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000145040 0247_ $$2ISSN$$a1420-682X
000145040 0247_ $$2ISSN$$a1420-9071
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000145040 037__ $$aDZNE-2020-00400
000145040 041__ $$aEnglish
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000145040 1001_ $$0P:(DE-HGF)0$$aSahaboglu, Ayse$$b0$$eCorresponding author
000145040 245__ $$aDrug repurposing studies of PARP inhibitors as a new therapy for inherited retinal degeneration.
000145040 260__ $$aCham (ZG)$$bSpringer International Publishing AG$$c2020
000145040 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2019-08-26
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000145040 520__ $$aThe enzyme poly-ADP-ribose-polymerase (PARP) has important roles for many forms of DNA repair and it also participates in transcription, chromatin remodeling and cell death signaling. Currently, some PARP inhibitors are approved for cancer therapy, by means of canceling DNA repair processes and cell division. Drug repurposing is a new and attractive aspect of therapy development that could offer low-cost and accelerated establishment of new treatment options. Excessive PARP activity is also involved in neurodegenerative diseases including the currently untreatable and blinding retinitis pigmentosa group of inherited retinal photoreceptor degenerations. Hence, repurposing of known PARP inhibitors for patients with non-oncological diseases might provide a facilitated route for a novel retinitis pigmentosa therapy. Here, we demonstrate and compare the efficacy of two different PARP inhibitors, BMN-673 and 3-aminobenzamide, by using a well-established retinitis pigmentosa model, the rd1 mouse. Moreover, the mechanistic aspects of the PARP inhibitor-induced protection were also investigated in the present study. Our results showed that rd1 rod photoreceptor cell death was decreased by about 25-40% together with the application of these two PARP inhibitors. The wealth of human clinical data available for BMN-673 highlights a strong potential for a rapid clinical translation into novel retinitis pigmentosa treatments. Remarkably, we have found that the efficacy of 3 aminobenzamide was able to decrease PARylation at the nanomolar level. Our data also provide a link between PARP activity with the Wnt/β-catenin pathway and the major intracellular antioxidant concentrations behind the PARP-dependent retinal degeneration. In addition, molecular modeling studies were integrated with experimental studies for better understanding of the role of PARP1 inhibitors in retinal degeneration.
000145040 536__ $$0G:(DE-HGF)POF3-345$$a345 - Population Studies and Genetics (POF3-345)$$cPOF3-345$$fPOF III$$x0
000145040 542__ $$2Crossref$$i2019-08-26$$uhttp://www.springer.com/tdm
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000145040 650_7 $$2NLM Chemicals$$aBenzamides
000145040 650_7 $$2NLM Chemicals$$aPhthalazines
000145040 650_7 $$2NLM Chemicals$$aPoly(ADP-ribose) Polymerase Inhibitors
000145040 650_7 $$08J365YF1YH$$2NLM Chemicals$$a3-aminobenzamide
000145040 650_7 $$09QHX048FRV$$2NLM Chemicals$$atalazoparib
000145040 650_7 $$0EC 2.4.2.30$$2NLM Chemicals$$aPoly(ADP-ribose) Polymerases
000145040 650_2 $$2MeSH$$aAnimals
000145040 650_2 $$2MeSH$$aBenzamides: therapeutic use
000145040 650_2 $$2MeSH$$aDrug Repositioning: methods
000145040 650_2 $$2MeSH$$aHumans
000145040 650_2 $$2MeSH$$aMice
000145040 650_2 $$2MeSH$$aPhthalazines: therapeutic use
000145040 650_2 $$2MeSH$$aPoly(ADP-ribose) Polymerase Inhibitors: therapeutic use
000145040 650_2 $$2MeSH$$aPoly(ADP-ribose) Polymerases: metabolism
000145040 650_2 $$2MeSH$$aRetina: drug effects
000145040 650_2 $$2MeSH$$aRetina: metabolism
000145040 650_2 $$2MeSH$$aRetina: pathology
000145040 650_2 $$2MeSH$$aRetinal Degeneration: drug therapy
000145040 650_2 $$2MeSH$$aRetinal Degeneration: metabolism
000145040 650_2 $$2MeSH$$aRetinal Degeneration: pathology
000145040 650_2 $$2MeSH$$aRetinitis Pigmentosa: drug therapy
000145040 650_2 $$2MeSH$$aRetinitis Pigmentosa: metabolism
000145040 650_2 $$2MeSH$$aRetinitis Pigmentosa: pathology
000145040 7001_ $$aMiranda, Maria$$b1
000145040 7001_ $$aCanjuga, Denis$$b2
000145040 7001_ $$aAvci-Adali, Meltem$$b3
000145040 7001_ $$0P:(DE-2719)2812754$$aSavytska, Natalia$$b4$$udzne
000145040 7001_ $$aSecer, Enver$$b5
000145040 7001_ $$aFeria-Pliego, Jessica Abigail$$b6
000145040 7001_ $$aKayık, Gülru$$b7
000145040 7001_ $$aDurdagi, Serdar$$b8
000145040 77318 $$2Crossref$$3journal-article$$a10.1007/s00018-019-03283-2$$b : Springer Science and Business Media LLC, 2019-08-26$$n11$$p2199-2216$$tCellular and Molecular Life Sciences$$v77$$x1420-682X$$y2019
000145040 773__ $$0PERI:(DE-600)1458497-9$$a10.1007/s00018-019-03283-2$$gVol. 77, no. 11, p. 2199 - 2216$$n11$$p2199-2216$$tCellular and molecular life sciences$$v77$$x1420-682X$$y2020
000145040 8564_ $$uhttps://pub.dzne.de/record/145040/files/DZNE-2020-00400_Restricted.pdf
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000145040 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812754$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b4$$kDZNE
000145040 9131_ $$0G:(DE-HGF)POF3-345$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lErkrankungen des Nervensystems$$vPopulation Studies and Genetics$$x0
000145040 9141_ $$y2020
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