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Ute M. Moll

Researcher at Stony Brook University

Publications -  160
Citations -  25186

Ute M. Moll is an academic researcher from Stony Brook University. The author has contributed to research in topics: Cancer & Apoptosis. The author has an hindex of 60, co-authored 156 publications receiving 21183 citations. Previous affiliations of Ute M. Moll include Institut Gustave Roussy & University of Göttingen.

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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Lorenzo Galluzzi, +103 more
TL;DR: A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
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p53 Has a Direct Apoptogenic Role at the Mitochondria

TL;DR: Evidence that p53 translocation to the mitochondria occurs in vivo in irradiated thymocytes is provided and it is shown that the p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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Regulation of autophagy by cytoplasmic p53

TL;DR: Evidence is provided of a key signalling pathway that links autophagy to the cancer-associated dysregulation of p53, which improved the survival of p 53-deficient cancer cells under conditions of hypoxia and nutrient depletion, allowing them to maintain high ATP levels.