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H. Peter Rodemann

Researcher at University of Tübingen

Publications -  94
Citations -  9630

H. Peter Rodemann is an academic researcher from University of Tübingen. The author has contributed to research in topics: Phosphorylation & Protein kinase B. The author has an hindex of 37, co-authored 93 publications receiving 8369 citations. Previous affiliations of H. Peter Rodemann include German Cancer Research Center.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Radiation-induced epidermal growth factor receptor nuclear import is linked to activation of DNA-dependent protein kinase

Klaus Dittmann, +8 more
- 02 Sep 2005 - 
TL;DR: The data implicate a novel function of the EGFR during DNA repair processes and radiation-induced activation of DNA-PK, inhibited DNA repair, and increased radiosensitivity of treated cells.
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Cellular basis of radiation-induced fibrosis

H. Peter Rodemann, +1 more
- 01 May 1995 - 
TL;DR: The cellular mechanism of radiation-induced fibrosis can be seen as a multicellular process involving various interacting cell systems in the target organ resulting in the fibrotic phenotype of the fibroblast/fibrocyte cell system.
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Autophagy contributes to resistance of tumor cells to ionizing radiation

Hassan Chaachouay, +5 more
- 01 Jun 2011 - 
TL;DR: The data clearly indicate that radioresistant breast tumor cells show a strong post-irradiation induction of autophagy, which thus serves as a protective and pro-survival mechanism in radioresistance.
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Blockage of epidermal growth factor receptor-phosphatidylinositol 3-kinase-AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair.

Mahmoud Toulany, +8 more
- 01 Jul 2006 - 
TL;DR: Targeting of the EGFR-dependent PI3K-AKT pathway in K-RAS-mutated A549 cells significantly affects postradiation survival by affecting the activation of DNA-PKcs, resulting in a decreased DSB repair capacity.