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K-Cl cotransporters are proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential.
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Mammalian Monoclonal SLC12A5 Primary Antibody für ISt, IHC - ABIN1304723
Lee, Walker, Williams, Goodier, Payne, Moss: Direct protein kinase C-dependent phosphorylation regulates the cell surface stability and activity of the potassium chloride cotransporter KCC2. in The Journal of biological chemistry 2007
Show all 11 Pubmed References
Mammalian Monoclonal SLC12A5 Primary Antibody für ISt, IHC - ABIN1304724
Law, Paquet, Kania: Emergence of motor circuit activity. in PLoS ONE 2014
These data clearly demonstrated that partially disrupted neuronal Cl(-) extrusion, mediated by two types of differentially impaired KCC2 mutant in an individual, causes epilepsy of infancy with migrating focal seizures.
Study describes the developmental patterns of cation-chloride cotransporters in the human brain from the fetal stage to senescence. Expression of KCC2 and its functionally associated proteins begins in early fetal period.
The authors show that APP (zeige APP Antikörper) can physically interact with KCC2, a neuron-specific K(+)-Cl(-) cotransporter (zeige SLC12A4 Antikörper) that is essential for Cl(-) homeostasis and fast GABAergic inhibition.
SLC12A5 promoted the migration and invasion of BUC by enhancing MMP-7 (zeige MMP7 Antikörper) expression.
Study shows that the overall expression of potassium-chloride cotransporter (zeige SLC12A7 Antikörper)-2 is increased in the hippocampi of temporal lobe epilepsy patients.
Our network model suggested the loss of KCC2 in a critical number of pyramidal cells increased external potassium and intracellular chloride concentrations leading to seizure-like field potential oscillations. These oscillations included transient discharges leading to ictal-like field events with frequency spectra as in vitro Restoration of KCC2 function suppressed seizure activity and thus may present a useful therapeut
The KCC2 exerts specific functions for the maturation of glycinergic synapses in cultured spinal cord neurons.
SLC12A5 plays a pivotal oncogenic role in colorectal carcinogenesis; its overexpression is an independent prognostic factor of patients with CRC (zeige CALR Antikörper).
the functional deficit of KCC2 may offer an explanation for the delayed onset of Rett symptoms.
A KCC2 mutation causes epilepsy of infancy with migrating focal seizures. Decreased KCC2 expression, reduced protein glycosylation and impaired Cl- extrusion contribute to loss of KCC2 activity, impairing synaptic inhibition and promoting excitability.
Study provides evidence for a proconvulsive role of GABAA (zeige GABRg1 Antikörper) receptor signaling that depends on the involvement of the KCC2 co-transporter.
Overall, the global native-KCC2 interactome and subsequent characterization revealed PACSIN1 (zeige PACSIN1 Antikörper) as a novel and potent negative regulator of KCC2.
This study directly implicates the dephosphorylation and downregulation of KCC2 in the peritumoral brain region in the pathophysiology of tumor-associated epilepsy in disease model mice; proposes that glutamate (zeige GRIN1 Antikörper) release from glioma cells mediate the dephosphorylation and downregulation of KCC2, revealing yet another target for the treatment of tumor-associated epilepsies.
Study showed that there is a transient dysregulation in the levels of NKCC1 (zeige SLC12A2 Antikörper) and KCC2 at disease onset, the time point when heightened nociceptive behaviors are most pronounced in mice with experimental autoimmune encephalomyelitis.
Neonatal maternal separation leads to KCC2 expression inhibition persisting until adolescence in hippocampus.
TGF-beta2 (zeige TGFB2 Antikörper) is a new regulatory factor for KCC2 functional activation and membrane trafficking.
GABAA (zeige GABRg1 Antikörper) receptor (GABAAR (zeige GABRG2 Antikörper)) and the Na(+)-K(+)-2Cl(-) cotransporter (zeige SLC12A1 Antikörper) (NKCC1 (zeige SLC12A2 Antikörper)), but not the K(+)-Cl(-) cotransporter (zeige SLC12A4 Antikörper) (KCC2), were expressed in the terminals of the CRH (zeige CRH Antikörper) neurons at the median eminence (ME). In contrast, CRH (zeige CRH Antikörper) neuronal somata were enriched with KCC2 but not with NKCC1 (zeige SLC12A2 Antikörper).
GluK2 (zeige GRIK2 Antikörper)-mediated increase in KCC2 recycling to the surface membrane translates to a hyperpolarization of the reversal potential for GABA (EGABA).
KCC2 expression supersedes NKCC1 (zeige SLC12A2 Antikörper) in mature fiber cells in mouse and rabbit lenses.
these data provide insight into the mechanism regulating Cl(-) homeostasis in immature neurons, and suggest that WNK1 (zeige WNK1 Antikörper)-regulated changes in KCC2 phosphorylation contribute to the developmental excitatory-to-inhibitory GABA sequence.
K-Cl cotransporters are proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential. The protein encoded by this gene is an integral membrane K-Cl cotransporter that can function in either a net efflux or influx pathway, depending on the chemical concentration gradients of potassium and chloride. The encoded protein can act as a homomultimer, or as a heteromultimer with other K-Cl cotransporters, to maintain chloride homeostasis in neurons. Alternative splicing results in two transcript variants encoding different isoforms.
solute carrier family 12 (potassium/chloride transporter), member 5
, K-Cl cotransporter 2
, electroneutral potassium-chloride cotransporter 2
, furosemide-sensitive K-Cl cotransporter
, neuronal K-Cl cotransporter
, neuronal-specific K-Cl cotransporter
, solute carrier family 12 member 5
, solute carrier family 12, member 5
, erythroid K-Cl cotransporter 2