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Péter Gál
Hungarian Academy of Sciences
Complement systemMolecular biologyLectin pathwayBiochemistryBiology
161Publications
32H-index
3,013Citations
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Publications 157
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#1Ditmer T. TalsmaH-Index: 3
#2Felix PoppelaarsH-Index: 8
Last. Marc A. SeelenH-Index: 23
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#1Márta L. Debreczeni (Semmelweis University)H-Index: 3
#2Inna SzekacsH-Index: 8
Last. Róbert Horváth (Semmelweis University)
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Tissue-on-a-chip technologies are more and more important in the investigation of cellular function and in the development of novel drugs by allowing the direct screening of substances on human cells. Constituting the inner lining of vessel walls, endothelial cells are the key players in various physiological processes, moreover, they are the first to be exposed to most drugs currently used. However, to date, there is still no appropriate technology for the label-free, real-time and high-through...
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#1V. Michael Holers (Anschutz Medical Campus)H-Index: 69
#2Anna BorodovskyH-Index: 10
Last. Dhruv DesaiH-Index: 2
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The complement system plays an important role in the pathogenesis of rheumatoid arthritis (RA). Besides driving lectin pathway (LP) activation, the mannan-binding lectin (MBL)-associated serine proteases (MASPs) also play a key role in regulating the alternative pathway (AP). We evaluated the effects of N-acetylgalactosamine (GalNAc)-conjugated MASP-1 and MASP-2 duplexes in vitro and in mice with and without arthritis to examine whether knockdown of MASP-1 and MASP-2 expression affects the devel...
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#1Zoltán Attila Nagy (ELTE: Eötvös Loránd University)H-Index: 1
#2Dávid Szakács (ELTE: Eötvös Loránd University)H-Index: 3
Last. Gábor Pál (ELTE: Eötvös Loránd University)H-Index: 22
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Ecotin is a serine protease inhibitor produced by hundreds of microbial species, including pathogens. Here we show, that ecotin orthologs from Escherichia coli, Yersinia pestis, Pseudomonas aeruginosa and Leishmania major are potent inhibitors of MASP-1 and MASP-2, the two key activator proteases of the complement lectin pathway. Factor D is the key activator protease of another complement activation route, the alternative pathway. We show that ecotin inhibits MASP-3, which is the sole factor D ...
1 CitationsSource
#1Péter Gál (MTA: Hungarian Academy of Sciences)H-Index: 32
#2József Dobó (MTA: Hungarian Academy of Sciences)H-Index: 23
Last. Gábor Pál (ELTE: Eötvös Loránd University)H-Index: 22
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#1Katalin SzilágyiH-Index: 8
#2István HajdúH-Index: 9
Last. György Dormán (University of Szeged)H-Index: 13
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The complement system is associated with various diseases such as inflammation or auto-immune diseases. Complement-targeted drugs could provide novel therapeutic intervention against the above diseases. C1s, a serine protease, plays an important role in the CS and could be an attractive target since it blocks the system at an early stage of the complement cascade. Designing C1 inhibitors is particularly challenging since known inhibitors are restricted to a narrow bioactive chemical space in add...
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#1Lorenz Jenny (University of Bern)H-Index: 5
#2Danilo Noser (University of Bern)
Last. Verena Schroeder (University of Bern)H-Index: 21
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Abstract Background The lectin pathway serine protease mannan-binding lectin-associated serine protease 1 (MASP-1) has been demonstrated to be a major link between complement and coagulation, yet little is known about its interactions with the fibrinolytic system. The aim of this work was to assess the effects of MASP-1 on fibrin clot lysis in different experimental settings. Methods Rotational thrombelastometry was used to evaluate the effect of MASP-1 on the lysis of clots formed in whole bloo...
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#1Dávid Szakács (ELTE: Eötvös Loránd University)H-Index: 3
#2Andrea Kocsis (MTA: Hungarian Academy of Sciences)H-Index: 7
Last. Gábor Pál (ELTE: Eötvös Loránd University)H-Index: 22
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1 CitationsSource
#1Márta L. Debreczeni (Semmelweis University)H-Index: 3
#2Zsuzsanna Németh (Semmelweis University)H-Index: 7
Last. László Cervenak (Semmelweis University)H-Index: 21
view all 14 authors...
Pathologically increased vascular permeability is an important dysfunction in the pathomechanism of life-threatening conditions, such as sepsis, ischemia/reperfusion or hereditary angioedema (HAE), diseases accompanied by uncontrolled activation of the complement system. HAE for example is caused by the deficiency of C1-inhibitor (the main regulator of early complement activation), which leads to edematous attacks threatening with circulatory collapse. We have previously reported that endothelia...
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