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1. THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Enzymes

Author

Alexander, Stephen PH, Fabbro, Doriano, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Sharman, Joanna L, Southan, Christopher, Davies, Jamie A, Beuve, Annie, Boison, Detlev, Brouckaert, Peter, Burnett, John C, Burns, Kathryn, Dessauer, Carmen, Friebe, Andreas, Garthwaite, John, Gertsch, Jürg, Helsby, Nuala, Izzo, Angelo A, Koesling, Doris, Kuhn, Michaela, Ostrom, Rennolds, Papapetropoulos, Andreas, Potter, Lincoln R, Pyne, Nigel J, Pyne, Susan, Russwurm, Michael, Schmidt, Harald HHW, Seifert, Roland, Stasch, Johannes‐Peter, Szabo, Csaba, van der Stelt, Mario, van der Vliet, Albert, and Watts, Val

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Generic health relevance, Animals, Databases, Pharmaceutical, Enzyme Inhibitors, Humans, Hydrolases, Isomerases, Ligands, Ligases, Lyases, Oxidoreductases, Transferases, CGTP Collaborators, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14752. Enzymes are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, ion channels, nuclear hormone receptors, catalytic receptors and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Published
2019

3. The Concise Guide to PHARMACOLOGY 2023/24: Catalytic receptors.

Author

Alexander, Stephen P. H., Fabbro, Doriano, Kelly, Eamonn, Mathie, Alistair A., Peters, John A., Veale, Emma L., Armstrong, Jane F., Faccenda, Elena, Harding, Simon D., Davies, Jamie A., Beuve, Annie, Brouckaert, Peter, Bryant, Clare, Burnett, John C., Farndale, Richard W., Friebe, Andreas, Garthwaite, John, Hobbs, Adrian J., Jarvis, Gavin E., and Koesling, Doris

Subjects
NUCLEAR receptors (Biochemistry), G protein coupled receptors, PHARMACOLOGY, CLINICAL pharmacology, DRUG target, ION channels, DATABASES
Abstract

The Concise Guide to PHARMACOLOGY 2023/24 is the sixth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of approximately 1800 drug targets, and nearly 6000 interactions with about 3900 ligands. There is an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (https://www.guidetopharmacology.org/), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes almost 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point‐in‐time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.16180. Catalytic receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein‐coupled receptors, ion channels, nuclear hormone receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid‐2023, and supersedes data presented in the 2021/22, 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC‐IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate. [ABSTRACT FROM AUTHOR]

Published
2023
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9. THE CONCISE GUIDE TO PHARMACOLOGY 2021/22: Catalytic receptors

Author

Alexander, Stephen P H, primary, Fabbro, Doriano, additional, Kelly, Eamonn, additional, Mathie, Alistair, additional, Peters, John A, additional, Veale, Emma L, additional, Armstrong, Jane F, additional, Faccenda, Elena, additional, Harding, Simon D, additional, Pawson, Adam J, additional, Southan, Christopher, additional, Davies, Jamie A, additional, Beuve, Annie, additional, Brouckaert, Peter, additional, Bryant, Clare, additional, Burnett, John C., additional, Farndale, Richard W., additional, Friebe, Andreas, additional, Garthwaite, John, additional, Hobbs, Adrian J., additional, Jarvis, Gavin E., additional, Kuhn, Michaela, additional, MacEwan, David, additional, Monie, Tom P., additional, Potter, Lincoln R., additional, Schmidt, Harald H.H.W., additional, and Waldman, Scott A., additional

Published
2021
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10. THE CONCISE GUIDE TO PHARMACOLOGY 2021/22: Catalytic receptors

Author

Alexander, Stephen PH, Fabbro, Doriano, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Southan, Christopher, Davies, Jamie A, Beuve, Annie, Brouckaert, Peter, Bryant, Clare, Burnett, John C, Farndale, Richard W, Friebe, Andreas, Garthwaite, John, Hobbs, Adrian J, Jarvis, Gavin E, Kuhn, Michaela, MacEwan, David, Monie, Tom P, Papapetropoulos, Andreas, Potter, Lincoln R, Schmidt, Harald H H W, Szabo, Csaba, Waldman, Scott A, Alexander, Stephen PH, Fabbro, Doriano, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Southan, Christopher, Davies, Jamie A, Beuve, Annie, Brouckaert, Peter, Bryant, Clare, Burnett, John C, Farndale, Richard W, Friebe, Andreas, Garthwaite, John, Hobbs, Adrian J, Jarvis, Gavin E, Kuhn, Michaela, MacEwan, David, Monie, Tom P, Papapetropoulos, Andreas, Potter, Lincoln R, Schmidt, Harald H H W, Szabo, Csaba, and Waldman, Scott A

