Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.1.99.3 (
PRE
)
1,923
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cyclobutane pyrimidine dimers (CPDs) are the most frequent and deleterious lesions generated in the mammalian genome after UV-C irradiation. The persistence of these lesions in DNA can be toxic and mutagenic, and also represents a specific signal to apoptosis. To investigate the CPDs repair in situ and consequent UV-induced apoptosis in human cells, we generated a recombinant adenovirus vector containing the gene encoding a CPD-
photolyase
-EGFP fusion protein (Adphr-EGFP). Adphr-EGFP-infected cells are proficient in photorepair, which prevents apoptotic cell death in comparison with samples kept in the dark, indicating that the fusion protein is functional in CPD recognition and removal. By using local UV irradiation, foci of the
photolyase
fusion protein were observed in UV-damaged areas of the nuclei in colocalization with
NER
enzymes. Phr-EGFP migration to CPD sites and redistribution after photorepair was followed, and shown to present similar kinetics in normal or DNA-repair-deficient cells. To our knowledge, this is the first report of an investigation of CPDs repair in situ employing a CPD-
photolyase
-EGFP enzyme. The Adphr-EGFP vector can be an informative tool to investigate the repair and cellular consequences of UV-induced lesions in primary human cells.
...
PMID:CPD-photolyase adenovirus-mediated gene transfer in normal and DNA-repair-deficient human cells. 1525 27
From the start of the first primitive life forms on earth ultraviolet (UV) light has been a seriously threatening factor. UV light is absorbed by the DNA causing several types of damage that can interfere with transcription and replication. In bacteria a number of different repair mechanisms have evolved to repair these UV-induced lesions. These mechanisms include direct reversal of the damage by a
photolyase
(photoreactivation), removing of the damaged base by a DNA glycosylase (base excision repair, BER), incision of the DNA adjacent to the damage by an endonuclease (UV-damage endonuclease, UVDE) or removal of a complete oligonucleotide containing the damage (nucleotide excision repair,
NER
). This paper presents an inventory of genes encoding enzymes involved in these repair pathways based on the analysis of complete genome sequences of a large number of eubacteria and archaebacteria. From the comparison of homologous sequences between the different species a picture emerges how the repair systems have been transmitted during evolution. In addition, a comparative analysis of amino acid sequences of homologous proteins allows the prediction of specific functions in as yet uncharacterized proteins or protein domains.
...
PMID:Repair of UV damage in bacteria. 1795 Nov 15