Recombinant Mouse Solute carrier family 12 member 5 (Slc12a5), partial

1. Enhancing GABAAR-mediated inhibition confines KCC2 to the plasma membrane, while antagonizing inhibition reduces KCC2 surface expression by increasing the lateral diffusion and endocytosis of the transporter. PMID: 29176664
2. the long-time considered "neuron-specific" KCC2 co-transporter is expressed in pancreatic islet beta-cells where it modulates Ca(2+)-dependent insulin secretion. PMID: 28496181
3. increase in KCC2 function mitigated induction of aberrant high-frequency activity during seizures, highlighting depolarizing GABA as a key contributor to the pathological neuronal synchronization seen in epilepsy. PMID: 30224498
4. our results demonstrate that local deficits in KCC2 activity within the hippocampus are sufficient to precipitate Mesial temporal lobe epilepsy . PMID: 29884458
5. Results demonstrate that KCC2 downregulation preceded convulsant induced epileptiform bursting activities both in vitro and in vivo. Suppression of its membrane expression induced spontaneous epileptiform bursting activities in vitro and Racine III seizure behaviors accompanied by epileptic EEG in vivo. PMID: 28279020
6. Disruption of Kcc2-dependent inhibition of olfactory bulb output neurons suggests its importance in odor discrimination. PMID: 27389623
7. Study provides evidence for a proconvulsive role of GABAA receptor signaling that depends on the involvement of the KCC2 co-transporter. PMID: 29045814
8. 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 release from glioma cells mediate the dephosphorylation and downregulation of KCC2, revealing yet another target for the treatment of tumor-associated epilepsies. PMID: 27513374
9. Neonatal maternal separation leads to KCC2 expression inhibition persisting until adolescence in hippocampus. PMID: 28962859
10. TGF-beta2 is a new regulatory factor for KCC2 functional activation and membrane trafficking. PMID: 27505893
11. GluK2-mediated increase in KCC2 recycling to the surface membrane translates to a hyperpolarization of the reversal potential for GABA (EGABA). PMID: 28235805
12. these data provide insight into the mechanism regulating Cl(-) homeostasis in immature neurons, and suggest that WNK1-regulated changes in KCC2 phosphorylation contribute to the developmental excitatory-to-inhibitory GABA sequence. PMID: 26126716
13. 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. PMID: 25596421
14. Results showed that the fast functional up-regulation of KCC2 in the mouse hippocampus following neonatal status epilepticus is dependent on BDNF PMID: 25229715
15. In these neurons, the plasmalemmal expression of KCC2, which establishes the low [Cl(-) ]i required for GABAA R-mediated inhibition PMID: 25066727
16. Decreased KCC2 protein expression, serine 940 dephosphorylation in motoneurons was found in mice with post-stroke spasticity. PMID: 25546454
17. study demonstrates that the level of KCC2 function sets the strength of postsynaptic inhibition. PMID: 25834055
18. Phosphorylation of S940 plays a critical role in potentiating KCC2 activity to limit the development of status epilepticus. PMID: 25733865
19. Results reveal KARs as regulators of KCC2, significantly advancing our growing understanding of the tight interplay between excitation and inhibition. PMID: 24910435
20. KCC2a and KCC2b isoforms have overlapping roles in neonatal neurons. PMID: 24639001
21. NO-mediated suppression of KCC2 can modulate synaptic inhibition in the superior paraolivary nucleus. PMID: 24987336
22. Suppressed expression of PRIPs induces an elevated expression of KCC2 in the spinal cord, resulting in inhibition of nociception and amelioration of neuropathic pain in DKO mice. PMID: 23639135
23. NL2 also regulates KCC2 to modulate GABA functional switch. PMID: 23663753
24. BPA can disrupt Kcc2 gene expression through epigenetic mechanisms PMID: 23440186
25. Loss of the Neto2:KCC2 interaction reduced KCC2-mediated Cl(-) extrusion, resulting in decreased synaptic inhibition in hippocampal neurons. PMID: 23401525
26. impaired Cl- extrusion capacity resulting from decreased KCC2 activity reduces the analgesic efficacy of certain GABAA receptor agonists and allosteric modulators. PMID: 22537560
27. ISO domain of KCC2 is required for neuronal chloride regulation PMID: 22723714
