Andreas Pichlmair

Prof. Andreas Pichlmair

orcid

Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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12 April 2021 in Nature
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Journal Article
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ASAlexey Stukalov
Alexey Stukalov
VGVirginie Girault
Virginie Girault
VGVincent Grass
Vincent Grass
OKOzge Karayel
Ozge Karayel
VBValter Bergant
Valter Bergant
APAndreas Pichlmair
Andreas Pichlmair

18 December 2017 in Nature Immunology
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CHCathleen Holze
Cathleen Holze
CMChloé Michaudel
Chloé Michaudel
CMClaire Mackowiak
Claire Mackowiak
DHDarya A. Haas
Darya A. Haas
CBChristian Benda
Christian Benda
APAndreas Pichlmair
Andreas Pichlmair

29 January 2021 in Science
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Journal Article
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SBStefan Bauernfried
Stefan Bauernfried
MSMatthias J. Scherr
Matthias J. Scherr
APAndreas Pichlmair
Andreas Pichlmair
KDKarl E. Duderstadt
Karl E. Duderstadt
VHVeit Hornung
Veit Hornung
A dsRNA detector in the immune toolkit: Nod-like receptor (NLR) proteins recognize pathogen-associated molecular patterns within cells, which triggers the formation of signaling complexes called inflammasomes. These complexes then initiate pyroptosis, a highly inflammatory form of cell death. Recent work has shown that a rhinovirus protease can activate the human NLRP1 inflammasome, but it was unclear whether this is the only pathogen-derived trigger for NLRP1. Bauernfried et al. report that long, double-stranded RNA (dsRNA) generated in the course of Semliki Forest virus infection binds and activates NLRP1 in epithelial cells. dsRNA binding triggered NLRP1 to acquire adenosine triphosphatase (ATPase) activity, a common feature of activated NLR proteins. Thus, in addition to its ability to recognize viral protease activity, human NLRP1 can act as a genuine sensor of virus-associated nucleic acids. Science , this issue p. eabd0811

4 March 2019 in Nature Immunology
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PHPhilipp Hubel
Philipp Hubel
CUChristian Urban
Christian Urban
VBValter Bergant
Valter Bergant
WSWilliam M. Schneider
William M. Schneider
BKBarbara Knauer
Barbara Knauer
APAndreas Pichlmair
Andreas Pichlmair

3 September 2018 in Nature
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PSPietro Scaturro
Pietro Scaturro
ASAlexey Stukalov
Alexey Stukalov
DHDarya A. Haas
Darya A. Haas
MCMirko Cortese
Mirko Cortese
KDKalina Draganova
Kalina Draganova
APAndreas Pichlmair
Andreas Pichlmair

14 July 2020 in Nature Communications
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Journal Article
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SSSepideh Sadegh
Sepideh Sadegh
JMJulian Matschinske
Julian Matschinske
DBDavid B. Blumenthal
David B. Blumenthal
GGGihanna Galindez
Gihanna Galindez
TKTim Kacprowski
Tim Kacprowski
Jan BaumbachJan Baumbach
Jan Baumbach
Coronavirus Disease-2019 (COVID-19) is an infectious disease caused by the SARS-CoV-2 virus. Various studies exist about the molecular mechanisms of viral infection. However, such information is spread across many publications and it is very time-consuming to integrate, and exploit. We develop CoVex, an interactive online platform for SARS-CoV-2 host interactome exploration and drug (target) identification. CoVex integrates virus-human protein interactions, human protein-protein interactions, and drug-target interactions. It allows visual exploration of the virus-host interactome and implements systems medicine algorithms for network-based prediction of drug candidates. Thus, CoVex is a resource to understand molecular mechanisms of pathogenicity and to prioritize candidate therapeutics. We investigate recent hypotheses on a systems biology level to explore mechanistic virus life cycle drivers, and to extract drug repurposing candidates. CoVex renders COVID-19 drug research systems-medicine-ready by giving the scientific community direct access to network medicine algorithms. It is available at https://exbio.wzw.tum.de/covex/.