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anti-Human SLC12A2 Antibodies:
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Mammalian Monoclonal SLC12A2 Primary Antibody for - ABIN1304870
Antoine, Hübner, Arezzo, Hébert: A causative link between inner ear defects and long-term striatal dysfunction. in Science (New York, N.Y.) 2013
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Cow (Bovine) Polyclonal SLC12A2 Primary Antibody for WB - ABIN2773831
Panet, Eliash, Atlan: Na+/K+/Cl- cotransporter activates MAP-kinase cascade downstream to protein kinase C, and upstream to MEK. in Journal of cellular physiology 2005
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Human Polyclonal SLC12A2 Primary Antibody for ELISA, IHC - ABIN4339820
Pawelczyk, Van Laer, Fransen, Rajkowska, Konings, Carlsson, Borg, Van Camp, Sliwinska-Kowalska: Analysis of gene polymorphisms associated with K ion circulation in the inner ear of patients susceptible and resistant to noise-induced hearing loss. in Annals of human genetics 2009
NKCC1 not only controls cell volume and Cl- concentration, but it can also regulate the actin cytoskeleton through Cofilin 1.
This new functional assay offered a robust working model for NKCC1 in determining reliable and concordant rank orders of the test compounds supporting its sensitivity and specificity.
we introduce the molecular mechanism by which flavonoids, specifically quercetin, act through elevation of [Cl(-) ]c via activation of NKCC1 on important factors controlling various body and cellular functions, such as (1) antihypertensive actions controlling blood volume dependent on the amounts of renal Na(+) reabsorption via expression of the epithelial Na(+) channel
NKCC1 and KCCs are coordinately regulated by L-WNK1 isoforms.
We also discovered and replicated three genome-wide significant variants in previously unreported loci for RDW (SLC12A2 rs17764730, PSMB5 rs941718), and hematocrit (PROX1 rs3754140) and an upstream anti-sense long-noncoding RNA, LINC01184, as the likely causal variant
NKCC1 high expression predicted a bad clinical outcome for lung adenocarcinoma patients and EGFR-mutated subgroup. Therefore, NKCC1 may play a role in lung adenocarcinoma and novel therapeutic tactics could be developed by targeting NKCC1 protein.
Study describes a functional missense variant in SLC12A2 in human schizophrenia, and suggest that genetically encoded dysregulation of NKCC1 may be a risk factor for, or contribute to the pathogenesis of, schizophrenia
The NKCC-1 is a Na(+)- dependent Cl(-) transporter that mediates the movement of Na(+), K(+), and Cl(-) ions across the plasma membrane and maintains cell volume and intracellular K(+) and Cl(-) homeostasis.
NKCC1 labeling was seen only in the basolateral membrane of the secretory coils.
Suggest that the expression of NKCC1 in esophageal squamous cell carcinoma may affect the G2/M checkpoint and may be related to the degree of histological differentiation of SCCs.
Functional expression of human NKCC1 from a synthetic cassette-based cDNA: introduction of extracellular epitope tags and removal of cysteines.
our data show a novel role for the WNK1/OSR1/NKCC1 pathway in glioma migration
NKCC activation involves movement of TM12 relative to TM10, which is likely tied to movement of the large C terminus
Reduced KCC2/NKCC1 ratio in the cerebrospinal fluid of Rett Syndrome patients suggests a disturbed process of GABAergic neuronal maturation and open up a new therapeutic perspective.
The hormone aldosterone was found to upregulate NKCC1 by increasing protein stability.
The rs10089 single nucleotide polymorphism was associated with increased susceptibility to noise-induced hearing loss.
Altered hippocampal area function and coupling in DISC1 and SLC12A2 minor allele carriers.
The results indicate a role for COMMD1 in the regulation of NKCC1 membrane expression and ubiquitination.
These findings suggest that NKCC1 and AQP1 participate in meningioma biology and invasion
A significant association is found between single nucleotide polymophisms in SLC12A2 and CTXN3 and schizophrenia in a Thai population.
Data show that the Na(+)/K(+)/2Cl(-) cotransporter (NKCC1) expressed in the luminal membrane of choroid plexus contributes approximately half of the cerebrospinal fluid (CSF) production.
Study showed that there is a transient dysregulation in the levels of NKCC1 and KCC2 at disease onset, the time point when heightened nociceptive behaviors are most pronounced in mice with experimental autoimmune encephalomyelitis.
This study identify neuronal up-regulation of NKCC1 and its mediation by TGFbeta, as a potential and important mechanism in the early post-traumatic seizures, and demonstrate the therapeutic potential of blocking this pathway.
Study suggests that astaxanthin may exert neuroprotection following traumatic brain injury by ameliorating AQP4/NKCC1-mediated cerebral edema, and NKCC1 inactivation inhibitions the upregulation of AQP4 after traumatic brain injury.
GABAA receptor (GABAAR) and the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1), but not the K(+)-Cl(-) cotransporter (KCC2), were expressed in the terminals of the CRH neurons at the median eminence (ME). In contrast, CRH neuronal somata were enriched with KCC2 but not with NKCC1.
These results identify NKCC1 as a novel target for Nedd4L-mediated down-regulation in vivo, which modulates ion and fluid transport in the distal colon together with epithelial Na(+) channel (ENaC).
NKCC1 inhibition protects neurons from traumatic brain injury via regulation of the ERK signal pathway.
We conclude that TRPV2 is involved in osmosensation in skeletal muscle fibres, acting in concert with P-SPAK-activated NKCC1
KCC2 expression supersedes NKCC1 in mature fiber cells in mouse and rabbit lenses.
GnRH neurons were immunopositive for NKCC1 and AE2.
NKCC1 may have a role in periventricular leukomalacia, as shown by bumetanide protection against white matter injury in a rodent model
our results suggest that NKCCs are involved in insulin secretion and that a single Slc12a2 allele may protect beta-cells from failure due to increased homeostatic expression of Slc12a1.
Repeated stress decreased KCC2 expression and increased NKCC1 expression in membranes of granular and pyramidal cells in the hippocampus.
Data indicate that ion transporter NKCC1 is involved in chloride accumulation but also reveals an impact in neurogenesis.
NKCC1 appeared down regulated in age related hearing loss.
The FAK inhibitor PF-573,228 augmented shrinkage-induced Src phosphorylation, and inhibited shrinkage-induced NKCC1 activity.
in addition to SPAK and OSR1, WNK4 is able to anchor itself to the N-terminal domain of NKCC1 and to promote cotransporter activation.
Fluid secretion is enhanced in a hypotonic challenge through the activation of NKCC1 in the mouse submandibular salivary gland.
angiotensin II activates the WNK-SPAK-NKCC1 phosphorylation cascade through the angiotensin II type 1 receptor.
Our results characterize an innovative mechanism of cardiogenic edema formation and identify NKCC1 as a unique therapeutic target in cardiogenic lung edema.
The protein encoded by this gene mediates sodium and chloride transport and reabsorption. The encoded protein is a membrane protein and is important in maintaining proper ionic balance and cell volume. This protein is phosphorylated in response to DNA damage. Three transcript variants encoding two different isoforms have been found for this gene.
solute carrier family 12 (sodium/potassium/chloride transporters), member 2
, solute carrier family 12 member 2-like
, basolateral Na-K-Cl symporter
, bumetanide-sensitive sodium-(potassium)-chloride cotransporter 1
, solute carrier family 12 member 2
, solute carrier family 12, member 2
, basolateral NaK(2Cl) cotransporter
, sodium/potassium/chloride cotransporters
, sodium/potassium/chloride transporters