Affinage

KCNJ10

ATP-sensitive inward rectifier potassium channel 10 · UniProt P78508

Length
379 aa
Mass
42.5 kDa
Annotated
2026-06-10
100 papers in source corpus 43 papers cited in narrative 43 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KCNJ10 (Kir4.1) is an inwardly rectifying, K+-selective channel that sets resting membrane potential and mediates K+ transport across glial, epithelial, and sensory cell membranes, where it generates the cochlear endocochlear potential and supports oligodendrocyte maturation and myelination (PMID:11788352, PMID:11466414, PMID:8995301). Its biophysical signature — inward rectification, single-channel conductance, and inhibition by intracellular acidification — is governed by defined pore and N-terminal residues including Glu158 in M2 and N-terminal lysines (Lys53, Lys67), with Glu158 and Thr128 also forming the binding site for antidepressant inhibitors such as fluoxetine and nortriptyline (PMID:10790154, PMID:11034617, PMID:11029294, PMID:19264848). Kir4.1 functions both as a homotetramer and as a heterotetramer with Kir5.1 (KCNJ16), the latter conferring markedly enhanced pH sensitivity and constituting the dominant basolateral K+ conductance of the renal distal nephron (PMID:11306656, PMID:20651251, PMID:25071208, PMID:18367659). In the distal convoluted tubule this Kir4.1/Kir5.1 channel acts as a sensor-effector that couples dietary K+, insulin/IGF-1 (via PI3K), and β-adrenergic/cAMP/PKA signaling to basolateral membrane potential and downstream SPAK/NCC activity, integrating salt and potassium homeostasis (PMID:25071208, PMID:26632606, PMID:30571558, PMID:30559144). Channel abundance and surface expression are controlled by Src-family kinase phosphorylation at Tyr8/Tyr9 (stimulatory), Nedd4-2-mediated ubiquitination scaffolded through Kir5.1 (inhibitory), Ca2+-sensing-receptor-driven Gαq/caveolin-1-dependent internalization, and PKC inhibition of the heteromer, while subcellular targeting depends on a C-terminal PDZ-binding motif and di-hydrophobic array linking the channel to syntrophin/dystroglycan complexes (PMID:23873931, PMID:29897283, PMID:17122384, PMID:21084311, PMID:17585871, PMID:16033858, PMID:16033419). In astrocytes, Kir4.1 performs osmotically neutral K+ spatial buffering that constrains neuronal excitability, and its expression is set by DNA methylation, MeCP2, and FMRP, linking the channel to motor neuron size via PI3K/mTOR signaling and to neuropsychiatric and pain phenotypes (PMID:21106816, PMID:21748805, PMID:24415225, PMID:29464197, PMID:38678030, PMID:29606582, PMID:29446379, PMID:36931588). Loss-of-function mutations in KCNJ10 cause EAST/SeSAME syndrome, and autoantibodies against the channel's first extracellular loop are pathogenic in a subset of multiple sclerosis patients (PMID:19420365, PMID:20651251, PMID:20807765, PMID:22784115).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1997 High

    Establishing that KCNJ10 encodes a functional K+-selective inwardly rectifying channel defined its core molecular identity and its pH-sensitive gating.

    Evidence cDNA cloning and two-electrode voltage clamp of the channel in Xenopus oocytes with pharmacological and pH characterization

    PMID:8995301

    Open questions at the time
    • Did not define which residues confer pH sensitivity or rectification
    • Native cell-type roles not yet addressed
  2. 2000 High

    Mutagenesis pinpointed the N-terminal lysines (Lys53, Lys67) and pore residue Glu158 as the molecular determinants of intracellular pH sensing and rectification, explaining how the channel acts as a proton sensor.

    Evidence Site-directed mutagenesis with whole-cell and single-channel patch clamp in Xenopus oocytes

    PMID:10790154 PMID:11029294 PMID:11034617

    Open questions at the time
    • Physiological context in which pH gating operates not defined
    • No structural model of the pH-sensing conformational change
  3. 2001 High

    Discovery that Kir5.1 only forms functional channels with Kir4.1 and shifts pH sensitivity established the Kir4.1/Kir5.1 heterotetramer as a distinct, more pH-sensitive entity.

