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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 Antibodies (73) and Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 6 Kits (1) and many more products for this protein.
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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 Proteins) may promote KCC3-mediated cervix tumor aggressiveness via the NF-kappaB (show NFKB1 Proteins)/p38 MAPK (show MAPK14 Proteins)/MMP2 (show MMP2 Proteins) 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 Proteins)-trafficking of mutant protein is an important pathophysiological feature of HMSN/ACC 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 protein isoforms have a similar effect on SLC12 cotransporters. NKCC1 (show SLC12A2 Proteins)/2 and NCC (show SLC12A3 Proteins) 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 Proteins) and KCC4 (show SLC12A7 Proteins) that could result in modulation of KCC activity
mutations of the KCC3 gene may result in non-syndromic childhood onset of demyelinating hereditary motor and sensory neuropathy
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 Proteins)-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 Proteins) activity and neutrophils activation
KCC3 contributes to Cl(-) extrusion in adult sensory neurons
K+-Cl-cotransporter (show SLC12A4 Proteins) KCC3 is expressed in neurons, interneurons and radial glial-like cells in the spinal cord.
This study demonstrated that the K(+)-Cl(-) cotransporter (show SLC12A4 Proteins) activity of KCC3 contributes to the propagation of action potentials along peripheral nerves.
Expression of Slc12a6 in the mouse nucleus accumbens is modulated by a sequence variant (B2 SINE indel) in the 3' UTR of Comt (catechol-O-methyltransferase (show COMT Proteins)).
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