Josef Penninger

ORCID: 0000-0002-8194-3777
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Bone Metabolism and Diseases
  • NF-κB Signaling Pathways
  • Cytokine Signaling Pathways and Interactions
  • Cell Adhesion Molecules Research
  • Immunotherapy and Immune Responses
  • Renin-Angiotensin System Studies
  • Immune Response and Inflammation
  • Apelin-related biomedical research
  • Bone health and treatments
  • Hormonal Regulation and Hypertension
  • Cell death mechanisms and regulation
  • SARS-CoV-2 and COVID-19 Research
  • COVID-19 Clinical Research Studies
  • Epigenetics and DNA Methylation
  • Ubiquitin and proteasome pathways
  • Congenital heart defects research
  • Developmental Biology and Gene Regulation
  • Receptor Mechanisms and Signaling
  • Viral Infections and Immunology Research
  • RNA modifications and cancer
  • interferon and immune responses
  • Melanoma and MAPK Pathways
  • Protein Kinase Regulation and GTPase Signaling

Austrian Academy of Sciences
2016-2025

Institute of Molecular Biotechnology
2016-2025

University of British Columbia
2019-2025

Medical University of Vienna
2020-2025

Helmholtz Centre for Infection Research
2023-2025

Vienna Biocenter
2015-2024

University of Michigan
2024

University of Applied Sciences Upper Austria
2024

BOKU University
2020-2024

Life Science Institute
2022-2023

During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world1,2,3. A new coronavirus (SARS-CoV) was as SARS pathogen4,5,6,7, which triggered pneumonia and acute, often lethal, lung failure8. Moreover, among infected individuals influenza such Spanish flu9,10 emergence disease viruses11,12 have caused high lethality resulting from failure13. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been potential...

10.1038/nm1267 article EN other-oa Nature Medicine 2005-07-10

A novel infectious disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was detected in Wuhan, China, December 2019.The disease (COVID-19) spread rapidly, reaching epidemic proportions and has been found 27 other countries.As of February 27, 2020, over 82,000 cases COVID-19 were reported, with > 2800 deaths.No specific therapeutics are available, current management includes travel restrictions, patient isolation, supportive medical care.There a number...

10.1007/s00134-020-05985-9 article EN cc-by-nc Intensive Care Medicine 2020-03-03

We have previously provided the first genetic evidence that angiotensin converting enzyme 2 (ACE2) is critical receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), and ACE2 protects lung from injury, providing a molecular explanation failure death due to SARS-CoV infections. has now also been identified as key SARS-CoV-2 infections, it proposed inhibiting this interaction might be used in treating patients with COVID-19. However, not known whether human recombinant soluble...

10.1016/j.cell.2020.04.004 article EN cc-by Cell 2020-04-24

Mark A. Lomaga, Wen-Chen Yeh, Ildiko Sarosi, Gordon S. Duncan, Caren Furlonger, Alexandra Ho, Sean Morony, Casey Capparelli, Gwyneth Van, Stephen Kaufman, Annette van der Heiden, Annick Itie, Andrew Wakeham, Wilson Khoo, Takehiko Sasaki, Zhaodan Cao, Josef M. Penninger, Christopher J. Paige, David L. Lacey, Colin R. Dunstan, William Boyle, V. Goeddel, and Tak W. Mak Department of Pharmaceutical Sciences, Faculty Pharmacy, University Toronto, Ontario, Canada M5S 2S2; Amgen Institute, Ontario...

10.1101/gad.13.8.1015 article EN Genes & Development 1999-04-15

Phosphoinositide 3-kinases (PI3Ks) regulate fundamental cellular responses such as proliferation, apoptosis, cell motility, and adhesion. Viable gene-targeted mice lacking the p110 catalytic subunit of PI3Kγ were generated. We show that controls thymocyte survival activation mature T cells but has no role in development or function B cells. PI3Kγ-deficient neutrophils exhibited severe defects migration respiratory burst response to heterotrimeric GTP-binding protein (G protein)–coupled...

10.1126/science.287.5455.1040 article EN Science 2000-02-11
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