Global ETD Search

1	The transcription factor p53: not a repressor, solely an activator Fischer, Martin 23 March 2015 (has links) (PDF) After almost two decades of research on direct repression by p53, I provide evidence that the transcription factor p53 solely acts as an activator of transcription. I evaluate the prominent models of transcriptional regulation by p53 based on a computational meta-analysis of genome-wide data. With this tool at hand, the major contradiction how p53 binding can result in activation of one target gene and repression of another is resolved. In contrast to most current models, solely genes activated by p53 are found to be enriched for p53 binding. Meta-analysis of large-scale data is unable to confirm reports on directly repressed p53 target genes and does not support models of direct repression. Consequently, as supported by experimental data, p53 is not a direct repressor of transcription, but solely activates its target genes. Moreover, models based on interference of p53 with activating transcription factors are also not supported by the meta-analysis. As an alternative to these models, the meta-analysis leads to the conclusion that p53 represses transcription indirectly by activation of the p53-p21- DREAM/RB pathway. Thus, results of the meta-analysis support only two models, namely activation by direct binding of p53 to target genes and repression through activating the p53-p21-DREAM/RB pathway. p53 Metaanalyse Zellstress Genrepression Zellzyklus p53 meta-analysis cell stress gene repression cell cycle ddc:610
2	Pathomechanismen der sporadischen Einschlusskörperchenmyositis / molekulare Interaktionen zwischen entzündlichem und ß-amyloid-assoziiertem Zellstress im Muskel / Pathomechanism of the sporadic Inclusion body Myositis / molecular interaction between inflammatory and ß-amyloid associated cell stress in the muscle Barthel, Konstanze 22 April 2009 (has links) No description available. 570 Biowissenschaften, Biologie Mathematics and Computer Science beta-Amyloid BACE-1 sIBM Entzündung Degeneration APP Zellstress Myotuben beta-amyloid BACE-1 sIBM inflammation degeneration APP cell stress myotubes W
3	The transcription factor p53: not a repressor, solely an activator Fischer, Martin 12 February 2015 (has links) After almost two decades of research on direct repression by p53, I provide evidence that the transcription factor p53 solely acts as an activator of transcription. I evaluate the prominent models of transcriptional regulation by p53 based on a computational meta-analysis of genome-wide data. With this tool at hand, the major contradiction how p53 binding can result in activation of one target gene and repression of another is resolved. In contrast to most current models, solely genes activated by p53 are found to be enriched for p53 binding. Meta-analysis of large-scale data is unable to confirm reports on directly repressed p53 target genes and does not support models of direct repression. Consequently, as supported by experimental data, p53 is not a direct repressor of transcription, but solely activates its target genes. Moreover, models based on interference of p53 with activating transcription factors are also not supported by the meta-analysis. As an alternative to these models, the meta-analysis leads to the conclusion that p53 represses transcription indirectly by activation of the p53-p21- DREAM/RB pathway. Thus, results of the meta-analysis support only two models, namely activation by direct binding of p53 to target genes and repression through activating the p53-p21-DREAM/RB pathway. info:eu-repo/classification/ddc/610 ddc:610
4	Molekulare Zellstressmechanismen bei der hereditären Einschlusskörpermyopathie / Molecular cell stress mechanisms in hereditary inclusion body myopathy Fischer, Charlotte Viola 05 June 2012 (has links) No description available. 610 Medizin, Gesundheit Medizin Medicine hereditäre Einschlusskörpermyopathie hIBM Nonaka Disease Myopathie Degeneration Zellstress iNOS αB-crystallin hereditary Inclusion Body myopathy hIBM Nonaka Disease myopathy degeneration cell stress iNOS αB-crystallin Medizin

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