Zobrazeno 1 - 10
of 53
pro vyhledávání: '"M. Jackson Stutts"'
Autor:
Agustin Garcia-Caballero, Maria A. Gandini, Shuo Huang, Lina Chen, Ivana A. Souza, Yan L. Dang, M. Jackson Stutts, Gerald W. Zamponi
Publikováno v:
Molecular Brain, Vol 12, Iss 1, Pp 1-9 (2019)
Abstract This study describes the functional interaction between Cav3.2 calcium channels and the Epithelial Sodium Channel (ENaC). β-ENaC subunits showed overlapping expression with endogenous Cav3.2 calcium channels in the thalamus and hypothalamus
Externí odkaz:
https://doaj.org/article/9e27b9858b4444059505c7694b8518ae
Publikováno v:
The Journal of General Physiology
A natural splice deletion of rat α-ENaC was previously reported to produce reduced ENaC current that was not attributable to reduced surface expression. Kota et al. show that this ENaC variant resists furin cleavage, implicating α-ENaC residues 34
Autor:
Ivana A. Souza, Maria A. Gandini, Lina Chen, Gerald W. Zamponi, Agustin Garcia-Caballero, M. Jackson Stutts, Yan L. Dang, Shuo Huang
Publikováno v:
Molecular Brain
Molecular Brain, Vol 12, Iss 1, Pp 1-9 (2019)
Molecular Brain, Vol 12, Iss 1, Pp 1-9 (2019)
This study describes the functional interaction between Cav3.2 calcium channels and the Epithelial Sodium Channel (ENaC). β-ENaC subunits showed overlapping expression with endogenous Cav3.2 calcium channels in the thalamus and hypothalamus as detec
Autor:
Matthew R. Redinbo, Ashley G. Henderson, Rui Cao, M. Jackson Stutts, Chong Da Tan, Sompop Bencharit, Carey A. Hobbs, Maxime G. Blanchard, Mehmet Kesimer, Robert Tarran, William G. Walton, Omar Alijevic, Stephan Kellenberger
Publikováno v:
American journal of physiology. Lung cellular and molecular physiology
American Journal of Physiology : Lung Cellular and Molecular Physiology, 305, L990-L1001
American Journal of Physiology : Lung Cellular and Molecular Physiology, 305, 12, pp. L990-L1001
American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 305, no. 12, pp. L990-L1001
American Journal of Physiology : Lung Cellular and Molecular Physiology, 305, L990-L1001
American Journal of Physiology : Lung Cellular and Molecular Physiology, 305, 12, pp. L990-L1001
American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 305, no. 12, pp. L990-L1001
The epithelial sodium channel (ENaC) is responsible for Na+and fluid absorption across colon, kidney, and airway epithelia. Short palate lung and nasal epithelial clone 1 (SPLUNC1) is a secreted, innate defense protein and an autocrine inhibitor of E
Autor:
Siobhan M. Hendrick, Brian J. Harvey, Robert Hamilton, Timothy Ferguson, Vinciane Saint-Criq, M. Jackson Stutts, J. Stuart Elborn, S. Lorraine Martin, Brian Walker, James Reihill
Publikováno v:
Reihill, J A, Walker, B, Hamilton, R A, Ferguson, T E G, Elborn, J S, Stutts, M J, Harvey, B J, Saint-Criq, V, Hendrick, S M & Martin, S L 2016, ' Inhibition of Protease–Epithelial Sodium Channel Signaling Improves Mucociliary Function in Cystic Fibrosis Airways ', American Journal of Respiratory and Critical Care Medicine, vol. 194, no. 6, pp. 701-710 . https://doi.org/10.1164/rccm.201511-2216OC
American Journal of Respiratory and Critical Care Medicine
American Journal of Respiratory and Critical Care Medicine, American Thoracic Society, 2016, 194 (6), pp.701-710. ⟨10.1164/rccm.201511-2216OC⟩
American Journal of Respiratory and Critical Care Medicine
American Journal of Respiratory and Critical Care Medicine, American Thoracic Society, 2016, 194 (6), pp.701-710. ⟨10.1164/rccm.201511-2216OC⟩
RATIONALE:In cystic fibrosis (CF) a reduction in airway surface liquid (ASL) height compromises mucociliary clearance, favoring mucus plugging and chronic bacterial infection. Inhibitors of the epithelial sodium channel (ENaC) have therapeutic potent
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::58cbf09671ff05a2839724191735a4e7
https://pure.qub.ac.uk/en/publications/inhibition-of-proteaseepithelial-sodium-channel-signaling-improves-mucociliary-function-in-cystic-fibrosis-airways(e8995c59-71df-44f5-9313-ffa3d7761878).html
https://pure.qub.ac.uk/en/publications/inhibition-of-proteaseepithelial-sodium-channel-signaling-improves-mucociliary-function-in-cystic-fibrosis-airways(e8995c59-71df-44f5-9313-ffa3d7761878).html
Autor:
Mahmoud Shobair, M. Jackson Stutts, Pradeep Kota, Yan L. Dang, Hong He, Onur Dagliyan, Nikolay V. Dokholyan
Sodium absorption in epithelial cells is rate-limited by the epithelial sodium channel (ENaC) activity in lung, kidney, and the distal colon. Pathophysiological conditions, such as cystic fibrosis and Liddle syndrome, result from water-electrolyte im
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b62f3b3856baa1be4bfe580c0d4c091
Autor:
Martina Gentzsch, Hong Dang, Agustin Garcia-Caballero, M. Jackson Stutts, Pradeep Kota, Nikolay V. Dokholyan
Publikováno v:
Biochemistry. 51:3460-3469
Limited proteolysis, accomplished by endopeptidases, is a ubiquitous phenomenon underlying the regulation and activation of many enzymes, receptors and other proteins synthesized as inactive precursors. Serine proteases are one of the largest and con
Autor:
Sharon L. Milgram, Yan Dang, Daniel Gillie, Susan S. Ishmael, Judith S. Bond, Agustin Garcia-Caballero, M. Jackson Stutts
Publikováno v:
Channels. 5:14-22
The Epithelial Na(+) Channel (ENaC) is an apical heteromeric channel that mediates Na(+) entry into epithelial cells from the luminal cell surface. ENaC is activated by proteases that interact with the channel during biosynthesis or at the extracellu
Autor:
Bernard C. Rossier, M. Jackson Stutts
Publikováno v:
Annual Review of Physiology. 71:361-379
The study of human monogenic diseases [pseudohypoaldosteronism type 1 (PHA-1) and Liddle's syndrome] as well as mouse models mimicking the salt-losing syndrome (PHA-1) or salt-sensitive hypertension (Liddle's syndrome) have established the epithelial