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K-Cl cotransporters are proteins that lower intracellular chloride concentrations below the electrochemical equilibrium potential. Zusätzlich bieten wir Ihnen Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 5 Antikörper (123) und Solute Carrier Family 12 (Potassium-Chloride Transporter) Member 5 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
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SLC12A5 promoted the migration and invasion of BUC by enhancing MMP-7 (zeige MMP7 ELISA Kits) expression.
Study shows that the overall expression of potassium-chloride cotransporter (zeige SLC12A7 ELISA Kits)-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 ELISA Kits).
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.
these data provide insight into the mechanism regulating Cl(-) homeostasis in immature neurons, and suggest that WNK1 (zeige WNK1 ELISA Kits)-regulated changes in KCC2 phosphorylation contribute to the developmental excitatory-to-inhibitory GABA sequence.
a novel signaling pathway that couples KCC2 to the cytoskeleton and regulates the formation of glutamatergic synapses.
These data describe a novel KCC2 variant significantly associated with a human disease and suggest genetically encoded impairment of KCC2 functional regulation may be a risk factor for the development of human IGE.
Study showed that there is a transient dysregulation in the levels of NKCC1 (zeige SLC12A2 ELISA Kits) 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 ELISA Kits) is a new regulatory factor for KCC2 functional activation and membrane trafficking.
GABAA (zeige GABRg1 ELISA Kits) receptor (GABAAR (zeige GABRG2 ELISA Kits)) and the Na(+)-K(+)-2Cl(-) cotransporter (zeige SLC12A1 ELISA Kits) (NKCC1 (zeige SLC12A2 ELISA Kits)), but not the K(+)-Cl(-) cotransporter (zeige SLC12A4 ELISA Kits) (KCC2), were expressed in the terminals of the CRH (zeige CRH ELISA Kits) neurons at the median eminence (ME). In contrast, CRH (zeige CRH ELISA Kits) neuronal somata were enriched with KCC2 but not with NKCC1 (zeige SLC12A2 ELISA Kits).
GluK2 (zeige GRIK2 ELISA Kits)-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 ELISA Kits) in mature fiber cells in mouse and rabbit lenses.
Repeated stress decreased KCC2 expression and increased NKCC1 (zeige SLC12A2 ELISA Kits) expression in membranes of granular and pyramidal cells in the hippocampus.
Decreasing [Cl(-)]i levels caused by increasing KCC2 levels in the 12 N could play important roles in regulating the frequency of respiration-related rhythmic activity during development.
Results showed that the fast functional up-regulation of KCC2 in the mouse hippocampus following neonatal status epilepticus is dependent on BDNF (zeige BDNF ELISA Kits)
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