Zobrazeno 1 - 10
of 207
pro vyhledávání: '"Manfred Schweiger"'
Publikováno v:
bchm. 389:1327-1332
Fanconi anemia is a fatal, hereditary chromosome instability syndrome of early childhood with progressive pancytopenia and cancer-proneness. Hypersensitivity to alkylating agents points to DNA repair inefficiency. Excess reactive oxygen intermediates
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7f07463ea17cbc9dc6d11b50bc88acd7
https://doi.org/10.1515/bc.2008.151
https://doi.org/10.1515/bc.2008.151
Publikováno v:
Cell Biology International. 29:1032-1037
Mutations in the lamin A gene have been shown, among other defects, to give rise to Hutchinson-Gilford progeria syndrome (HGPS) and to atypical Werner syndrome (WS), both of which are progeroid disorders. Here, we have investigated well-characterized
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dbfb516015eadc40d478f2e98ab9b4b5
https://doi.org/10.1016/j.cellbi.2005.10.011
https://doi.org/10.1016/j.cellbi.2005.10.011
Autor:
Annemarie Poustka, Maria Kontou, Rainer Wittig, Manfred Schweiger, Rainer Will, Monica Hirsch-Kauffmann, Caroline Adelfalk
Publikováno v:
Oncogene. 23:2146-2152
Cancer cells have high levels of thioredoxin (Trx) and of glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Cells from patients with the cancer-prone disease Fanconi anemia (FA) exhibit reduced Trx levels. We found the activity of GAPDH to correlate
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::389c2039afdbe454c6d65c071fe6e9a5
https://doi.org/10.1038/sj.onc.1207334
https://doi.org/10.1038/sj.onc.1207334
Autor:
Manfred Schweiger, Caroline Adelfalk, Maria Kontou, Monica Hirsch-Kauffmann, Maria Helena Ramirez
Publikováno v:
Biological Chemistry. 384:169-174
Fanconi anemia (FA) is a hereditary disease of unknown pathogenic mechanisms, although mutations in seven different genes can be causative. Six of these genes have been cloned and sequenced. Only slight homology to the DNA of any other known gene has
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::270e5e544c903cea790fbeb4783b1697
https://doi.org/10.1515/bc.2003.018
https://doi.org/10.1515/bc.2003.018
Autor:
Maria Helena Ramirez, Manfred Schweiger, Monica Hirsch-Kauffmann, Caroline Adelfalk, Maria Kontou, Werner Ruppitsch
Publikováno v:
Oncogene. 21:2406-2412
The cause of the molecular defect of Fanconi anemia (FA) remains unknown. Cells from patients with FA exert an elevated spontaneous chromosomal instability which is further triggered by mitomycin C. The induced lability is reduced by overexpression o
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e96c62f155925e9849e4b2675ba7640f
https://doi.org/10.1038/sj.onc.1205299
https://doi.org/10.1038/sj.onc.1205299
Publikováno v:
FEBS Letters. 516:239-244
The final step in the biosynthesis of nicotinamide-adenine dinucleotide, a major coenzyme in cellular redox reactions and involved in intracellular signaling, is catalyzed by the enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT). The X-r
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::20b23c50b5a600693ae02bd5264ee260
https://doi.org/10.1016/s0014-5793(02)02556-5
https://doi.org/10.1016/s0014-5793(02)02556-5
Autor:
Manfred Schweiger, Thomas von Zglinicki, Caroline Adelfalk, Violeta Serra, Monica Hirsch-Kauffmann, Mario Lorenz
Publikováno v:
FEBS Letters. 506:22-26
Fanconi anemia (FA) is a fatal inherited disease displaying chromosomal instability, disturbances in oxygen metabolism and a high burden of intracellular radical oxygen species. Oxygen radicals can damage DNA including telomeric regions. Insufficient
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::326fe0e82bc0b52f624d2a9f8cadf328
https://doi.org/10.1016/s0014-5793(01)02869-1
https://doi.org/10.1016/s0014-5793(01)02869-1
Autor:
Dierk Jorcke, Siham M.A. Bakhit, Mathias Ziegler, Christoph Weise, Manfred Schweiger, Andrés Herrero-Yraola, Peter Franke
Publikováno v:
The EMBO Journal. 20:2404-2412
Mitochondrial ADP-ribosylation leads to modification of two proteins of approximately 26 and 53 kDA: The nature of these proteins and, hence, the physiological consequences of their modification have remained unknown. Here, a 55 kDa protein, glutamat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9053498e3dc262fdefe0e00b8148678d
https://doi.org/10.1093/emboj/20.10.2404
https://doi.org/10.1093/emboj/20.10.2404
Autor:
Christoph Weise, Monica Hirsch-Kauffmann, Felicitas Lerner, Mathias Ziegler, Thomas Specht, Shiao Li Oei, Klaus Hennig, Manfred Schweiger, Marc Niere
Publikováno v:
FEBS Letters. 492:95-100
Nicotinamide mononucleotide adenylyl transferase (NMNAT) is an essential enzyme in all organisms, because it catalyzes a key step of NAD synthesis. However, little is known about the structure and regulation of this enzyme. In this study we establish
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e68782612d9426bad0591169c84c29fc
https://doi.org/10.1016/s0014-5793(01)02180-9
https://doi.org/10.1016/s0014-5793(01)02180-9
Publikováno v:
Europe PubMed Central
The nuclear enzyme poly(ADP-ribosyl) transferase (pADPRT) catalyzes the formation of poly(ADP-ribose) from NAD+. Several nuclear proteins and pADPRT itself are targets for the modification by poly(ADP-ribosyl)ation. It is demonstrated here that poly(
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1919dbcb229984c3fd18b56da47ed84c
https://doi.org/10.1006/bbrc.1999.0824
https://doi.org/10.1006/bbrc.1999.0824