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1,043 results on '"Nichols, Colin G."'

1. Inwardly rectifying potassium channels (KIR) in GtoPdb v.2021.3

Author

Adelman, John P, Clapham, David E, Hibino, Hiroshi, Inanobe, Atsushi, Jan, Lily Y, Karschin, Andreas, Kubo, Yoshihiro, Kurachi, Yoshihisa, Lazdunski, Michel, Miki, Takashi, Nichols, Colin G, Palmer, Lawrence G, Pearson, Wade L, Sackin, Henry, Seino, Susumu, Slesinger, Paul A, Tucker, Stephen, and Vandenberg, Carol A

Abstract

The 2TM domain family of K channels are also known as the inward-rectifier K channel family. This family includes the strong inward-rectifier K channels (Kir2.x) that are constitutively active, the G-protein-activated inward-rectifier K channels (Kir3.x) and the ATP-sensitive K channels (Kir6.x, which combine with sulphonylurea receptors (SUR1-3)). The pore-forming α subunits form tetramers, and heteromeric channels may be formed within subfamilies (e.g. Kir3.2 with Kir3.3).

Published
2023

3. Inwardly rectifying potassium channels (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Author

Adelman, John P, Clapham, David E, Hibino, Hiroshi, Inanobe, Atsushi, Jan, Lily Y, Karschin, Andreas, Kubo, Yoshihiro, Kurachi, Yoshihisa, Lazdunski, Michel, Miki, Takashi, Nichols, Colin G, Palmer, Lawrence G, Pearson, Wade L, Sackin, Henry, Seino, Susumu, Slesinger, Paul A, Tucker, Stephen, and Vandenberg, Carol A

Abstract

The 2TM domain family of K channels are also known as the inward-rectifier K channel family. This family includes the strong inward-rectifier K channels (Kir2.x) that are constitutively active, the G-protein-activated inward-rectifier K channels (Kir3.x) and the ATP-sensitive K channels (Kir6.x, which combine with sulphonylurea receptors (SUR1-3)). The pore-forming α subunits form tetramers, and heteromeric channels may be formed within subfamilies (e.g. Kir3.2 with Kir3.3).

Published
2022

7. How many SARS-CoV-2 “viroporins” are really ion channels?

Author

Harrison, Neil L, Abbott, Geoffrey W, Gentzsch, Martina, Aleksandrov, Andrei, Moroni, Anna, Thiel, Gerhard, Grant, Stephen, Nichols, Colin G, Lester, Henry A, Hartel, Andreas, Shepard, Kenneth, Garcia, David Cabrera, and Yazawa, Masayuki

Subjects
Biological Sciences, Biomedical and Clinical Sciences, COVID-19, Humans, Ion Channels, SARS-CoV-2, Viral Proteins, Viroporin Proteins, Biological sciences, Biomedical and clinical sciences
Published
2022

11. Novel loss-of-function variants expand ABCC9-related intellectual disability and myopathy syndrome

Author

Efthymiou, Stephanie, primary, Scala, Marcello, additional, Nagaraj, Vini, additional, Ochenkowska, Katarzyna, additional, Komdeur, Fenne L, additional, Liang, Robin A, additional, Abdel-Hamid, Mohamed S, additional, Sultan, Tipu, additional, Barøy, Tuva, additional, Van Ghelue, Marijke, additional, Vona, Barbara, additional, Maroofian, Reza, additional, Zafar, Faisal, additional, Alkuraya, Fowzan S, additional, Zaki, Maha S, additional, Severino, Mariasavina, additional, Duru, Kingsley C, additional, Tryon, Robert C, additional, Brauteset, Lin Vigdis, additional, Ansari, Morad, additional, Hamilton, Mark, additional, van Haelst, Mieke M, additional, van Haaften, Gijs, additional, Zara, Federico, additional, Houlden, Henry, additional, Samarut, Éric, additional, Nichols, Colin G, additional, Smeland, Marie F, additional, and McClenaghan, Conor, additional

Published
2024
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12. Glibenclamide reverses cardiovascular abnormalities of Cantu syndrome driven by [K.sub.ATP] channel overactivity

Author

McClenaghan, Conor, Huang, Yan, Yan, Zihan, Harter, Theresa M., Halabi, Carmen M., Chalk, Rod, Kovacs, Attila, van Haaften, Gijs, Remedi, Maria S., and Nichols, Colin G.

