the incision complex. In TCR the Cockayne syndrome (CS) gene 
products are key players in the recognition of a stalled RNA polymerase the 
presumed signaling structure for repair of transcribed strands. In this study, 
we show that the extent of recovery of UV-inhibited transcription and TCR 
strictly depends on the amount of CSB protein as well as the amount of DNA 
damage present in the cell. This indicates that the ratio between DNA damage 
frequency and CSB protein concentration in the cell is rather critical for acute 
cellular response, i.e. recovery of inhibited transcription upon DNA damage 
infliction, and hence cellular survival.