Abstract

The Concise Guide to PHARMACOLOGY 2021/22 is the fifth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of nearly 1900 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes over 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/bph.15541. Catalytic receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, ion channels, nuclear hormone receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2021, and supersedes data presented in the 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Published
2021

11. Genetic modifiers of hypertension in soluble guanylate cyclase α1-deficient mice

Author

Buys, Emmanuel S., Raher, Michael J., Kirby, Andrew, Mohd, Shahid, Baron, David M., Hayton, Sarah R., Tainsh, Laurel T., Sips, Patrick Y., Rauwerdink, Kristen M., Yan, Qingshang, Tainsh, Robert E.T., Shakartzi, Hannah R., Stevens, Christine, Decaluwe, Kelly, Rodrigues-Machado, Maria da Gloria, Malhotra, Rajeev, de Voorde, Johan Van, Wang, Tong, Brouckaert, Peter, Daly, Mark J., and Bloch, Kenneth D.

Subjects
Blood pressure -- Measurement, Guanylate cyclase -- Properties, Hypertension -- Diagnosis -- Care and treatment -- Genetic aspects, Health care industry
Abstract

Nitric oxide (NO) plays an essential role in regulating hypertension and blood flow by inducing relaxation of vascular smooth muscle. Male mice deficient in a NO receptor component, the α1 subunit of soluble guanylate cyclase (sGCα1), are prone to hypertension in some, but not all, mouse strains, suggesting that additional genetic factors contribute to the onset of hypertension. Using linkage analyses, we discovered a quantitative trait locus (QTL) on chromosome 1 that was linked to mean arterial pressure (MAP) in the context of sGCα1 deficiency. This region is syntenic with previously identified blood pressure-related QTLs in the human and rat genome and contains the genes coding for renin. Hypertension was associated with increased activity of the renin-angiotensin-aldosterone system (RAAS). Further, we found that RAAS inhibition normalized MAP and improved endothelium-dependent vasorelaxation in sGCα1-deficient mice. These data identify the RAAS as a blood pressure-modifying mechanism in a setting of impaired NO/cGMP signaling., Introduction Systemic arterial hypertension is one of the most widespread public health problems in the developed world and the most prevalent modifiable risk factor for cardiovascular disease (CVD) in both [...]

Published
2012
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15. Anaphylactic shock depends on PI3K and eNOS-derived NO

Author

Cauwels, Anje, Janssen, Ben, Buys, Emmanuel, Sips, Patrick, and Brouckaert, Peter

Subjects
Anaphylaxis -- Causes of, Anaphylaxis -- Research, Nitric oxide -- Health aspects, Nitric oxide -- Research
Abstract

Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. Platelet-activating factor (PAF) is implicated in the cardiovascular dysfunctions occurring in various shock syndromes, including anaphylaxis. Excessive production [...]