    Evidence Heterologous co-expression and single-channel analysis in Xenopus oocytes with immunolocalization

    PMID:11306656

    Open questions at the time
    • In vivo stoichiometry and tissue-specific assembly not resolved here
    • Functional consequence of heteromerization in native tissue not yet shown
  4. 2002 High

    Tissue-specific knockouts revealed the channel's distinct physiological roles — endocochlear potential generation, oligodendrocyte maturation/myelination, and RPE apical K+ transport — establishing it as a key K+ transport pathway across multiple specialized epithelia and glia.

    Evidence Conditional/constitutive knockout mice with electrophysiology, ion measurement, immunostaining, and developmental single-channel recordings (RPE)

    PMID:10523406 PMID:11466414 PMID:11788352

    Open questions at the time
    • Molecular partners coordinating K+ transport in each tissue only partly defined
    • Mechanism linking channel loss to spongiform degeneration not detailed
  5. 2004 Medium

    Identifying region-specific homomeric versus Kir4.1/Kir5.1 heteromeric channels in astrocytes and their association with PDZ-domain syntrophins clarified how channel composition and targeting are spatially organized in the brain.

    Evidence Reciprocal immunoprecipitation and subunit-specific immunolabeling across brain regions

    PMID:15310750

    Open questions at the time
    • Single lab; functional consequence of regional heteromerization not measured
    • Syntrophin-binding interface not mapped
  6. 2005 Medium

    Mapping the C-terminal PDZ-binding motif and di-hydrophobic array, and their dependence on laminin/dystroglycan/syntrophin, explained how the channel achieves polarized basolateral and Muller-cell domain localization.

    Evidence Site-directed mutagenesis with confocal imaging and electrophysiology in MDCK/HEK293T and Muller cell cultures

    PMID:16033419 PMID:16033858

    Open questions at the time
    • Single labs; in vivo requirement of these motifs not tested
    • Direct PDZ partner in each cell type not definitively identified
  7. 2006 High

    Demonstrating a direct CaR–Kir4.1 physical interaction that inactivates the channel placed Kir4.1 under Ca2+-sensing-receptor control in the distal nephron.

    Evidence Yeast two-hybrid, reciprocal co-IP from cells and kidney, and functional inactivation in Xenopus oocytes

    PMID:17122384

    Open questions at the time
    • Downstream physiological output of CaR-mediated inhibition not yet defined
    • Mechanism of current inactivation (gating vs trafficking) not resolved at this stage
  8. 2007 Medium

    Defining PKC inhibition of the heteromer, low-K+-induced Ca2+ influx through the channel, hyperpolarization-driven cell-cycle arrest in glioma, and antidepressant pore block expanded the channel's regulatory and effector repertoire.

    Evidence Voltage clamp with PKC pharmacology and in vitro kinase assay, Ca2+ imaging in WT/knockout slices, gain-of-function in glioma cells with cell-cycle analysis, and selectivity-profiled antidepressant patch clamp

    PMID:17284334 PMID:17585871 PMID:17876807 PMID:17920044

    Open questions at the time
    • PKC phosphorylation sites not identified
    • Physiological significance of low-K+ Ca2+ transients in vivo unclear
  9. 2009 High

    Linkage analysis identifying homozygous KCNJ10 mutations as the cause of EAST/SeSAME syndrome, with concordant renal salt wasting in knockout mice, established the channel as essential for renal salt handling and a Mendelian disease gene.

    Evidence Genome linkage, Sanger sequencing, Xenopus oocyte functional assays, and Kcnj10 knockout mouse phenotyping; also antidepressant pore-residue mapping

    PMID:19264848 PMID:19420365

    Open questions at the time
    • Tissue-level mechanism linking channel loss to each EAST symptom not yet dissected
    • Genotype–phenotype relationships across mutations incomplete
  10. 2010 High

    Single-channel and surface-expression analysis of individual EAST mutations resolved distinct loss-of-function mechanisms (altered pH gating, disrupted folding via the Cys108–Cys140 disulfide, reduced surface trafficking) and localized the Kir4.1/Kir5.1 heteromer to the DCT basolateral membrane.

