Results 61 to 70 of about 7,018 (220)

Kir4.1 channel activation in NG2 glia contributes to remyelination in ischemic strokeResearch in context

open access: yesEBioMedicine, 2023
Summary: Background: Stroke is one of the most common neurological diseases in the world and is clinically manifested by transient or permanent brain dysfunction.
Xiaoqi Hong   +9 more
doaj   +1 more source

Impaired CO2 sensitivity of astrocytes in a mouse model of Rett syndrome [PDF]

open access: yes, 2015
Rett syndrome is a prototypical neurological disorder characterised by abnormal breathing pattern and reduced ventilatory CO2 sensitivity. Medullary astrocytes are a crucial component of central CO2 /pH chemosensitivity.
Abdala, AP   +3 more
core   +1 more source

KIR4.1: K+ channel Illusion or Reality in the autoimmune pathogenesis of multiple sclerosis

open access: yesFrontiers in Molecular Neuroscience, 2016
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Many believe autoimmune pathogenesis plays a key role in MS, but its target(s) remains elusive.
Chen Gu
doaj   +1 more source

Role of Kir4.1 channels in growth control of glia [PDF]

open access: yesGlia, 2007
AbstractThe inwardly rectifying potassium channel Kir4.1 is widely expressed by astrocytes throughout the brain. Kir4.1 channels are absent in immature, proliferating glial cells. The progressive expression of Kir4.1 correlates with astrocyte differentiation and is characterized by the establishment of a negative membrane potential (> −70 mV) and an
Haruki, Higashimori, Harald, Sontheimer
openaire   +2 more sources

Novel KCNJ10 Compound Heterozygous Mutations Causing EAST/SeSAME-Like Syndrome Compromise Potassium Channel Function

open access: yesFrontiers in Genetics, 2019
Inwardly rectifying K+ channel 4.1 (Kir4.1), encoded by KCNJ10, is a member of the inwardly rectifying potassium channel family. In the brain, Kir4.1 is predominant in astrocytic glia and accounts for the spatial buffering of K+ released by neurons ...
Hongfeng Zhang   +14 more
doaj   +1 more source

Diverse functions of the inward-rectifying potassium channel Kir5.1 and its relationship with human diseases

open access: yesFrontiers in Physiology, 2023
The inward-rectifying potassium channel subunit Kir5.1, encoded by Kcnj16, can form functional heteromeric channels (Kir4.1/5.1 and Kir4.2/5.1) with Kir4.1 (encoded by Kcnj10) or Kir4.2 (encoded by Kcnj15).
Chaojie Zhang   +7 more
doaj   +1 more source

Identification and functional characterization of two novel mutations in KCNJ10 and PI4KB in SeSAME syndrome without electrolyte imbalance

open access: yesHuman Genomics, 2019
Background Dysfunction in inwardly rectifying potassium channel Kir4.1 has been implicated in SeSAME syndrome, an autosomal-recessive (AR), rare, multi-systemic disorder.
Ravi K. Nadella   +15 more
doaj   +1 more source

Effects of aquaporin 4 and inward rectifier potassium channel 4.1 on medullospinal edema after methylprednisolone treatment to suppress acute spinal cord injury in rats [PDF]

open access: yesActa Cirúrgica Brasileira, 2018
Purpose: To investigate the effects of aquaporin 4 (AQP4) and inward rectifier potassium channel 4.1 (Kir4.1) on medullospinal edema after treatment with methylprednisolone (MP) to suppress acute spinal cord injury (ASCI) in rats.
Ye Li   +4 more
doaj   +1 more source

Dystroglycan and Kir4.1 coclustering in retinal Müller glia is regulated by laminin‐1 and requires the PDZ‐ligand domain of Kir4.1 [PDF]

open access: yesJournal of Neurochemistry, 2005
AbstractInwardly rectifying potassium (Kir) channels in Müller glia play a critical role in the spatial buffering of potassium ions that accumulate during retinal activity. To this end, Kir channels show a polarized subcellular distribution with the predominant channel subunit in Müller glia, Kir4.1, clustered in the endfeet of these cells at the inner
Geoffrey, Noël   +5 more
openaire   +2 more sources

Neuron-oligodendrocyte potassium shuttling at nodes of Ranvier protects against inflammatory demyelination

open access: yesThe Journal of Clinical Investigation, 2023
Multiple sclerosis (MS) is a progressive inflammatory demyelinating disease of the CNS. Increasing evidence suggests that vulnerable neurons in MS exhibit fatal metabolic exhaustion over time, a phenomenon hypothesized to be caused by chronic ...
Hannah Kapell   +41 more
doaj   +1 more source

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