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SLC12A6 is a member of the K-Cl cotransporter (KCC) family. De plus, nous expédions Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 Protéines (9) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 73 products:
Human Polyclonal SLC12A6 Primary Antibody pour ELISA, WB - ABIN564298
Salin-Cantegrel, Shekarabi, Holbert, Dion, Rochefort, Laganière, Dacal, Hince, Karemera, Gaspar, Lapointe, Rouleau: HMSN/ACC truncation mutations disrupt brain-type creatine kinase-dependant activation of K+/Cl- co-transporter 3. dans Human molecular genetics 2008
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Human Polyclonal SLC12A6 Primary Antibody pour IHC (p), IHC - ABIN449540
Simard, Bergeron, Frenette-Cotton, Carpentier, Pelchat, Caron, Isenring: Homooligomeric and heterooligomeric associations between K+-Cl- cotransporter isoforms and between K+-Cl- and Na+-K+-Cl- cotransporters. dans The Journal of biological chemistry 2007
Human Polyclonal SLC12A6 Primary Antibody pour ICC, IF - ABIN4328465
Shiozaki, Takemoto, Ichikawa, Fujiwara, Konishi, Kosuga, Komatsu, Okamoto, Kishimoto, Marunaka, Otsuji: The K-Cl cotransporter KCC3 as an independent prognostic factor in human esophageal squamous cell carcinoma. dans BioMed research international 2014
Neurodegenerative deficits in hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum are primarily caused by an axonopathy superimposed upon abnormal development, affecting peripheral but also central nervous system axons, all ultimately because of a genetic defect in the axonal cotransporter KCC3.
These results suggest that the function of the peripheral nervous system depends on finely tuned, kinase-regulated KCC3 activity and implicate abnormal cell volume homeostasis as a previously unreported mechanism of axonal degeneration.
These results suggest that the expression of KCC3 in ESCC may affect cellular invasion and be related to a worse prognosis in patients with ESCC.
SPAK (Montrer STK39 Anticorps) may promote KCC3-mediated cervix tumor aggressiveness via the NF-kappaB (Montrer NFKB1 Anticorps)/p38 MAPK (Montrer MAPK14 Anticorps)/MMP2 (Montrer MMP2 Anticorps) axis.
SLC12A6 has been shown to be causative in Andermann Syndrome.
serine residue 96 of human KCC3 is a third site that has to be dephosphorylated for full activation of the cotransporter during hypotonicity.
mis (Montrer AMH Anticorps)-trafficking of mutant protein is an important pathophysiological feature of HMSN/ACC (Montrer ACACA Anticorps) causative KCC3 mutations.
Neuropathic features of hereditary motor and sensory neuropathy/agenesis of corpus callosum in transgenic mouse lines are predominantly due to a neuronal KCC3 deficit, while the auditory impairment is due to loss of non-neuronal KCC3 expression.
The Wnk3 (Montrer WNK3 Anticorps) protein isoforms have a similar effect on SLC12 cotransporters. NKCC1 (Montrer SLC12A2 Anticorps)/2 and NCC (Montrer SLC12A3 Anticorps) were inhibited, even in hypertonicity, while KCCs were activated, even in isotonic conditions.
KCC3 is the dominant isoform in erythrocytes, with variable expression of KCC1 (Montrer SLC12A4 Anticorps) and KCC4 (Montrer SLC12A7 Anticorps) that could result in modulation of KCC activity
Results reveal the role of electrical activity in the process of neuromuscular junction (NMJ) denervation and subsequent neurodegeneration in Andermann syndrome. Study found that loss of KCC3 function is associated with an abnormal intrinsic neuronal electrical activity. Notably, we show that pharmacologically decreasing the firing frequency of Slc12a6-/- motoneurons partially rescues innervation at the NMJ.
electrophysiological studies using the threshold tracking technique indicated a reduced stimulus-response curve slope with an elevated rheobase, a decreased strength-duration time constant, diminished persistent Na(+) currents, and an outward deviation of threshold electrotonus in KCC3(-/-) nerves compared to wild-type nerves
Kcc3 inactivation caused systemic vascular resistance and ventricular mass to increase while preventing extracellular fluid volume to accumulate.
The results establish that the parvalbumin (Montrer PVALB Anticorps)-positive neuronal population is an important player in the pathogenic development of peripheral neuropathy associated with agenesis of the corpus callosum.
Data are consistent with a role for KCC3 in the proximal tubule glucose reabsorption mechanism.
KCC3 regulates NADPH oxidase (Montrer NOX1 Anticorps) activity and neutrophils activation
KCC3 contributes to Cl(-) extrusion in adult sensory neurons
K+-Cl-cotransporter (Montrer SLC12A4 Anticorps) KCC3 is expressed in neurons, interneurons and radial glial-like cells in the spinal cord.
This gene is a member of the K-Cl cotransporter (KCC) family. K-Cl cotransporters are integral membrane proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential. The proteins encoded by this gene are activated by cell swelling induced by hypotonic conditions. Alternate splicing results in multiple transcript variants encoding different isoforms. Mutations in this gene are associated with agenesis of the corpus callosum with peripheral neuropathy.
solute carrier family 12 member 6
, furosemide-sensitive KCl cotransporter 3
, K-Cl cotransporter 3
, electroneutral potassium-chloride cotransporter 3
, potassium chloride cotransporter 3
, potassium chloride cotransporter KCC3a-S3
, potassium-chloride transporter-3a
, potassium-chloride transporter-3b
, solute carrier family 12 (potassium/chloride transporters), member 6