    Evidence Single-channel and inside-out patch clamp in CHO/HEK293/COSm6 cells, radiotracer efflux, mutagenesis, and immunostaining/EM of patient kidney

    PMID:20651251 PMID:20807765

    Open questions at the time
    • In vivo consequences of each mutation class not separately tested
    • Structural basis of folding defects not directly visualized
  11. 2010 High

    Showing that CaR drives Kir4.1 internalization through Gαq and caveolin-1 (not clathrin) defined the trafficking mechanism by which Ca2+ sensing downregulates surface channel.

    Evidence Co-IP, surface biotinylation, siRNA knockdown, and patch clamp with dominant constructs in HEK293

    PMID:21084311

    Open questions at the time
    • In vivo relevance of caveolin-1-dependent internalization not demonstrated
    • Endosomal fate of internalized channel not traced
  12. 2011 High

    In vivo glial-conditional knockouts established that Kir4.1 sets glial membrane potential and mediates osmotically neutral K+ spatial buffering, mechanistically linking channel loss to the epilepsy phenotype.

    Evidence In vivo and slice K+-sensitive microelectrode recordings with simultaneous extracellular space volume measurement in glia-specific knockout mice

    PMID:21106816 PMID:21748805

    Open questions at the time
    • Relative contributions of Kir4.1 versus other K+ clearance mechanisms not yet quantified
    • Gastric parietal-cell role (PMID 21367857) reflects a separate epithelial function not integrated here
  13. 2013 High

    Identifying Src-family kinase phosphorylation at Tyr8/Tyr9 as stimulatory for surface expression and channel activity, alongside KCNJ16-dependent pathogenicity of A167V, defined post-translational and heteromer-dependent control of the DCT channel.

    Evidence LC/MS phosphoproteomics, mutagenesis, surface biotinylation, and patch clamp; plus co-expression of mutant KCNJ10 with KCNJ16 in oocytes

    PMID:23873931 PMID:24193250

    Open questions at the time
    • Upstream signals activating SFK toward Kir4.1 not defined
    • Whether Tyr phosphorylation regulates trafficking or gating directly is not fully separated
  14. 2014 High

    Knockout patch-clamp studies established the Kir4.1/Kir5.1 heteromer as the dominant DCT1 basolateral K+ conductance whose loss depolarizes the membrane and suppresses the SPAK–NCC axis, placing the channel upstream of WNK/NCC salt transport; parallel work delimited its astrocytic buffering role and DNA-methylation control of its expression.

    Evidence DCT1 patch clamp with immunostaining/Western in knockout mice; K+/volume electrode recordings in hippocampal slices; ChIP and bisulfite sequencing across development

    PMID:24415225 PMID:24482245 PMID:25071208

    Open questions at the time
    • Methylation findings from a single lab
    • Precise molecular coupling of basolateral potential to WNK/SPAK not fully resolved
  15. 2015 Medium

    Demonstrating PI3K-dependent activation of Kir4.1/Kir5.1 by insulin/IGF-1 in the collecting duct identified a hormonal input that hyperpolarizes the basolateral membrane.

    Evidence Single-channel and whole-cell patch clamp in native CCD with PI3K inhibition

    PMID:26632606

    Open questions at the time
    • Single lab; in vivo physiological output of insulin regulation not tested
    • Intermediate steps between PI3K and channel opening unknown
  16. 2016 Medium

    Showing compensatory ENaC and AQP2 upregulation in collecting-duct segments after Kir4.1 disruption clarified how downstream nephron segments adapt to impaired DCT Na+ transport.

    Evidence Patch clamp, Western blot, and immunostaining in CNT/CCD of Kcnj10 knockout mice

    PMID:26887833

    Open questions at the time
    • Single lab; signaling driving the compensatory response not identified
    • Whether compensation is direct or systemic not resolved
  17. 2018 High

    A cluster of studies established the channel as a node integrating transcriptional, RNA-binding, and ubiquitination control with disease and behavioral outputs: MeCP2 and FMRP set astrocytic Kir4.1, Nedd4-2/Kir5.1 limit it, and bidirectional astrocytic manipulation drives depression-like states and motor-neuron size via PI3K/mTOR.