28. Ablation of Kcc2 from granule cells impaired consolidation of long-term phase learning of the vestibulo-ocular reflex, whereas baseline performance, short-term gain-decrease learning and gain consolidation remained intact. PMID: 22252133
29. KCC2 gene regulation plays a crucial role in the development of immature neurons via Egr4 downstream of the MAPK/ERK signaling pathway PMID: 21837281
30. Data show that neuronal networks within the spinal cord are more excitable in KCC2 mutant mice, which suggests that KCC2 strongly modulates the excitability of spinal cord networks. PMID: 21255132
31. Egr4 is an important component in the mechanism of BDNF-dependent KCC2 gene regulation via the ERK1/2 pathway in immature neurons. PMID: 21228173
32. These results point to a role of KCC2 in neuronal differentiation and migration during early development mediated by its direct structural interactions with the neuronal cytoskeleton. PMID: 20529123
33. Tyrosine phosphorylation of KCC2 is thus likely to play a key role in regulating the degradation of KCC2, a process that may be responsible for pathological losses of KCC2 function that are evident in status epilepticus and other forms of epilepsy. PMID: 20600929
34. These results suggest that absence of KCC2 preserves the depolarizing action of GABA in CR cells and support the notion that KCC2 is a key factor controlling Cl- homeostasis and preventing hyperexcitability. PMID: 18789906
35. chromosome 5 mapping PMID: 11701957
36. Hyperexcitability and epilepsy associated with disruption of the mouse neuronal-specific K-Cl cotransporter gene. PMID: 12000122
37. KCC2 was localized to approximately 34% of GnRH neurons. PMID: 12810559
38. tyrosine-phosphorylation seems to be less important in the emergence of low intracellular chloride than the transcriptional upregulation of KCC2 PMID: 14648690
39. Neither neuronal spiking nor ionotropic glutamatergic and GABAergic transmission are required for the developmental expression of KCC2 in mouse hippocampal neurons in vitro. PMID: 14686894
40. Cortical neurons lacking KCC2, not only fail to show a developmental decrease in [Cl-]i, but also are unable to regulate [Cl-]i on Cl- loading or maintain [Cl]i during membrane depolarization. PMID: 15469961
41. We propose a model for functional coupling between the Na+, K+-ATPase alpha2 subunit and KCC2, which excludes Cl- from the cytosol in respiratory center neurons. PMID: 15564586
42. the functional activity of KCC2 in vivo parallels the developmental expression of the protein, whereas cultured neurons require an additional activation step (mimicked by staurosporine) for KCC2 to become functional. PMID: 15787696
43. Almost all KCC2-positive dendrites (more than 98%) attached to and formed synapses with mossy fiber terminals. As development proceeded, the number of KCC2-positive granule cells increased, and all granule cells became positive by P21. PMID: 17008020
44. The KCC2 was first detected within the Purkinje cells in the Purkinje cell layer of the hemisphere at embryonic day 15 (E15) and the vermis at E17, but the ventricular and intermediate zones were negative. PMID: 17134779
45. Analysis of KCC2 potassium-chloride cotransporter (Slc12a5) promoter and proximal intron-1 regions reveals 10 candidate transcription factor binding sites that are highly conserved in mammalian KCC2 genes. PMID: 17192429
46. The novel KCC2a isoform differs from the only previously known KCC2 isoform (now termed KCC2b) by 40 unique N-terminal amino acid residues, including a putative Ste20-related proline alanine-rich kinase-binding site. PMID: 17715129
47. KCC2 interacts with the dendritic cytoskeleton to promote spine development. PMID: 18093524
48. a reduction of KCC2 expression by half results in increased susceptibility to seizure PMID: 18394864
49. Deregulation of KCC2 expression may break the balance of intracellular and extracellular chloride concentration which contributes to the mechanism of hyperexcitability leading to seizures. PMID: 18550034
50. Injured neurons reverse their response to BDNF by switching the BDNF-induced downregulation of KCC2 to upregulation. PMID: 18596173

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KEGG: mmu:57138

STRING: 10090.ENSMUSP00000096690

UniGene: Mm.252987