M
Markus Löbrich
Researcher at Technische Universität Darmstadt
Publications - 109
Citations - 16221
Markus Löbrich is an academic researcher from Technische Universität Darmstadt. The author has contributed to research in topics: DNA repair & Homologous recombination. The author has an hindex of 56, co-authored 107 publications receiving 15057 citations. Previous affiliations of Markus Löbrich include University of California, Berkeley & Lawrence Berkeley National Laboratory.
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Journal ArticleDOI
Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses
Kai Rothkamm,Markus Löbrich +1 more
TL;DR: Evidence is presented that foci of γ-H2AX (a phosphorylated histone), detected by immunofluorescence, are quantitatively the same as DSBs and are capable of quantifying the repair of individual D SBs, allowing the investigation of DSB repair after radiation doses as low as 1 mGy, an improvement by several orders of magnitude over current methods.
Journal ArticleDOI
Pathways of DNA double-strand break repair during the mammalian cell cycle.
TL;DR: It is shown here that NHEJ-defective hamster cells (CHO mutant V3 cells) have strongly reduced repair in all cell cycle phases after 1 Gy of irradiation, and HR is particularly important in late S/G2, where both pathways contribute to repair and radioresistance.
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ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation.
TL;DR: It is shown that under most normal growth conditions, IR-induced H2AX phosphorylation can be carried out by ATM and DNA-PK in a redundant, overlapping manner.
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A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci.
Enriqueta Riballo,Martin Kühne,Nicole Rief,Aidan J. Doherty,Graeme C. M. Smith,Marı́a-José Recio,Caroline Reis,Kirsten Dahm,Andreas Fricke,Andrea Krempler,Antony R. Parker,Stephen P. Jackson,Andrew R. Gennery,Penny A. Jeggo,Markus Löbrich +14 more
TL;DR: It is shown that ataxia telangiectasia mutated protein (ATM) and Artemis, the protein defective in patients with RS-SCID, function in a common double-strand break repair pathway that also requires H2AX, 53BP1, Nbs1, Mre11, and DNA-PK.
Journal ArticleDOI
ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin.
Aaron A. Goodarzi,Angela T. Noon,Dorothee Deckbar,Yael Ziv,Yosef Shiloh,Markus Löbrich,Penny A. Jeggo +6 more
TL;DR: It is shown that < or =25% of DSBs require ATM signaling for repair, and this percentage correlates with increased chromatin but not damage complexity, which suggests that the importance of ATM signalling for DSB repair increases as the heterochromatic component of a genome expands.