Magdalena Ganz
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View article: The oncoprotein DEK affects the outcome of PARP1/2 inhibition during mild replication stress
The oncoprotein DEK affects the outcome of PARP1/2 inhibition during mild replication stress Open
DNA replication stress is a major source of genomic instability and is closely linked to tumor formation and progression. Poly(ADP-ribose)polymerases1/2 (PARP1/2) enzymes are activated in response to replication stress resulting in poly(AD…
View article: The oncoprotein DEK affects the outcome of PARP1/2 inhibition during replication stress
The oncoprotein DEK affects the outcome of PARP1/2 inhibition during replication stress Open
DNA replication stress is a major source of genomic instability and is closely linked to tumor formation and progression. Poly(ADP-ribose)polymerases1/2 (PARP1/2) enzymes are activated in response to replication stress resulting in poly(AD…
View article: The C-terminal domain of p53 orchestrates the interplay between non-covalent and covalent poly(ADP-ribosyl)ation of p53 by PARP1
The C-terminal domain of p53 orchestrates the interplay between non-covalent and covalent poly(ADP-ribosyl)ation of p53 by PARP1 Open
The post-translational modification poly(ADPribosyl)ation (PARylation) plays key roles in genome maintenance and transcription. Both non-covalent poly(ADP-ribose) binding and covalent PARylation control protein functions, however, it is un…
View article: Analyzing structure–function relationships of artificial and cancer-associated PARP1 variants by reconstituting TALEN-generated HeLa<i>PARP1</i>knock-out cells
Analyzing structure–function relationships of artificial and cancer-associated PARP1 variants by reconstituting TALEN-generated HeLa<i>PARP1</i>knock-out cells Open
Genotoxic stress activates PARP1, resulting in the post-translational modification of proteins with poly(ADP-ribose) (PAR). We genetically deleted PARP1 in one of the most widely used human cell systems, i.e. HeLa cells, via TALEN-mediated…