Published
2006

23. THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein-coupled receptors

Author

Alexander, Stephen PH, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Sharman, Joanna L, Southan, Christopher, Davies, Jamie A, Arumugam, Thiruma V, Bennett, Andrew, Sjogren, Benita, Sobey, Christopher, Wong, Szu Shen, Abbracchio, Maria P, Alexander, Wayne, Al-hosaini, Khaled, Back, Magnus, Beaulieu, Jean-Martin, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel JM, Blaho, Victoria, Bousquet, Corinne, Brauner-Osborne, Hans, Burnstock, Geoffrey, Calo, Girolamo, Castano, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chun, Jerold, Cianciulli, Antonia, Clapp, Lucie H, Couture, Rejean, Csaba, Zsolt, Dent, Gordon, Singh, Khuraijam Dhanachandra, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward, Fong, Tung M, Fumagalli, Marta, Gainetdinov, Raul R, de Gasparo, Marc, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jorg, Hanson, Julien, Hauger, Richard L, Hay, Debbie, Heinemann, Akos, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, Laszlo, Husain, Ahsan, Ijzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kozielewicz, Pawel, Kreienkamp, Hans-Juergen, Kukkonen, Jyrki P, Langenhan, Tobias, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jerome, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence, Mitolo, Vincenzo, Mouillac, Bernard, Murphy, Philip M, Nahon, Jean-Louis, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria A, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric, Ramachandran, Rithwik, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth, Schoeneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie, Thomas, Walter, Timmermans, Pieter BMWM, Tirupula, Kalyan, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Ward, Donald T, Wester, Hans-Juergen, Willars, Gary B, Williams, Tom Lloyd, Woodruff, Trent M, Yao, Chengcan, Aldrich, Richard W, Becirovic, Elvir, Biel, Martin, Catterall, William A, Conner, Alex C, Davies, Paul, Delling, Markus, Di Virgilio, Francesco, Falzoni, Simonetta, George, Chandy, Goldstein, Steve AN, Grissmer, Stephan, Ha, Kotdaji, Hammelmann, Verena, Hanukoglu, Israel, Jarvis, Mike, Jensen, Anders A, Kaczmarek, Leonard K, Kellenberger, Stephan, King, Brian, Lynch, Joseph W, Perez-Reyes, Edward, Plant, Leigh D, Rash, Lachlan D, Ren, Dejian, Sivilotti, Lucia G, Smart, Trevor G, Snutch, Terrance P, Tian, Jinbin, Van den Eynde, Charlotte, Vriens, Joris, Wei, Aguan D, Winn, Brenda T, Wulff, Heike, Xu, Haoxing, Yue, Lixia, Zhang, Xiaoli, Zhu, Michael, Coons, Laurel, Fuller, Peter, Korach, Kenneth S, Young, Morag, Bryant, Clare, Farndale, Richard W, Hobbs, Adrian, Jarvis, Gavin E, MacEwan, David, Monie, Tom P, Waldman, Scott, Beuve, Annie, Boison, Detlev, Brouckaert, Peter, Burnett, John C, Burns, Kathryn, Dessauer, Carmen, Friebe, Andreas, Garthwaite, John, Gertsch, Jurg, Helsby, Nuala, Izzo, Angelo A, Koesling, Doris, Kuhn, Michaela, Ostrom, Rennolds, Papapetropoulos, Andreas, Potter, Lincoln R, Pyne, Nigel J, Pyne, Susan, Russwurm, Michael, Schmidt, Harald HHW, Seifert, Roland, Stasch, Johannes-Peter, Szabo, Csaba, van der Stelt, Mario, van der Vliet, Albert, Watts, Val, Anderson, Catriona MH, Broer, Stefan, Dawson, Paul, Hagenbuch, Bruno, Hammond, James R, Hancox, Jules, Inui, Ken-ichi, Kanai, Yoshikatsu, Kemp, Stephan, Thwaites, David T, Verri, Tiziano, University of Nottingham, UK (UON), Monash university, University of Cambridge [UK] (CAM), University of Bristol [Bristol], University of Greenwich, Ninewells Hospital and Medical School [Dundee], University of Edinburgh, Institut de Génomique Fonctionnelle (IGF), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Drug Design and Pharmacology [Copenhagen] (ILF), Faculty of Health and Medical Sciences, University of Copenhagen = Københavns Universitet (KU)-University of Copenhagen = Københavns Universitet (KU), University of Córdoba [Córdoba], Neuroprotection du Cerveau en Développement / Promoting Research Oriented Towards Early Cns Therapies (PROTECT), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Novartis Institutes for BioMedical Research (NIBR), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Différenciation et communication neuronale et neuroendocrine (DC2N), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), ARVALIS - Institut du végétal [Paris], Laboratoire de Recherche Vasculaire Translationnelle (LVTS (UMR_S_1148 / U1148)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Max Planck Institute for Heart and Lung Research (MPI-HLR), Max-Planck-Gesellschaft, Glaxo Smith Kline [Harlow], University of Antwerp (UA), Neuroendocrinologie cellulaire et moléculaire, European Synchrotron Radiation Facility (ESRF), Experimental Medicine and Immunotherapeutics [Cambridge, UK], Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University [Riyadh] (KSU), Department of Cardiology, Karolinska University Hospital, Karolinska Institutet [Stockholm], Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Department of Medical Sciences, Università degli Studi di Ferrara (UniFE), Department of Pharmacological Sciences and Biomolecular, University of Milan, Department of Molecular Biology Helen L. Dorris, The Scripps Research Institute, Département de Physiologie, Université de Montréal (UdeM), Department of Pharmacology, Université de Sherbrooke (UdeS), Departments of Physiology & Pharmacology, and Medicine [Calgary, Canada] (School of Medicine), University of Calgary, Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Université Paris Diderot - Paris 7 (UPD7)-Université Paris 13 (UP13)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institute of Biochemistry, Medical Faculty, University of Leipzig, Department of Molecular and Biochemical Pharmacology, and Pleinlaan 2

