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Andras Kapus
Researcher at University of Toronto
Publications - 145
Citations - 10462
Andras Kapus is an academic researcher from University of Toronto. The author has contributed to research in topics: Phosphorylation & Proto-oncogene tyrosine-protein kinase Src. The author has an hindex of 57, co-authored 137 publications receiving 9729 citations. Previous affiliations of Andras Kapus include University Health Network & Toronto General Hospital.
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Journal ArticleDOI
TGF-β1 regulates the expression and transcriptional activity of TAZ protein via a Smad3-independent, myocardin-related transcription factor-mediated mechanism.
Maria Zena Miranda,Maria Zena Miranda,Janne Folke Bialik,Janne Folke Bialik,Pam Speight,Qinghong Dan,Tony Yeung,Katalin Szászi,Stine F. Pedersen,Andras Kapus +9 more
TL;DR: The results uncover an important aspect of the cross-talk between TGF β and Hippo signaling, showing that TGFβ induces TAZ via a Smad3-independent, p38- and MRTF-mediated and yet MRTF translocation-independent mechanism.
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Regulation of the epithelial Na(+) /H(+) exchanger isoform by the cytoskeleton.
TL;DR: Members of the Na+/H+ exchanger (NHE) family mediate electroneutral countertransport of H+ for Na+ across cellular membranes and mediate transepithelial Na+ transport processes and housekeeping functions such as the regulation of cellular and organellar pH and volume.
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In vivo and in vitro modulation of intercellular adhesion molecule (ICAM)-1 expression by hypertonicity.
George Oreopoulos,Julia E. Hamilton,Sandro Rizoli,Jie Fan,Z. Lu,Yue Hua Li,John Marshall,Andras Kapus,Ori D. Rotstein +8 more
TL;DR: Hypertonicity modulates endothelial ICAM-1 expression as one possible protective mechanism against I/R injury and minimizes PMN-mediated injury.
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Oxidative Stress Reprograms Lipopolysaccharide Signaling via Src Kinase-dependent Pathway in RAW 264.7 Macrophage Cell Line
Rachel G. Khadaroo,Andras Kapus,Kinga A. Powers,Myron I. Cybulsky,John C. Marshall,Ori D. Rotstein +5 more
TL;DR: These studies show that oxidant stress is able to augment macrophage responsiveness to LPS as evidenced by earlier and increased NF-κB translocation, and provide a novel potential mechanism whereby oxidants might prime alveolar macrophages for altered responsiveness to subsequent inflammatory stimuli and suggest different cellular targets for immunomodulation following ischemia/reperfusion.
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Hypertonic resuscitation of hemorrhagic shock upregulates the anti-inflammatory response by alveolar macrophages
TL;DR: HTS resuscitation exerts an immunomodulatory effect on alveolar macrophages by shifting the balance of pro- and counter-inflammatory cytokine production in favor of an anti-inflammatory response.