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David A. Leib

Researcher at Dartmouth College

Publications -  108
Citations -  18697

David A. Leib is an academic researcher from Dartmouth College. The author has contributed to research in topics: Herpes simplex virus & Virus. The author has an hindex of 44, co-authored 100 publications receiving 16817 citations. Previous affiliations of David A. Leib include Saint Louis University & Osaka University.

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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.
Journal ArticleDOI

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.
Journal ArticleDOI

HSV-1 ICP34.5 confers neurovirulence by targeting the Beclin 1 autophagy protein.

Anthony Orvedahl, +8 more
- 15 Mar 2007 - 
TL;DR: It is shown that the herpes simplex virus type 1 (HSV-1)-encoded neurovirulence protein ICP34.5 binds to the mammalian autophagy protein Beclin 1 and inhibits its Autophagy function, which is essential for viral Neurovirulence.
Journal ArticleDOI

Regulation of starvation- and virus-induced autophagy by the eIF2α kinase signaling pathway

Zsolt Tallóczy, +7 more
- 08 Jan 2002 - 
TL;DR: Autophagy is a novel evolutionarily conserved function of the eIF2α kinase pathway that is targeted by viral virulence gene products.
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Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9.

Anne Krug, +10 more
- 15 Feb 2004 - 
TL;DR: Though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 orTLR9 are capable of controlling HSV -1 replication in vivo after local infection, demonstrating that TLR 9- and MyD 88-independent pathways in cells other than IPCs can effectively compensate for defective IPC responders.