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Ordered disorder of the astrocytic dystrophin (Montrer DMD Protéines)-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 (Montrer SLC1A2 Protéines) may follow in pathogenesis of cortical degeneration. This is the first demonstration of decrease of AQP4 and its association with EAAT-2 (Montrer SLC1A2 Protéines) decrease in AIDS brain, suggesting a role in the pathogenesis of HIV-associated neurocognitive disorders.
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 (Montrer CRK Protéines) 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 (Montrer AQP5 Protéines), 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 (Montrer MKI67 Protéines) expression, and cell count.
AQP4 antibodies were higher in neuromyelitis optica Chinese Han patients with circulating auto-antibodies.
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 (Montrer GFAP Protéines), AQP4 appeared predominantly at later stages of plaque formation, in older mice, and within the processes of astrocytes. In combination with GFAP (Montrer GFAP Protéines), AQP4 differentiated plaques into three progression stages.
in vivo studies demonstrated that LPS (Montrer TLR4 Protéines)-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 (Montrer CSAD Protéines) and identify AQP4 as a new target for therapy.
Aquaporin-4 (AQP4) water channels in astrocytes regulate basal brain water content.
Apelin (Montrer APLN Protéines)-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 (Montrer EPHB2 Protéines) and PI3K/Akt (Montrer AKT1 Protéines) 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 (Montrer ARSE Protéines)) of the M1 promoter is connected to the putative M23 core promoter, it also works in astrocytes.
In anhedonic mice, the expression of the water channel aquaporin 4 (AQP4), a factor in glymphatic pathway dysfunction, was down-regulated in cortex and hippocampus.
AQP4 plays an important role in mediating brain edema in hypoxic-ischemic encephalopathy.
constitutive recycling of AQP2 (Montrer AQP2 Protéines) does not require phosphorylation at any C-terminal sites
In conclusion, HPO (Montrer GFER Protéines) 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 (Montrer RDH11 Protéines).
In the guinea pig AQP4 is localised to enteric glial cells.
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