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Thomas G. Hofmann

Researcher at German Cancer Research Center

Publications -  80
Citations -  9972

Thomas G. Hofmann is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: DNA damage & Phosphorylation. The author has an hindex of 39, co-authored 73 publications receiving 8606 citations. Previous affiliations of Thomas G. Hofmann include Heinrich Pette Institute & Heidelberg University.

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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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Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2

Thomas G. Hofmann, +7 more
- 01 Jan 2002 - 
TL;DR: It is demonstrated that the human serine/threonine kinase homeodomain-interacting protein kinase-2 colocalizes and interacts with p53 and CREB-binding protein (CBP) within promyelocytic leukaemia (PML) nuclear bodies and implies that HIPK2 is a novel regulator of p53 effector functions involved in cell growth, proliferation and apoptosis.
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The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy

Ahmet Ucar, +25 more
- 25 Sep 2012 - 
TL;DR: Pharmacological inhibition of miR-132 by antagomir injection rescues cardiac hypertrophy and heart failure in mice, offering a possible therapeutic approach for cardiac failure.
Journal Article

The Antiinflammatory Sesquiterpene Lactone Parthenolide Inhibits NF-κB by Targeting the IκB Kinase Complex

Steffen P. Hehner, +3 more
- 15 Nov 1999 - 
TL;DR: The sesquiterpene lactone parthenolide could serve as a lead compound for the development of antiinflammatory remedies and is suitable as a molecular tool, allowing the dissection of TNF-α-derived signaling pathways leading to the activation of NF-κB, c-Jun N-terminal kinase, and p38.
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Hydrogen peroxide-induced apoptosis is CD95-independent, requires the release of mitochondria-derived reactive oxygen species and the activation of NF-κB

Andreas Dumont, +5 more
- 21 Jan 1999 - 
TL;DR: This study shows that hydrogen peroxide-induced apoptosis in T-cells did not require tyrosine kinase p56lck, phosphatase CD45, the CD95 receptor and its associated Caspase-8, and that pharmacological and genetic inhibition of transcription factor NF-κB protected cells from hydrogenperoxide-elicited cell death.