Subjects
Heart hypertrophy -- Genetic aspects -- Analysis, Cardiovascular abnormalities -- Genetic aspects -- Analysis, Heart -- Analysis, Glyburide -- Analysis, Medical schools, Cardiovascular diseases, Smooth muscle, Hypertrophy, Phenotypes, Health care industry
Abstract

Cantu syndrome (CS) is a complex disorder caused by gain-of-function (GoF) mutations in ABCC9 and KCNJ8, which encode the SUR2 and Kir6.1 subunits, respectively, of vascular smooth muscle (VSM) [K.sub.ATP] channels. CS includes dilated vasculature, marked cardiac hypertrophy, and other cardiovascular abnormalities. There is currently no targeted therapy, and it is unknown whether cardiovascular features can be reversed once manifest. Using combined transgenic and pharmacological approaches in a knockin mouse model of CS, we have shown that reversal of vascular and cardiac phenotypes can be achieved by genetic downregulation of [K.sub.ATP] channel activity specifically in VSM, and by chronic administration of the clinically used [K.sub.ATP] channel inhibitor, glibenclamide. These findings demonstrate that VSM [K.sub.ATP] channel GoF underlies CS cardiac enlargement and that CS-associated abnormalities are reversible, and provide evidence of in vivo efficacy of glibenclamide as a therapeutic agent in CS., Introduction Cantu syndrome (CS) is a complex disorder with multiple cardiovascular abnormalities, including edema, dilated and tortuous blood vessels with decreased systemic vascular resistance, patent ductus arteriosus (PDA), and marked [...]

Published
2020
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16. Preferential Gq signaling in diabetes: an electrical switch in incretin action and in diabetes progression?

Author

Nichols, Colin G., York, Nathaniel W., and Remedi, Maria S.

Subjects
Type 2 diabetes -- Genetic aspects -- Development and progression -- Care and treatment, Peptides -- Health aspects, Gene expression -- Health aspects, Health care industry
Abstract

Patients with type 2 diabetes (T2D) fail to secrete insulin in response to increased glucose levels that occur with eating. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are two incretins secreted from gastrointestinal cells that amplify insulin secretion when glucose is high. In this issue of the JCI, Oduori et al. explore the role of ATP-sensitive [K.sup.+] ([K.sub.ATP]) channels in maintaining glucose homeostasis. In persistently depolarized [beta] cells from [K.sub.ATP] channel knockout (KO) mice, the researchers revealed a shift in G protein signaling from the Gs family to the Gq family. This shift explains why GLP-1, which signals via Gq, but not GIP, which signals preferentially via Gs, can effectively potentiate secretion in islets from the [K.sub.ATP] channel-deficient mice and in other models of [K.sub.ATP] deficiency, including diabetic KK-Ay mice. Their results provide one explanation for differential insulinotropic potential of incretins in human T2D and point to a potentially unifying model for T2D progression itself., Switching G protein signaling in hyperexcited [beta] cells The textbook progression of type 2 diabetes (T2D) involves development of insulin resistance that is frequently associated with obesity and that is [...]

Published
2020
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18. KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer’s disease–related pathology

Author

Grizzanti, John, primary, Moritz, William R., additional, Pait, Morgan C., additional, Stanley, Molly, additional, Kaye, Sarah D., additional, Carroll, Caitlin M., additional, Constantino, Nicholas J., additional, Deitelzweig, Lily J., additional, Snipes, James A., additional, Kellar, Derek, additional, Caesar, Emily E., additional, Pettit-Mee, Ryan J., additional, Day, Stephen M., additional, Sens, Jonathon P., additional, Nicol, Noelle I., additional, Dhillon, Jasmeen, additional, Remedi, Maria S., additional, Kiraly, Drew D., additional, Karch, Celeste M., additional, Nichols, Colin G., additional, Holtzman, David M., additional, and Macauley, Shannon L., additional

Published
2023
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22. ABCC9-related Intellectual disability Myopathy Syndrome is a KATP channelopathy with loss-of-function mutations in ABCC9

Author

Smeland, Marie F., McClenaghan, Conor, Roessler, Helen I., Savelberg, Sanne, Hansen, Geir Åsmund Myge, Hjellnes, Helene, Arntzen, Kjell Arne, Müller, Kai Ivar, Dybesland, Andreas Rosenberger, Harter, Theresa, Sala-Rabanal, Monica, Emfinger, Chris H., Huang, Yan, Singareddy, Soma S., Gunn, Jamie, Wozniak, David F., Kovacs, Attila, Massink, Maarten, Tessadori, Federico, Kamel, Sarah M., Bakkers, Jeroen, Remedi, Maria S., Van Ghelue, Marijke, Nichols, Colin G., and van Haaften, Gijs

Published
2019
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