Janin Knop
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Janin Knop has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Harald Wajant
Division of Molecular Internal Medicine Department of Internal Medicine II University Hospital Würzburg Würzburg Germany
1 shared publication - Lazaros Vasilikos
Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland
1 shared publication - Lisanne M. Spilgies
Institute of Experimental Immunology, University of Zurich, CH-8057 Zürich, Switzerland
1 shared publication - Mark D. Robinson
Institute of Molecular Life Sciences and SIB Swiss Institute of Bioinformatics, University of Zurich
1 shared publication - Monica Yabal
Institute of Molecular Immunology, TUM School of Medicine, Technical University of Munich, Munich, Germany
1 shared publication - Philipp Jakob Jost
Division of Oncology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria
1 shared publication
Latest Publications
- Open Access
- 15 February 2019
- Published by Cold Spring Harbor Laboratory in bioRxiv
- p. 550749
TNFR2 induced priming of NLRP3-inflammasome via RIPK1 leads to pyroptosis in XIAP deficient cells
Summary: Recent data suggests that LPS stimulation can trigger inflammasome activation through a TNFR2/TNF/TNFR1 mediated loop inxiap−/−macrophages. Yet, the direct role TNFR2-specific activation plays in the absence of XIAP is unknown. We found TNFR2-specific activation lead to cell death inxiap−/−myeloid cells, particularly in the absence the RING domain. RIPK1/TAK1 kinase activity downstream of TNFR2 resulted in a TNF/TNFR1 cell death independent of necroptosis. TNFR2-specific activation lead to a similar inflammatory NF-kB driven transcriptional profile as TNFR1 activation with the exception of up-regulation of NLRP3 and caspase-11. Activation and up-regulation of the canonical inflammasome was mediated by RIPK1 kinase activity and ROS production. While both RIPK1 kinase activity and ROS production reduced cell death as well as release of IL-1β, the release of IL-18 was not reduced to basal levels. This study supports, targeting TNFR2 specifically to reduce IL-18 release in XIAP deficient (XLP-2) patients.
- 15 February 2019
- Published by Cold Spring Harbor Laboratory in bioRxiv
- p. 550749
Open AccessTNFR2 induced priming of NLRP3-inflammasome via RIPK1 leads to pyroptosis in XIAP deficient cells
Summary: Recent data suggests that LPS stimulation can trigger inflammasome activation through a TNFR2/TNF/TNFR1 mediated loop inxiap−/−macrophages. Yet, the direct role TNFR2-specific activation plays in the absence of XIAP is unknown. We found TNFR2-specific activation lead to cell death inxiap−/−myeloid cells, particularly in the absence the RING domain. RIPK1/TAK1 kinase activity downstream of TNFR2 resulted in a TNF/TNFR1 cell death independent of necroptosis. TNFR2-specific activation lead to a similar inflammatory NF-kB driven transcriptional profile as TNFR1 activation with the exception of up-regulation of NLRP3 and caspase-11. Activation and up-regulation of the canonical inflammasome was mediated by RIPK1 kinase activity and ROS production. While both RIPK1 kinase activity and ROS production reduced cell death as well as release of IL-1β, the release of IL-18 was not reduced to basal levels. This study supports, targeting TNFR2 specifically to reduce IL-18 release in XIAP deficient (XLP-2) patients.