Subjects
0301 basic medicine, RM, Databases, Pharmaceutical, Computer science, Drug classification, Pharmacology, Ligands, Receptors, G-Protein-Coupled, NO, law.invention, 03 medical and health sciences, Databases, G-Protein-Coupled, 0302 clinical medicine, law, Summary information, Receptors, Animals, Humans, Pharmacology & Pharmacy, The Concise Guide to Pharmacology 2019/20, ComputingMilieux_MISCELLANEOUS, G protein-coupled receptor, Clinical pharmacology, Science & Technology, Extramural, POTENT, Pharmaceutical Preparations, 3. Good health, 030104 developmental biology, Pharmaceutical, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Catalytic receptors, Life Sciences & Biomedicine, 030217 neurology & neurosurgery
Abstract

© 2019 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of The British Pharmacological Society. The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14748. G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Published
2019
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25. Human TNF mutants with selective activity on the p55 receptor

Author

Van Ostade, Xaveer, Vandenabeele, Peter, Everaerdt, Bart, Loetscher, Hansruedi, Gentz, Reiner, Brockhaus, Manfred, Lesslauer, Werner, Tavernier, Jan, Brouckaert, Peter, and Fiers, Walter

Subjects
Tumor necrosis factor -- Innovations, Antineoplastic agents -- Innovations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Human tumor necrosis factor (TNF) mutants have been isolated that attach to the human TNF-R55 cell receptor but not to the TNF-R75 receptor. Binding tests involving cell lines from human larynx carcinomas showed that the mutant forms will not bind to both receptors as was the case with previous forms of TNF. The TNF mutants may become powerful tumor-fighting drugs since they cause much less systemic toxicity than earlier TNF.

Published
1993

26. Do-it-yourself: construction of a custom cDNA macroarray platform with high sensitivity and linear range

Author

Vander Beken Seppe, Van den Bergh Rafael, Houthuys Erica, Boonefaes Tom, Raes Geert, Brouckaert Peter, De Baetselier Patrick, and Grooten Johan

Subjects
Biotechnology, TP248.13-248.65
Abstract

Abstract Background Research involving gene expression profiling and clinical applications, such as diagnostics and prognostics, often require a DNA array platform that is flexibly customisable and cost-effective, but at the same time is highly sensitive and capable of accurately and reproducibly quantifying the transcriptional expression of a vast number of genes over the whole transcriptome dynamic range using low amounts of RNA sample. Hereto, a set of easy-to-implement practical optimisations to the design of cDNA-based nylon macroarrays as well as sample 33P-labeling, hybridisation protocols and phosphor screen image processing were analysed for macroarray performance. Results The here proposed custom macroarray platform had an absolute sensitivity as low as 50,000 transcripts and a linear range of over 5 log-orders. Its quality of identifying differentially expressed genes was at least comparable to commercially available microchips. Interestingly, the quantitative accuracy was found to correlate significantly with corresponding reversed transcriptase - quantitative PCR values, the gold standard gene expression measure (Pearson's correlation test p < 0.0001). Furthermore, the assay has low cost and input RNA requirements (0.5 μg and less) and has a sound reproducibility. Conclusions Results presented here, demonstrate for the first time that self-made cDNA-based nylon macroarrays can produce highly reliable gene expression data with high sensitivity and covering the entire mammalian dynamic range of mRNA abundances. Starting off from minimal amounts of unamplified total RNA per sample, a reasonable amount of samples can be assayed simultaneously for the quantitative expression of hundreds of genes in an easily customisable and cost-effective manner.

