Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
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
Show all 4 Pubmed References
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
Show all 2 Pubmed References
Human Monoclonal Aquaporin 4 Primary Antibody for EIA, IHC (fro) - ABIN119570
Bódis, Nagy, Németh, Mózsik: Active water selective channels in the stomach: investigation of aquaporins after ethanol and capsaicin treatment in rats. in Journal of physiology, Paris 2001
Show all 3 Pubmed References
Human Monoclonal Aquaporin 4 Primary Antibody for EIA, IHC (fro) - ABIN119571
Esposito, Imitola, Lu, De Filippis, Scuderi, Ganesh, Folkerth, Hecht, Shin, Iuvone, Chesnut, Steardo, Sheen: Genomic and functional profiling of human Down syndrome neural progenitors implicates S100B and aquaporin 4 in cell injury. in Human molecular genetics 2008
Show all 2 Pubmed References
Ordered disorder of the astrocytic dystrophin (show DMD Antibodies)-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 (show SLC1A2 Antibodies) may follow in pathogenesis of cortical degeneration. This is the first demonstration of decrease of AQP4 and its association with EAAT-2 (show SLC1A2 Antibodies) decrease in AIDS brain, suggesting a role in the pathogenesis of HIV-associated neurocognitive disorders.
This study demonstrated that Concentrations of microparticles expressing GFAP (show GFAP Antibodies) 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 (show FBN1 Antibodies) and indicate an abnormal distribution of AQP4 in SGs (show FBN1 Antibodies) from SS patients, which could be responsible for the decreased saliva (show RAG1AP1 Antibodies) secretion in these patients.
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 (show CRK Antibodies) signal transduction pathway
The findings of this study demonstrated a novel molecular mechanism involving the SUR1 (show ABCC8 Antibodies)-TRPM4 (show TRPM4 Antibodies)-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 (show GJA1 Antibodies) 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 (show SLC1A2 Antibodies).
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 (show GFAP Antibodies), AQP4 appeared predominantly at later stages of plaque formation, in older mice, and within the processes of astrocytes. In combination with GFAP (show GFAP Antibodies), AQP4 differentiated plaques into three progression stages.
AQP4 plays an important role in mediating brain edema in hypoxic-ischemic encephalopathy.
constitutive recycling of AQP2 (show AQP2 Antibodies) does not require phosphorylation at any C-terminal sites
In conclusion, HPO (show GFER Antibodies) 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 (show RDH11 Antibodies).
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