Results 41 to 50 of about 1,066 (149)

Differential Assembly of Inwardly Rectifying K+ Channel Subunits, Kir4.1 and Kir5.1, in Brain Astrocytes [PDF]

open access: yesJournal of Biological Chemistry, 2004
The inwardly rectifying K+ channel subunit Kir5.1 is expressed abundantly in the brain, but its precise distribution and function are still largely unknown. Because Kir5.1 is co-expressed with Kir4.1 in retinal glial Muller cells, we have compared the biochemical and immunological properties of Kir5.1 and Kir4.1 in the mouse brain.
Hiroshi, Hibino   +4 more
openaire   +2 more sources

The central role of aquaporins in the pathophysiology of ischemic stroke [PDF]

open access: yes, 2015
Stroke is a complex and devastating neurological condition with limited treatment options. Brain edema is a serious complication of stroke. Early edema formation can significantly contribute to infarct formation and thus represents a promising target ...
Di Giovanni, Giuseppe   +4 more
core   +2 more sources

Structural basis of control of inward rectifier Kir2 channel gating by bulk anionic phospholipids [PDF]

open access: yes, 2016
Inward rectifier potassium (Kir) channel activity is controlled by plasma membrane lipids. Phosphatidylinositol-4,5-bisphosphate (PIP(2)) binding to a primary site is required for opening of classic inward rectifier Kir2.1 and Kir2.2 channels, but ...
Anna Stary-Weinzinger   +55 more
core   +2 more sources

EAST syndrome: Clinical, pathophysiological, and genetic aspects of mutations in KCNJ10 [PDF]

open access: yes, 2016
EAST syndrome is a recently described autosomal recessive disorder secondary to mutations in KCNJ10 (Kir4.1), a gene encoding a potassium channel expressed in the brain, eye, ear and kidney.
Abdelhadi, O   +4 more
core   +1 more source

HNF1B as a New Transcriptional Activator of the Renal KIR4.1/KIR5.1 Potassium Channel [PDF]

open access: yesThe FASEB Journal, 2017
Background Hepatocyte nuclear factor 1 homeobox B ( HNF1B) is an essential transcription factor for the development and functioning of the kidney.
Kompatscher, A.   +7 more
openaire   +1 more source

An in vivo protein landscape of the mouse DCT during high dietary K+ or low dietary Na+ intake [PDF]

open access: yes, 2021
The hormone aldosterone is essential for maintaining K+ and Na+ balance and controlling blood pressure. Aldosterone has different effects if it is secreted due to hypovolemia or hyperkalemia.
Cheng, Lei   +3 more
core   +1 more source

High dietary potassium causes ubiquitin-dependent degradation of the kidney sodium-chloride cotransporter [PDF]

open access: yes, 2021
The thiazide-sensitive sodium-chloride cotransporter (NCC) in the renal distal convoluted tubule (DCT) plays a critical role in regulating blood pressure (BP) and K+ homeostasis.
Dimke, Henrik   +5 more
core   +1 more source

Kir4.1 Potassium Channel Subunit Is Crucial for Oligodendrocyte Development and In Vivo Myelination [PDF]

open access: yes, 2001
To understand the cellular and in vivo functions of specific K^+ channels in glia, we have studied mice with a null mutation in the weakly inwardly rectifying K^+ channel subunit Kir4.1.
Jacobs, Russell E.   +4 more
core   +1 more source

Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function? [PDF]

open access: yes, 2021
Despite significant advances in our understanding of the pathophysiology of multiple sclerosis (MS), knowledge about contribution of individual ion channels to axonal impairment and remyelination failure in progressive MS remains incomplete.
Boscia, Francesca   +3 more
core   +2 more sources

Functional interaction between aquaporins and Kir4.1/Kir4.1‐Kir5.1 channels

open access: yesThe FASEB Journal, 2007
In the CNS glial cells, Kir4.1 and Kir4.1‐Kir5.1 channels are involved in clearance of K + during neuronal activity. A number of studies have shown that Kir channels are co‐localized with aquaporins (AQP4) in the glial cells, and coupled water and K ...
Rikke Søe, Dan Arne Klærke
openaire   +1 more source

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