Published
2011
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30. Nitroglycerine limits infarct size through S-nitrosation of cyclophilin D: a novel mechanism for an old drug

Author

Bibli, Sofia-Iris, primary, Papapetropoulos, Andreas, primary, Iliodromitis, Efstathios K, primary, Daiber, Andreas, primary, Randriamboavonjy, Voahanginirina, primary, Steven, Sebastian, primary, Brouckaert, Peter, primary, Chatzianastasiou, Athanasia, primary, Kypreos, Kyriakos E, primary, Hausenloy, Derek J, primary, Fleming, Ingrid, primary, and Andreadou, Ioanna, primary

Published
2018
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34. The Ability of Nitric Oxide to Lower Intraocular Pressure Is Dependent on Guanylyl Cyclase

Author

Muenster, Stefan, primary, Lieb, Wolfgang S., additional, Fabry, Gregor, additional, Allen, Kaitlin N., additional, Kamat, Shivani S., additional, Guy, Ann H., additional, Dordea, Ana C., additional, Teixeira, Leandro, additional, Tainsh, Robert E., additional, Yu, Binglan, additional, Zhu, Wei, additional, Ashpole, Nicole E., additional, Malhotra, Rajeev, additional, Brouckaert, Peter, additional, Bloch, Donald B., additional, Scherrer-Crosbie, Marielle, additional, Stamer, W. Daniel, additional, Kuehn, Markus H., additional, Pasquale, Louis R., additional, and Buys, Emmanuel S., additional

Published
2017
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35. Sensitivity to Sevoflurane anesthesia is decreased in mice with a congenital deletion of Guanylyl Cyclase-1 alpha

Author

Nagasaka, Yasuko, primary, Wepler, Martin, additional, Thoonen, Robrecht, additional, Sips, Patrick Y., additional, Allen, Kaitlin, additional, Graw, Jan A., additional, Yao, Vincent, additional, Burns, Sara M., additional, Muenster, Stefan, additional, Brouckaert, Peter, additional, Miller, Keith, additional, Solt, Ken, additional, Buys, Emmanuel S., additional, Ichinose, Fumito, additional, and Zapol, Warren M., additional

Published
2017
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37. Nitroglycerine limits infarct size through S-nitrosation of cyclophilin D: a novel mechanism for an old drug.

Author

Bibli, Sofia-Iris, Papapetropoulos, Andreas, Iliodromitis, Efstathios K, Daiber, Andreas, Randriamboavonjy, Voahanginirina, Steven, Sebastian, Brouckaert, Peter, Chatzianastasiou, Athanasia, Kypreos, Kyriakos E, Hausenloy, Derek J, Fleming, Ingrid, and Andreadou, Ioanna

Subjects
ENDOTHELIUM diseases, NITRIC-oxide synthases, MYOCARDIAL infarction, KNOCKOUT mice
Abstract

Aims Nitroglycerine (NTG) given prior to an ischaemic insult exerts cardioprotective effects. However, whether administration of an acute low dose of NTG in a clinically relevant manner following an ischaemic episode limits infarct size, has not yet been explored. Methods and results Adult mice were subjected to acute myocardial infarction in vivo and then treated with vehicle or low-dose NTG prior to reperfusion. This treatment regimen minimized myocardial infarct size without affecting haemodynamic parameters but the protective effect was absent in mice rendered tolerant to the drug. Mechanistically, NTG was shown to nitrosate and inhibit cyclophilin D (CypD), and NTG administration failed to limit infarct size in CypD knockout mice. Additional experiments revealed lack of the NTG protective effect following genetic (knockout mice) or pharmacological inhibition (L-NAME treatment) of the endothelial nitric oxide synthase (eNOS). The protective effect of NTG was attributed to preservation of the eNOS dimer. Moreover, NTG retained its cardioprotective effects in a model of endothelial dysfunction (ApoE knockout) by preserving CypD nitrosation. Human ischaemic heart biopsies revealed reduced eNOS activity and exhibited reduced CypD nitrosation. Conclusion Low-dose NTG given prior to reperfusion reduces myocardial infarct size by preserving eNOS function, and the subsequent eNOS-dependent S-nitrosation of CypD, inhibiting cardiomyocyte necrosis. This novel pharmacological action of NTG warrants confirmation in clinical studies, although our data in human biopsies provide promising preliminary results. [ABSTRACT FROM AUTHOR]

Published
2019
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40. Paracrine nitric oxide induces expression of cardiac sarcomeric proteins in adult progenitor cells through soluble guanylyl cyclase/cyclic-guanosine monophosphate and Wnt/β-catenin inhibition

