Zobrazeno 1 - 10
of 769
pro vyhledávání: '"A. S. Verkman"'
Publikováno v:
Fluids and Barriers of the CNS, Vol 21, Iss 1, Pp 1-12 (2024)
Abstract It has been proposed that cerebrospinal fluid (CSF) can enter and leave the retina and optic nerve along perivascular spaces surrounding the central retinal vessels as part of an aquaporin-4 (AQP4) dependent ocular ‘glymphatic’ system. H
Externí odkaz:
https://doaj.org/article/140b21ad8e6848179326dc2c9943a577
Publikováno v:
Scientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
Abstract Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system. Most NMOSD patients are seropositive for immunoglobulin G (IgG) autoantibodies against astrocyte water channel aquaporin-4 (A
Externí odkaz:
https://doaj.org/article/3ee501b270e4462e877685fc11073ca9
Publikováno v:
JCI Insight, Vol 7, Iss 13 (2022)
Nephrolithiasis is a common and recurrent disease affecting 9% of the US population. Hyperoxaluria is major risk factor for calcium oxalate kidney stones, which constitute two-thirds of all kidney stones. SLC26A3 (DRA, downregulated in adenoma) is an
Externí odkaz:
https://doaj.org/article/90984ad7720347c687441ffc4c72772e
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-14 (2020)
Aquaporin 3 (AQP3) is a transporter of water, glycerol and hydrogen peroxide, and hydrogen peroxide mediated oxidative stress has been implicated in liver injury. Here, the authors report the development of an anti-AQP3 monoclonal antibody, which all
Externí odkaz:
https://doaj.org/article/e318202226c44321ab0d1805baa94b42
Publikováno v:
Acta Neuropathologica Communications, Vol 7, Iss 1, Pp 1-16 (2019)
Abstract Cellular injury in AQP4-IgG seropositive neuromyelitis spectrum disorder (herein called NMO) involves AQP4-IgG binding to astrocytes, resulting in astrocyte injury by complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cy
Externí odkaz:
https://doaj.org/article/808b5c3dc01e4ce68803301318f50d4f
Publikováno v:
Acta Neuropathologica Communications, Vol 7, Iss 1, Pp 1-11 (2019)
Abstract Redistribution of the water channel aquaporin-4 (AQP4) away from astrocyte endfeet and into parenchymal processes is a striking histological feature in mouse models of Alzheimer’s disease (AD) and other neurological conditions with promine
Externí odkaz:
https://doaj.org/article/10d43df501334b6989400e71771dc976
Publikováno v:
Journal of Neuroinflammation, Vol 16, Iss 1, Pp 1-13 (2019)
Abstract Background Neuromyelitis optica spectrum disorder (herein called NMO) is an inflammatory demyelinating disease that can be initiated by binding of immunoglobulin G autoantibodies (AQP4-IgG) to aquaporin-4 on astrocytes, causing complement-de
Externí odkaz:
https://doaj.org/article/7bf22072265d4d4ea106b6ab162a119d
Autor:
Chung-Ming Tse, Jianyi Yin, Varsha Singh, Rafiquel Sarker, Ruxian Lin, Alan S. Verkman, Jerrold R. Turner, Mark Donowitz
Publikováno v:
Cellular and Molecular Gastroenterology and Hepatology, Vol 7, Iss 3, Pp 641-653 (2019)
Background & Aims: SLC26A3 (DRA) is an electroneutral Cl-/HCO3- exchanger that is present in the apical domain of multiple intestinal segments. An area that has continued to be poorly understood is related to DRA regulation in acute adenosine 3′,5
Externí odkaz:
https://doaj.org/article/565a8fd73e2844858353410d7094d254
Publikováno v:
JCI Insight, Vol 6, Iss 11 (2021)
SLC26A6 (also known as putative anion transporter 1 [PAT1]) is a Cl–/HCO3– exchanger expressed at the luminal membrane of enterocytes where it facilitates intestinal Cl– and fluid absorption. Here, high-throughput screening of 50,000 synthetic
Externí odkaz:
https://doaj.org/article/335b699909b6487cab0a1d9d87cc57cd
Publikováno v:
JCI Insight, Vol 6, Iss 4 (2021)
Diarrhea is a major cause of global mortality, and outbreaks of secretory diarrhea such as cholera remain an important problem in the developing world. Current treatment of secretory diarrhea primarily involves supportive measures, such as fluid repl
Externí odkaz:
https://doaj.org/article/96273d8dd05a47629cd870fee1f98ad6