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Eva Szegezdi

Researcher at National University of Ireland, Galway

Publications -  88
Citations -  11610

Eva Szegezdi is an academic researcher from National University of Ireland, Galway. The author has contributed to research in topics: Apoptosis & Receptor. The author has an hindex of 33, co-authored 78 publications receiving 10554 citations. Previous affiliations of Eva Szegezdi include Hungarian Academy of Sciences & University College Hospital.

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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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Mediators of endoplasmic reticulum stress-induced apoptosis.

Eva Szegezdi, +3 more
- 01 Sep 2006 - 
TL;DR: The role of the molecules that are activated during the UPR is examined in order to identify the molecular switch from the adaptive phase to apoptosis and how the activation of these molecules leads to the commitment of death and the mechanisms that are responsible for the final demise of the cell.
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Caspase-12 and ER-stress-mediated apoptosis: the story so far.

Eva Szegezdi, +2 more
- 01 Dec 2003 - 
TL;DR: The complex role of the ER and its signaling pathways provides a novel angle on apoptosis research and may offer a key to apoptosis‐associated diseases.
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TRAIL receptor signalling and modulation: Are we on the right TRAIL?

Devalingam Mahalingam, +4 more
- 01 May 2009 - 
TL;DR: The current status of TRAIL receptor-targeting for cancer therapy, the apoptotic signalling pathway induced by TRAIL receptors, the prognostic implications of TRAils receptor expression and modulation of TRAil sensitivity of tumour cells by combination therapies are addressed.
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Transglutaminase 2-/- mice reveal a phagocytosis-associated crosstalk between macrophages and apoptotic cells.

Zsuzsa Szondy, +16 more
- 24 Jun 2003 - 
TL;DR: It is reported that apoptosis could be induced in TGase2-/- mice; however, the clearance of apoptotic cells was defective during the involution of thymus elicited by dexamethasone, anti-CD3 antibody, or γ-irradiation, and in the liver after induced hyperplasia.