Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Telomere shortening is associated with cellular senescence. We investigated whether UVA, which contributes to photoaging, accelerates telomere shortening in human cultured cells. The terminal restriction fragment (TRF) from WI-38 fibroblasts irradiated with UVA (365-nm light) decreased with increasing irradiation dose. Furthermore, UVA irradiation dose-dependently increased the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in both WI-38 fibroblasts and HL-60 cells. To clarify the mechanism of the acceleration of telomere shortening, we investigated site-specific DNA damage induced by UVA irradiation in the presence of endogenous photosensitizers using (32)P 5'-end-labeled DNA fragments containing the telomeric oligonucleotide (TTAGGG)(4). UVA irradiation with riboflavin induced 8-oxodG formation in the DNA fragments containing telomeric sequence, and Fpg protein treatment led to chain cleavages at the central guanine of 5'-GGG-3' in telomere sequence. The amount of 8-oxodG formation in DNA fragment containing telomere sequence [5'-CGC(TTAGGG)(7)CGC-3'] was approximately 5 times more than that in DNA fragment containing nontelomere sequence [5'-CGC(TGTGAG)(7)CGC-3']. Catalase did not inhibit this oxidative DNA damage, indicating no or little participation of H(2)O(2) in DNA damage. These results indicate that the photoexcited endogenous photosensitizer specifically oxidizes the central guanine of 5'-GGG-3' in telomere sequence to produce 8-oxodG probably through an electron-transfer reaction. It is concluded that the site-specific damage in telomere sequence induced by UVA irradiation may participate in the increase of telomere shortening rate.
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PMID:Site-specific DNA damage at the GGG sequence by UVA involves acceleration of telomere shortening. 1129 44

The telomerase complex and Telosome regulate, maintenance and repair telomeres. The telomerase complex is formed by complex of protein (TERT, Dyskerin, GAR, NHP2, NOP10) and nucleic acid (TERC) that together work as a reverse transcriptase. The Telosoma comprises a network of protein (TRF2, TRF1, TIN2, RAP1, TPP1 and POT1). Furthermore, dyskeratosis congenita (DC) (ORPHA1775) is a rare disease with similar characteristics to premature aging. DC is a genetically heterogeneous disease caused by mutations in the genes that encoding for different subunits of the telomerase complex and Telosome. It is known that the telomeric DNA is susceptible to oxidative stress, and telomerase activity dependent cellular redox environment. Recently a correlation between telomerase activity and catalase activity was established, and it has suggested a role of antioxidant extranuclear telomerase. However, it is not yet clear whether there is any relationship or connection between molecular telomerase activity and cellular antioxidant defense. In this paper, by using the technology of RNA interference (siRNA) silencing DKC1, NOP10 genes of telomerase complex and TINF2 of Telosoma in HeLa cells, on cellular antioxidant capacity will be presented. It was intended to see if there is a cellular effect related to the production of oxidative stress or alteration of antioxidant systems after silencing these components involved in telomere maintenance. In this paper we have evaluated the levels of DKC1, NOP10, TINF2 levels of antioxidant enzymes (CuZnSOD, MnSOD, Catalase, Gpx1, Grx1 and Trx1) by RT- qPCR and Western blotting. We analyzed the production of reactive oxygen species by fluorimetry and also assessed the activity of the telomerase complex by Sybr Green RT- QTrap.
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PMID:Characterization of the antioxidant systems in different complementation groups of Dyskeratosis Congenita. 2646 48