Author

De Pauw, Aurelia, primary, Massion, Paul, additional, Sekkali, Belaid, additional, Andre, Emilie, additional, Dubroca, Caroline, additional, Kmecova, Jana, additional, Bouzin, Caroline, additional, Friart, Ann, additional, Sibille, Catherine, additional, Gilon, Patrick, additional, De Mulder, Delphine, additional, Esfahani, Hrag, additional, Strapart, Adrien, additional, Martherus, Ruben, additional, Payen, Valéry, additional, Sonveaux, Pierre, additional, Brouckaert, Peter, additional, Janssens, Stefan, additional, and Balligand, Jean-Luc, additional

Published
2016
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41. Androgen-sensitive hypertension associated with soluble guanylate cyclase-α1 deficiency is mediated by 20-HETE

Author

Dordea, Ana C., primary, Vandenwijngaert, Sara, additional, Garcia, Victor, additional, Tainsh, Robert E. T., additional, Nathan, Daniel I., additional, Allen, Kaitlin, additional, Raher, Michael J., additional, Tainsh, Laurel T., additional, Zhang, Fan, additional, Lieb, Wolfgang S., additional, Mikelman, Sarah, additional, Kirby, Andrew, additional, Stevens, Christine, additional, Thoonen, Robrecht, additional, Hindle, Allyson G., additional, Sips, Patrick Y., additional, Falck, John R., additional, Daly, Mark J., additional, Brouckaert, Peter, additional, Bloch, Kenneth D., additional, Bloch, Donald B., additional, Malhotra, Rajeev, additional, Schwartzman, Michal L., additional, and Buys, Emmanuel S., additional

Published
2016
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42. The Role of Soluble Guanylyl Cyclase in Chronic Obstructive Pulmonary Disease

Author

Glynos, Constantinos Dupont, Lisa L. Vassilakopoulos, Theodoros and Papapetropoulos, Andreas Brouckaert, Peter Giannis, Athanassios Joos, Guy F. Bracke, Ken R. Brusselle, Guy G.

Subjects
inorganic chemicals, cardiovascular system, heterocyclic compounds, respiratory tract diseases
Abstract

Rationale: Soluble guanylyl cyclase (sGC), a cyclic guanosine 5’-monophosphate-generating enzyme, regulates smooth muscle tone and exerts antiinflammatory effects in animal models of asthma and acute lung injury. In chronic obstructive pulmonary disease (COPD), primarily caused by cigarette smoke (CS), lung inflammation persists and smooth muscle tone remains elevated, despite ample amounts of nitric oxide that could activate sGC. Objectives: To determine the expression and function of sGC in patients with COPD and in a murine model of COPD. Methods: Expression of sGC alpha 1, alpha 2, and beta 1 subunits was examined in lungs of never-smokers, smokers without airflow limitation, and patients with COPD; and in C57BL/6 mice after 3 days, 4 weeks, and 24 weeks of CS exposure. The functional role of sGC was investigated in vivo by measuring bronchial responsiveness to serotonin in mice using genetic and pharmacologic approaches. Measurements and Main Results: Pulmonary expression of sGC, both at mRNA and protein level, was decreased in smokers without airflow limitation and in patients with COPD, and correlated with disease severity (FEV1%). In mice, exposure to CS reduced sGC, cyclic guanosine 5’-monophosphate levels, and protein kinase G activity. sGC alpha 1(-/-) mice exposed to CS exhibited bronchial hyperresponsiveness to serotonin. Activation of sGC by BAY 58-2667 restored the sGC signaling and attenuated bronchial hyperresponsiveness in CS-exposed mice. Conclusions: Down-regulation of sGC because of CS exposure might contribute to airflow limitation in COPD.

Published
2013

43. Soluble guanylate cyclase α₁-deficient mice: a novel murine model for primary open angle glaucoma

Author

Buys, Emmanuel S, Ko, Yu-Chien, Alt, Clemens, Hayton, Sarah R, Jones, Alexander, Tainsh, Laurel T, Ren, Ruiyi, Giani, Andrea, Clerté, Maeva, Abernathy, Emma, Tainsh, Robert ET, Oh, Dong-Jin, Malhotra, Rajeev, Arora, Pankaj, de Waard, Nadine, Yu, Binglan, Turcotte, Raphael, Nathan, Daniel, Scherrer-Crosbie, Marielle, Loomis, Stephanie J, Kang, Jae H, Lin, Charles P, Gong, Haiyan Y, Rhee, Douglas J, Brouckaert, Peter, Wiggs, Janey L, Gregory, Meredith S, Pasquale, Louis R, Bloch, Kenneth D, and Ksander, Bruce R

