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Anita C. Truttmann

Researcher at University of Lausanne

Publications -  36
Citations -  6805

Anita C. Truttmann is an academic researcher from University of Lausanne. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 19, co-authored 33 publications receiving 6118 citations. Previous affiliations of Anita C. Truttmann include University Hospital of Lausanne.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy 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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Beclin 1-independent autophagy contributes to apoptosis in cortical neurons.

TL;DR: Beclin 1-independent autophagy is an important contributor to both the caspase-dependent and -independent components of neuronal apoptosis and may be considered as an important therapeutic target in neural conditions involving apoptosis.
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Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury.

TL;DR: Findings reveal that selective neuronal deletion of Atg7 is strongly protective against neuronal death and overall brain injury occurring after HI and suggest that inhibition of HI-enhanced autophagy should be considered as a potential therapeutic target for the treatment of human newborns developing severe hypoxic-ischemic encephalopathy.
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Enhancement of autophagic flux after neonatal cerebral hypoxia-ischemia and its region-specific relationship to apoptotic mechanisms.

TL;DR: A role of enhanced autophagy in delayed neuronal death after severe hypoxia-ischemia that is differentially linked to apoptosis according to the cerebral region is suggested.
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Involvement of autophagy in hypoxic-excitotoxic neuronal death

TL;DR: Results clearly show a death-mediating role of autophagy in hypoxic-excitotoxic conditions and suggest that inhibition of Autophagy should be considered as a neuroprotective strategy in HI brain injuries.