Kyra Michalova
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Kyra Michalova has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Alexander Dejneka
Institute of Physics, Academy of Sciences of the Czech Republic 2 , Na Slovance 2, 18221 Prague
1 shared publication - Barbora Smolková
Department of Optical and Biophysical Systems, Institute of Physics of the Czech Academy of Sciences, 18221 Prague, Czech Republic
1 shared publication - Jan Kubovciak
Laboratory of Genomics and Bioinformatics, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic
1 shared publication - Mariia Lunova
FZU - Institute of Physics of the Czech Academy of Sciences, Prague, 18200, Czech Republic; Institute for Clinical & Experimental Medicine (IKEM), Prague, 14021, Czech Republic
1 shared publication - Mariia Uzhytchak
Department of Optical and Biophysical Systems, Institute of Physics of the Czech Academy of Sciences, 18221 Prague, Czech Republic
1 shared publication - Milan Jirsa
Institute for Clinical & Experimental Medicine (IKEM), Prague, 14021, Czech Republic
1 shared publication
Latest Publications
- Open Access
- 4 March 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (5) , 2560
Expression of Interferons Lambda 3 and 4 Induces Identical Response in Human Liver Cell Lines Depending Exclusively on Canonical Signaling
Lambda interferons mediate antiviral immunity by inducing interferon-stimulated genes (ISGs) in epithelial tissues. A common variant rs368234815TT/∆G creating functional gene from an IFNL4 pseudogene is associated with the expression of major ISGs in the liver but impaired clearance of hepatitis C. To explain this, we compared Halo-tagged and non-tagged IFNL3 and IFNL4 signaling in liver-derived cell lines. Transfection with non-tagged IFNL3, non-tagged IFNL4 and Halo-tagged IFNL4 led to a similar degree of JAK-STAT activation and ISG induction; however, the response to transfection with Halo-tagged IFNL3 was lower and delayed. Transfection with non-tagged IFNL3 or IFNL4 induced no transcriptome change in the cells lacking either IL10R2 or IFNLR1 receptor subunits. Cytosolic overexpression of signal peptide-lacking IFNL3 or IFNL4 in wild type cells did not interfere with JAK-STAT signaling triggered by interferons in the medium. Finally, expression profile changes induced by transfection with non-tagged IFNL3 and IFNL4 were highly similar. These data do not support the hypothesis about IFNL4-specific non-canonical signaling and point out that functional studies conducted with tagged interferons should be interpreted with caution.
- 4 March 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (5) , 2560
Open AccessExpression of Interferons Lambda 3 and 4 Induces Identical Response in Human Liver Cell Lines Depending Exclusively on Canonical Signaling
Lambda interferons mediate antiviral immunity by inducing interferon-stimulated genes (ISGs) in epithelial tissues. A common variant rs368234815TT/∆G creating functional gene from an IFNL4 pseudogene is associated with the expression of major ISGs in the liver but impaired clearance of hepatitis C. To explain this, we compared Halo-tagged and non-tagged IFNL3 and IFNL4 signaling in liver-derived cell lines. Transfection with non-tagged IFNL3, non-tagged IFNL4 and Halo-tagged IFNL4 led to a similar degree of JAK-STAT activation and ISG induction; however, the response to transfection with Halo-tagged IFNL3 was lower and delayed. Transfection with non-tagged IFNL3 or IFNL4 induced no transcriptome change in the cells lacking either IL10R2 or IFNLR1 receptor subunits. Cytosolic overexpression of signal peptide-lacking IFNL3 or IFNL4 in wild type cells did not interfere with JAK-STAT signaling triggered by interferons in the medium. Finally, expression profile changes induced by transfection with non-tagged IFNL3 and IFNL4 were highly similar. These data do not support the hypothesis about IFNL4-specific non-canonical signaling and point out that functional studies conducted with tagged interferons should be interpreted with caution.