Subjects
genetic structures, BLOOD-FLOW, OCULAR PERFUSION-PRESSURE, TRABECULAR MESHWORK, eye diseases, I COLLAGEN MUTATION, HUMOR OUTFLOW FACILITY, INTRAOCULAR-PRESSURE, CLINICAL-TRIAL, OPTIC-NERVE HEAD, ENDOTHELIAL DYSFUNCTION, Medicine and Health Sciences, sense organs, NITRIC-OXIDE SYNTHASE
Abstract

Primary open angle glaucoma (POAG) is a leading cause of blindness worldwide. The molecular signaling involved in the pathogenesis of POAG remains unknown. Here, we report that mice lacking the alpha(1) subunit of the nitric oxide receptor soluble guanylate cyclase represent a novel and translatable animal model of POAG, characterized by thinning of the retinal nerve fiber layer and loss of optic nerve axons in the context of an open iridocorneal angle. The optic neuropathy associated with soluble guanylate cyclase alpha(1)-deficiency was accompanied by modestly increased intraocular pressure and retinal vascular dysfunction. Moreover, data from a candidate gene association study suggests that a variant in the locus containing the genes encoding for the alpha(1) and beta(1) subunits of soluble guanylate cyclase is associated with POAG in patients presenting with initial paracentral vision loss, a disease subtype thought to be associated with vascular dysregulation. These findings provide new insights into the pathogenesis and genetics of POAG and suggest new therapeutic strategies for POAG.

Published
2013

45. Cardiovascular and pharmacological implications of haem-deficient NO-unresponsive soluble guanylate cyclase knock-in mice

Author

Thoonen, Robrecht, primary, Cauwels, Anje, additional, Decaluwe, Kelly, additional, Geschka, Sandra, additional, Tainsh, Robert E., additional, Delanghe, Joris, additional, Hochepied, Tino, additional, De Cauwer, Lode, additional, Rogge, Elke, additional, Voet, Sofie, additional, Sips, Patrick, additional, Karas, Richard H., additional, Bloch, Kenneth D., additional, Vuylsteke, Marnik, additional, Stasch, Johannes-Peter, additional, Van de Voorde, Johan, additional, Buys, Emmanuel S., additional, and Brouckaert, Peter, additional

Published
2015
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46. Androgen-sensitive hypertension associated with soluble guanylate cyclase alpha1 deficiency is mediated by 20-HETE

Author

Vandenwijngaert, Sara, primary, Dordea, Ana C, additional, Garcia, Victor, additional, Tainsh, Robert E, additional, Nathan, Daniel I, additional, Raher, Michael J, additional, Allen, Kaitlin, additional, Zhang, Fan, additional, Lieb, Wolfgang S, additional, Mikelman, Sarah, additional, Kirby, Andrew, additional, Stevens, Christine, additional, Thoonen, Robrecht, additional, Hindle, Allyson, additional, Sips, Patrick Y, additional, Malhotra, Rajeev, additional, Daly, Mark J, additional, Brouckaert, Peter, additional, Bloch, Kenneth D, additional, Schwartzman, Michal, additional, and Buys, Emmanuel S, additional

Published
2015
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48. Cardiac soluble guanylate cyclase protects against the cardiac dysfunction induced by chronic doxorubicin treatment in mice

Author

Vandenwijngaert, Sara, primary, Swinnen, Melissa, additional, Gillijns, Hilde, additional, Caluwé, Ellen, additional, Tainsh, Robert E, additional, Nathan, Daniel I, additional, Allen, Kaitlin, additional, Bartunek, Jozef, additional, Brouckaert, Peter, additional, Scherrer-Crosbie, Marielle, additional, Bloch, Kenneth D, additional, Janssens, Stefan P, additional, and Buys, Emmanuel S, additional

Published
2015
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50. Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, additional, Huyghe, Leander, additional, De Jonge, Natalie, additional, Blanchetot, Christophe, additional, Hanssens, Valérie, additional, De Boeck, Gitte, additional, Silence, Karen, additional, Festjens, Els, additional, Heukers, Raimond, additional, Roux, Benjamin, additional, Lamballe, Fabienne, additional, Ginestier, Christophe, additional, Charafe-Jauffret, Emmanuelle, additional, Maina, Flavio, additional, Brouckaert, Peter, additional, Saunders, Michael, additional, Thibault, Alain, additional, Dreier, Torsten, additional, de Haard, Hans, additional, and Michieli, Paolo, additional

Published
2015
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