|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for AQP4(NM_004028.5) Search again
Product ID:
HQP149805
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MIWC, MLC4, WCH4, hAQP4
Gene Description:
aquaporin 4
Target Gene Accession:
NM_004028.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. [provided by RefSeq].
Gene References into function
- Restricted to astrocytes. Detectable in subpial and subependymal zone in normal condition. More intense in ischemic foci. May reflect participation in development of brain edema in human brains by playing role in water transport.
- AQP4 mRNA failed to localize in parietal cells but was identified in neighboring mucosal cells that were triangular in shape and smaller than parietal cells in size, and in columnar cells at the base of the gastric gland.
- Increased expression. Over-expression occurred on astrocytic processes. Induction of AQP1 and AQP4 on reactive astrocytes in subarachnoid hemorrhage. May be involved in brain edema formation or resolution.
- The expression of AQP4 is affected by nerve supply and is down-regulated in human muscles with neurogenic atrophy.
- aquaporin-4 has species-specific roles in astrocytes and a functional relationship with Connexin43
- Up-regulation of AQP4 was found in astrocytes in various inflammatory lesions. Distribution of AQP4-positve astrocytes differed according to disease and was'nt related to brain edema. Thus, functions and regulation of AQP4 in human brains are multiple.
- Astrocytic impairment and humoral immunity against AQP4 may be primarily involved in the lesion formation of NEUROMYELITIS OPTICA, contrarely to MULTIPLE SCLEROSIS in which demyelination is the primary pathology.
- These results in human fetal brain lend morphological support to the previous findings that aquaporin-1 and aquaporin-4 play different roles in the regulation of the water homeostasis of the brain.
- The distribution of NMO-characteristic brain lesions corresponds to sites of high AQP4 expression in neuromyelitis optica
- Significant increased expression levels of AQP1 and AQP4 were seen in Creutzfeldt-Jakob disease, but not in advanced Alzheimer's disease and diffuse Lewy body disease.
- Unexpectedly high AQP4 levels in pilocytic astrocytomas and present AQP4 as tumor progression marker in WHO grade II-IV astrocytomas.
- Only the presence of AQP1, but not AQP4, enhanced cell growth and migration, typical properties of gliomas, while AQP4 enhanced cell adhesion suggesting differential biological roles for AQP1 and AQP4 in glioma cell biology.
- We did not find any variation in exon 4 of the AQP4 gene in our considerable large sample of traumatic brain edema.
- increased AQP-4 expression in sCJD is an early pathologic event and appears to remain until the late disease stage
- upregulated expression of chromosome 21 genes such as S100B and amyloid precursor protein activated the stress response kinase pathways, and furthermore, could be linked to upregulation of the water channel aquaporin 4 in Down syndrome neural progenitors
- AQP4-mediated maternal-fetal fluid exchange could play an important role in the control of ion homeostasis and water balance in the human placenta throughout pregnancy
- Review highlights an understanding of the major role of aquaporin-4 in maintenance of the microenvironment of neurons, axons, and oligodendrocytes and its importance as a therapeutic target in neurologic disease.
- Upregulation of APQ4 by tumor cells and reactive astroglia were major factors of cerebral edema
- AQP4 is not expressed in human airway epithelial cells from the A549 adeoncarcinoma cell line.
- genetic variation in AQP4 might contribute to brain edema formation after middle cerebral artery occlusion
- Our study shows that AQP4 downregulation can occur in muscular dystrophies with either normal or disrupted expression of dystrophin-associated proteins, and that this might be associated with upregulation of AQP1.
- These data suggest that changes are apparent in markers for abnormal glial-neuronal communication (connexin 43 and aquaporin 4) in brains of subjects with autism.
- Presence of anti-AQP4 antibodies correlates with clinical severity and poor prognosis in opticospinal multiple sclerosis.
- Elevated anti-AQP4 antibody titers in serum were found in 15 (71%) of 21 patients with neuromyelitis optica, 4.3% of 46 patients with multiple sclerosis, none of 51 normal controls, and 2.6% of 115 patients with other neurological diseases.
- Aquaporin-4-specific IgG in some cases of NMO may reflect a paraneoplastic immune response. The clinical utility of this autoantibody as a cancer marker warrants prospective investigation.
- Changes in AQP4 expression & blood-brain barrier integrity, both of which can be regulated by CNS inflammation, contribute to inductive events for anti-AQP4-specific immune response in neuromyelitis optica. Review.
- 24 variants in AQP4 including four novel nsSNPs (I128T, D184E, I205L and M224T) were identified.
- may be involved in the pathogenesis of Neuromyelitis optica.
- AQP4 expression was analyzed in muscle biopsies from patients affected by Limb Girdle Muscular Dystrophies.
- This study was designed to analyze changes in the expression of AQP4 following elevation of intraocular pressure (IOP) and after intravitreal endothelin-1 injection and the potential involvement of the ubiquitin-dependent proteasome.
- These observations indicate that the C-terminal domain of AQP4 is constitutively phosphorylated at least in part by protein kinase CK2 and it is required for Golgi transition.
- the emergence of anti-AQP4 antibody is reinforced by the presence of the HLA-DPB1*0501 allele in Japanese.