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anti-Human Aquaporin 4 Antibodies:
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Human Polyclonal Aquaporin 4 Primary Antibody for IHC (fro), IHC (p) - ABIN3043789
Zhang, Chen, Dang, Liu, Ito, Sun: Neuroprotective effects of total steroid saponins on cerebral ischemia injuries in an animal model of focal ischemia/reperfusion. in Planta medica 2015
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Human Polyclonal Aquaporin 4 Primary Antibody for IF (p), IHC (p) - ABIN671181
Duan, Hao, Fan, Wang, Liu, Hao, Xu, Liu, Zhang: The role of neuropeptide Y and aquaporin 4 in the pathogenesis of intestinal dysfunction caused by traumatic brain injury. in The Journal of surgical research 2013
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Human Polyclonal Aquaporin 4 Primary Antibody for WB - ABIN3043706
Chen, Huang, Ruan, He, Li: Ulinastatin attenuates cerebral ischemia-reperfusion injury in rats. in International journal of clinical and experimental medicine 2014
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Human Polyclonal Aquaporin 4 Primary Antibody for IHC (p), WB - ABIN3044015
Wang, Bu, Zhang, Chen, Zhang, Bao: Expression pattern of aquaporins in patients with primary nephrotic syndrome with edema. in Molecular medicine reports 2016
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Polyclonal Aquaporin 4 Primary Antibody for WB - ABIN540593
Lennon, Kryzer, Pittock, Verkman, Hinson: IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel. in The Journal of experimental medicine 2005
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Human Polyclonal Aquaporin 4 Primary Antibody for ICC, IF - ABIN4281307
Lopez-Rodriguez, Acaz-Fonseca, Viveros, Garcia-Segura: Changes in cannabinoid receptors, aquaporin 4 and vimentin expression after traumatic brain injury in adolescent male mice. Association with edema and neurological deficit. in PLoS ONE 2015
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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.
The locus belongs to a linkage disequilibrium block showing expression quantitative trait loci effects on three putative cis-regulated genes, including the aquaporin 4 (AQP4) locus. AQP4 is already known to mediate the formation of ischemic edema in the brain and heart, increasing the size and extent of resulting lesions. Our findings indicate that AQP4 may also play a role in the etiopathology of vascular depression.
Perivascular AQP4 expression is attenuated in idiopathic normal pressure hydrocephalus.
Seropositivity for AQP4-IgG was confirmed in 46% of patients with longitudinally extensive transverse myelitis (LETM), confirming an AQP4-IgG-seropositive neuromyelitis optica spectrum disorder diagnosis rather than antiphospholipid-associated LETM. Recurrent LETM was exclusive to AQP4-IgG-positive patients. Clotting disorders are common in patients with LETM with AQP4-IgG and antiphospholipid antibody dual positivity.
AQP4 supramolecular structure is different in brain and skeletal muscle, which is likely to result in different tissues susceptibility to the Neuromyelitis optica disease.
Study provides the first integrative evidence for a gliogenetic basis that involves AQP4, underlying language-associated brain plasticity.
This study showed that the high percentage (64-99%) of MHC-fast positive fibers showed immunoreaction for AQP4.
There was no clear relationship between AQP4 expression and degree of edema.
aquaporin-4 (AQP4) expression and correlation with hypoxia, and neuroinflammation in human Traumatic brain injury, were examined.
cortical AQP4 immunoreactivity was more intense in the Alzheimer disease group than in the control group.
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.
AQP-1 was decreased in renal papilla and AQP-4 expressions were increased in proximal tubule by suppressing renin activity or supplement of Vitamin D analogue. After injecting renin into the lateral ventricle of the 1alpha(OH)ase knockout mice, the renin expression level was decreased in the kidney, followed by the decrease of AQP-1 in renal papilla and increase of AQP-4 in proximal tubule
Data show that hypoxia is involved in the development of age-related hydrocephalus by a process depending on Aqp4 channels as a main route for cerebrospinal fluid movement. Significant increase in Aqp4 expression occurring over the course of aging, together with reduced cerebrospinal fluid outflow rate and ventricular compliance, contribute to produce more severe hydrocephalus related to hypoxic events in aged mice.
A significant decrease in tracer transport in water channel aquaporin-4 (AQP4) knock-out (KO) mice [Meta-analysis].
The data of this study suggested that AQP4 deletion protects BBB integrity by reducing inflammatory responses due to the upregulation of PPAR-gamma expression and attenuation of proinflammatory cytokine release.
Study findings in primary rat astrocytes and in middle cerebral artery occlusion/reperfusion mouse model indicated that miR29a prevented astrocyte injury in vitro by inhibiting AQP4.
Aquaporin-4 (AQP4) is involved in the hypoxia-dependent VEGF upregulation in the retina of a mouse model of oxygen-induced retinopathy
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.
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.
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