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Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology.
the AQP4 could play a role in the regulation of water balance and ion transport in the sensory cells of zebrafish, bringing new data for the utilizing of this experimental model in the biology of sensory system.
These results suggest that AQP4 is damaged first and decrease of EAAT-2 may follow in pathogenesis of cortical degeneration. This is the first demonstration of decrease of AQP4 and its association with EAAT-2 decrease in AIDS brain, suggesting a role in the pathogenesis of HIV-associated neurocognitive disorders.
AQP4 genetic variation moderates the relationship between sleep and brain Abeta-amyloid burden.
our results suggested that miRNA-320a could suppress the aggressive capacity of tumors by targeting AQP4, and that miRNA-320a could serve as a new effective therapeutic target for glioma surgical and therapeutic strategies.
This study demonstrated that Concentrations of microparticles expressing GFAP and AQP4 were significantly higher in the traumatic brain injury group compared with healthy controls.
Review speculated that the diverse expression of AQP4 isoforms and complement regulatory factors may determine individual susceptibility to disease onset, the expression difference in AQP4 isoforms and complement regulatory factors in different organs may determine the extent of involvement and the severity of the disease. AQP4-IgG-mediated immune injury in peripheral organs may not be rare.
Hypothermia-mediated increase in AQP4 surface abundance on human astrocytes, which was blocked using either calmodulin antagonist; TRPV4 antagonist or calcium chelation. A TRPV4 agonist mimicked the effect of hypothermia compared with untreated normothermic astrocytes. Hypothermia increased surface localization of AQP4 in human astrocytes likely through TRPV4 calcium channels and calmodulin activation.
AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA.
the overall results of this study allowed us to provide the first description of the localization of AQP4 in human SGs and indicate an abnormal distribution of AQP4 in SGs from SS patients, which could be responsible for the decreased saliva secretion in these patients.
CC genotype of rs72878794 associated with sudden infant death syndrome
Aquaporin 4 (AQP-4) are recognized as essential for two unique functions, namely, neurovascular coupling and glymphatic flow, the brain equivalent of systemic lymphatics [Review].
In neuromyelitis optica spectrum disorder-AQP4 patients, gender impacts on disease onset age and site of attack
Findings suggest that a defined population of AQP4- and AQP1-expressing reactive astrocytes may modify alpha-syn deposition in the neocortex of patients with Parkinson's Disease.
Report the value of spinal cord biopsy in the diagnosis of aquaporin-4 antibody positive neuromyelitis optica spectrum disorder.
identified that TMZ might have therapeutic potential for controlling proliferation, invasion of malignant glioma by inhibiting AQP4 expression through activation of p38 signal transduction pathway
The purpose of this study was to determine whether or not aquaporin-4 (AQP4) gene mutations are related to the pathogenesis of inflammatory demyelinating diseases in the central nervous system.
Comparative molecular dynamics study of neuromyelitis optica-immunoglobulin G binding to AQP4 extracellular domains has been presented.
Osmotic water permeabilities of aquaporins AQP4, AQP5, and GlpF from near-equilibrium simulations have been presented.
A clear correlation between AQP4 expression and ADCmax values in grade I meningioma was identified.
Peritumoral brain edema in patients with meningiomas may depend on AQP4 expression grades and not on tumor grade, tumor volume, Ki-67 expression, and cell count.
AQP4 antibodies were higher in neuromyelitis optica Chinese Han patients with circulating auto-antibodies.
Retinal nerve fiber layer may be better preserved in MOG-IgG versus AQP4-IgG optic neuritis.
AQP4 deficiency alleviates proinflammatory cytokine release from astrocytes, in association with the SPHK1/MAPK/AKT pathway.
Low expression of AQP4 is associated with Human immunodeficiency virus-associated nephropathy.
This study demonstrated that the significant improvement in blood-brain barrier (BBB) permeability was observed in the AQP4-deficient ALS mouse model.
Brain water content decreased following treatment with 3% HS relative to the TBI group. This was accompanied by decreases in AQP4, TNF-alpha, and IL-1beta mRNA and protein levels.
Treatment with goreisan significantly decreased both brain water content and AQP4 expression in the ischemic brain at 24 hours after middle cerebral artery occlusion.
The findings of this study demonstrated a novel molecular mechanism involving the SUR1-TRPM4-AQP4 complex to account for bulk water influx during astrocyte swelling.
The findings of this study suggest that AQP4 KO leads to increased aggregation of Cx43 into gap junctions and provide a putative mechanistic basis for the enhanced tracer coupling in hippocampi of AQP4 KO mice.
Interaction of the IgG-AQP4 complex with FcgammaRs triggers coendocytosis of the excitatory amino acid transporter 2.
The diffusive and AQP4-independent solute transport in rodent brain parenchyma has been demonstrated.
Present study demonstrated that AQP4 depolarization is a widespread pathological condition and may contribute to motor neuron degeneration in ALS.
Dataindicate that astrocytes in the substantia nigra differ from those in neocortex by showing a higher level of aquaporin-4, particularly in those endfoot membrane domains that mediate water exchange between brain and blood.
AQP4-specific T cells contribute to AQP4-targeted CNS autoimmunity
AQP-4 expression was significantly elevated in the ipsilateral hemisphere in the first 24h following cerebral cortical injury in mice and this could be correlated with worsening of neurological function. Over the next 48h, there was a trend towards decrease in AQP-4 expression that was associated with partial recovery of neurological function.
Study shows that the size of the aquaporin-4 (Aqp4) pool differs considerably between brain regions, roughly mirroring regional differences in Aqp4 mRNA copy numbers.
tg-ArcSwe mouse model of Alzheimer's disease demonstrated a robust upregulation of AQP4 expression in areas of plaques. Compared to GFAP, AQP4 appeared predominantly at later stages of plaque formation, in older mice, and within the processes of astrocytes. In combination with GFAP, AQP4 differentiated plaques into three progression stages.
in vivo studies demonstrated that LPS-induced activated microglia did not express AQP4, and in vitro that AQP4 deficiency inhibited astrocyte activation and reduced the release of proinflammatory cytokines from astrocytes.
The present data point to a salient glial contribution to CSD and identify AQP4 as a new target for therapy.
Aquaporin-4 (AQP4) water channels in astrocytes regulate basal brain water content.
Apelin-13 protects blood brain barrier from disruption after cerebral ischemia both morphologically and functionally, which is highly associated with the increased levels of AQP4, possibly through the activation of ERK and PI3K/Akt pathways.
Aquaporin-4 has two isoforms, M1 and M23, whose transcripts are driven by distinct promoters. A fragment located between exons 0 and 1 of the aquaporin-4 gene, which had been thought to be the promoter for M23, lacked enhancers functioning in astrocytes. When the astrocyte-specific enhancer (ASE) of the M1 promoter is connected to the putative M23 core promoter, it also works in astrocytes.
AQP4 plays an important role in mediating brain edema in hypoxic-ischemic encephalopathy.
constitutive recycling of AQP2 does not require phosphorylation at any C-terminal sites
In conclusion, HPO can decrease AQP4 expression in brain tissue of rabbits with cerebral hemorrhage to suppress the progression of brain edema and promote repairing of injured tissue.
AQP4 may play an important role in brain edema after severe scald.
This gene encodes a member of the aquaporin family of intrinsic membrane proteins that function as water-selective channels in the plasma membranes of many cells. The encoded protein is the predominant aquaporin found in brain. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
, aquaporin 4
, aquaporin type4
, mercurial-insensitive water channel
, aquaporin 4.M23
, mercurial insensitive water channel
, water channel