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Gisela Taucher-Scholz

Researcher at Technische Universität Darmstadt

Publications -  74
Citations -  4094

Gisela Taucher-Scholz is an academic researcher from Technische Universität Darmstadt. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 33, co-authored 73 publications receiving 3647 citations. Previous affiliations of Gisela Taucher-Scholz include Darmstadt University of Applied Sciences.

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Factors determining DNA double-strand break repair pathway choice in G2 phase.

TL;DR: It is proposed that NHEJ initially attempts to repair DSBs and, if rapid rejoining does not ensue, then resection occurs promoting repair by HR, and novel roles for ATM in regulating DSB end resection are identified.
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Autophosphorylation of DNA-PKCS regulates its dynamics at DNA double-strand breaks

TL;DR: A model in which DNA-PKCS phosphorylation/autophosphorylation facilitates NHEJ by destabilizing the interaction of DNA- PKCS with the DNA ends is suggested.
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DNA double-strand breaks in heterochromatin elicit fast repair protein recruitment, histone H2AX phosphorylation and relocation to euchromatin

TL;DR: This work demonstrates that H2AX is early phosphorylated within HC, but the damage site is subsequently expelled from the center to the periphery of chromocenters within ∼20 min, and describes a local decondensation of HC at the sites of ion hits, potentially allowing for DSB movement via physical forces.
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Autophosphorylation and ATM Activation: ADDITIONAL SITES ADD TO THE COMPLEXITY*

TL;DR: This work targeted the ATM phosphorylation sites, Ser367 and Ser2996, for further study by generating phosphospecific antibodies against these sites and demonstrated thatosphorylation of both was rapidly induced by radiation, providing further support for the importance of autophosphorylated in the activation and function of ATM in vivo.
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Live cell microscopy analysis of radiation-induced DNA double-strand break motion

TL;DR: The hypothesis that spatial proximity of DNA breaks is required for the formation of radiation-induced chromosomal exchanges is supported, as long-range displacements of damaged chromatin domains do not generally occur during DNA double-strand break repair after introduction of multiple damaged sites by charged particles.