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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

Extracellular signal-regulated kinase and GEF-H1 mediate depolarization-induced Rho activation and paracellular permeability increase

Faiza Waheed, +5 more
- 17 Mar 2010 - 
TL;DR: The ERK/GEF-H1/Rho/ROK/pMLC pathway could be a central mechanism whereby electrogenic transmembrane transport processes control myosin phosphorylation and regulate paracellular transport in the tubular epithelium.
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Is myosin light-chain phosphorylation a regulatory signal for the osmotic activation of the Na+-K+-2Cl- cotransporter?

Caterina Di Ciano-Oliveira, +6 more
- 23 Feb 2005 - 
TL;DR: Results indicate that an increase in MLC phosphorylation is neither a sufficient nor a necessary signal to stimulate NKCC in tubular cells, however, basal myosin activity plays a permissive role in the optimal osmotic responsiveness of NKCC.
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Hypertonic preconditioning prevents hepatocellular injury following ischemia/reperfusion in mice: a role for interleukin 10.

George Oreopoulos, +8 more
- 01 Jul 2004 - 
TL;DR: Findings define a novel mechanism responsible for the anti‐inflammatory effects of hypertonic saline and also suggest a potential clinical role for hyperosmolar solutions in the prevention of liver injury associated with I/R.
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The Protein Kinase C Cascade Regulates Recruitment of Matrix Metalloprotease 9 to Podosomes and Its Release and Activation

Helan Xiao, +7 more
- 01 Dec 2010 - 
TL;DR: The data suggest that multiple PKC isozymes form a signaling cascade that controls podosome formation and dynamics and MMP-9 recruitment, release, and activation in a coordinated fashion.
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Loss of SMAD3 Promotes Vascular Remodeling in Pulmonary Arterial Hypertension via MRTF Disinhibition

Diana Zabini, +17 more
- 12 Jan 2018 - 
TL;DR: Loss of SMAD3 presents a novel pathomechanism in PAH that promotes vascular cell proliferation and—via MRTF disinhibition—hypertrophy of huPASMCs, thereby reconciling the parallel induction of a synthetic and contractile hu PASMC phenotype.