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SLC12A6 is a member of the K-Cl cotransporter (KCC) family. Additionally we are shipping Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 Proteins (9) and many more products for this protein.
Showing 10 out of 73 products:
Human Polyclonal SLC12A6 Primary Antibody for 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. in Human molecular genetics 2008
Show all 4 Pubmed References
Human Polyclonal SLC12A6 Primary Antibody for 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. in The Journal of biological chemistry 2007
Human Polyclonal SLC12A6 Primary Antibody for 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. in 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 (show STK39 Antibodies) may promote KCC3-mediated cervix tumor aggressiveness via the NF-kappaB (show NFKB1 Antibodies)/p38 MAPK (show MAPK14 Antibodies)/MMP2 (show MMP2 Antibodies) 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 (show AMH Antibodies)-trafficking of mutant protein is an important pathophysiological feature of HMSN/ACC (show ACACA Antibodies) 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 (show WNK3 Antibodies) protein isoforms have a similar effect on SLC12 cotransporters. NKCC1 (show SLC12A2 Antibodies)/2 and NCC (show SLC12A3 Antibodies) 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 (show SLC12A4 Antibodies) and KCC4 (show SLC12A7 Antibodies) 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 (show PVALB Antibodies)-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 (show NOX1 Antibodies) activity and neutrophils activation
KCC3 contributes to Cl(-) extrusion in adult sensory neurons
K+-Cl-cotransporter (show SLC12A4 Antibodies) 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