P
Pavel Kovarik
Researcher at Max F. Perutz Laboratories
Publications - 63
Citations - 6196
Pavel Kovarik is an academic researcher from Max F. Perutz Laboratories. The author has contributed to research in topics: Innate immune system & Phosphorylation. The author has an hindex of 36, co-authored 60 publications receiving 5653 citations. Previous affiliations of Pavel Kovarik include University of Vienna.
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Journal ArticleDOI
Serine phosphorylation of STATs
Thomas Decker,Pavel Kovarik +1 more
TL;DR: This review addresses recent advances in understanding the regulation of STAT serine phosphorylation, as well as the kinases and other signal transducers implied in this process.
Journal ArticleDOI
Partial Impairment of Cytokine Responses in Tyk2-Deficient Mice
Marina Karaghiosoff,Hans Neubauer,Caroline Lassnig,Pavel Kovarik,Heike Schindler,Hanspeter Pircher,Barbara McCoy,Christian Bogdan,Thomas Decker,Gottfried Brem,Klaus Pfeffer,Mathias Müller,Mathias Müller +12 more
TL;DR: Tyk2-/- mice are unable to clear vaccinia virus and show a reduced T cell response after LCMV challenge, which imply a selective contribution of Tyk2 to the signals triggered by various biological stimuli and cytokine receptors.
Journal ArticleDOI
GAS elements: a few nucleotides with a major impact on cytokine-induced gene expression.
TL;DR: This review focuses on the identification and definition of GAS elements, their interaction with Stat transcription factors, and their contribution to the specificity of cytokine-induced gene expression.
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Central role for type I interferons and Tyk2 in lipopolysaccharide-induced endotoxin shock.
Marina Karaghiosoff,Ralf Steinborn,Pavel Kovarik,Gernot Kriegshäuser,Manuela Baccarini,Birgit Donabauer,Ursula Reichart,Thomas Kolbe,Christian Bogdan,Tomas Leanderson,David E. Levy,Thomas Decker,Mathias Müller +12 more
TL;DR: It is reported that mice devoid of the JAK protein tyrosine kinase family member, Tyk2, were resistant to shock induced by high doses of LPS, and IFN-β–null but not STAT1-null mice were also resistant to high dose LPS treatment, suggesting thatTyk2 and IFn-β are essential effectors in LPS induced lethality.
Journal ArticleDOI
Stress-induced phosphorylation of STAT1 at Ser727 requires p38 mitogen-activated protein kinase whereas IFN-gamma uses a different signaling pathway.
Pavel Kovarik,Dagmar Stoiber,Patrick A. Eyers,Rossella Menghini,Armin Neininger,Matthias Gaestel,Philip Cohen,Thomas Decker +7 more
TL;DR: The data suggest that STAT1 is phosphorylated at Ser727 by a stress-activated signaling pathway either through p38 MAPK directly or through an unidentified kinase downstream of p38MAPK.