    Evidence ChIP, FMRP RNA binding with viral rescue, co-IP/GST pull-down/ubiquitination assays with conditional knockouts, and astrocyte-specific gain/loss-of-function with electrophysiology and behavior

    PMID:29446379 PMID:29464197 PMID:29606582 PMID:29897283 PMID:38678030

    Open questions at the time
    • How multiple regulators are integrated on a single channel pool is unclear
    • Cell-type-specific contribution of each pathway to phenotypes not fully separated
  18. 2019 High

    Establishing that norepinephrine stimulates the DCT heteromer via β-adrenergic→cAMP→PKA signaling and that dietary K+ tunes channel activity, both required for NCC modulation, defined the channel as the sensor-effector coupling neural and dietary signals to renal salt handling.

    Evidence Single-channel/whole-cell patch clamp, adrenergic and dietary manipulation, and renal clearance in kidney-specific Kir4.1 knockout mice

    PMID:30559144 PMID:30571558

    Open questions at the time
    • Direct PKA phosphorylation site on the channel not mapped
    • Integration of adrenergic and dietary inputs not modeled together
  19. 2012 High

    Identification of pathogenic anti-Kir4.1 IgG targeting the first extracellular loop in multiple sclerosis patients established an autoimmune channelopathy mechanism distinct from the inherited EAST mutations.

    Evidence Proteomic identification, ELISA, and intracisternal serum IgG injection in mice with complement analysis

    PMID:22784115

    Open questions at the time
    • Fraction of MS patients with pathogenic antibodies and clinical specificity not fully defined here
    • Mechanism of channel loss (internalization vs complement lysis) not separated
  20. 2023 Medium

    Demonstrating MeCP2-dependent spinal astrocytic Kir4.1 regulation in neuropathic pain extended the channel's astrocyte-buffering role to nociceptive circuits.

    Evidence scRNA-seq, conditional knockout and viral overexpression with slice electrophysiology and behavioral pain testing

    PMID:36931588

    Open questions at the time
    • Single lab; molecular link from MeCP2 to pain circuit excitability incomplete
    • Generalizability beyond CCI model not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple converging regulatory inputs (SFK phosphorylation, Nedd4-2 ubiquitination, CaR/Gαq internalization, PKA, PI3K, PKC, and transcriptional control) are integrated on the same channel pool to produce tissue-specific outputs remains unresolved, as does a high-resolution structural model of pH gating and heteromer assembly.
  • No structural model of pH-dependent gating or Kir4.1/Kir5.1 assembly in the corpus
  • Quantitative hierarchy among competing regulators not established
  • Cross-tissue differences in regulation not mechanistically unified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0140299 molecular sensor activity 3
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3 R-HSA-382551 Transport of small molecules 3
Partners
CASRCAV1FMR1KCNJ16MECP2NEDD4LSLC12A3
Complex memberships
Kir4.1 homotetramerKir4.1/Kir5.1 heterotetramer

Evidence

Reading pass · 43 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 KCNJ10 (Kir4.1) knockout in strial intermediate cells of the cochlea abolishes the endocochlear potential and reduces endolymph volume and K+ concentration, establishing KCNJ10 as the molecular mechanism for endocochlear potential generation in concert with other transport pathways. Conditional knockout mouse, electrophysiology, ion measurement American journal of physiology. Cell physiology High 11788352
2001 Kir4.1 forms the major K+ conductance of oligodendrocytes in the spinal cord; Kir4.1-null mice show depolarized oligodendrocyte membrane potentials, immature oligodendrocyte morphology, hypomyelination, and spongiform degeneration, while spinal cord neurons remain physiologically normal. Kir4.1 knockout mouse, whole-cell patch clamp of cultured oligodendrocytes and neurons, immunostaining The Journal of neuroscience High 11466414
2009 Homozygous missense mutations in KCNJ10 cause EAST syndrome (epilepsy, ataxia, sensorineural deafness, tubulopathy); when expressed in Xenopus oocytes, these mutations cause significant and specific decreases in K+ currents; Kcnj10 knockout mice become dehydrated with renal salt wasting, demonstrating KCNJ10's major role in renal salt handling. Genome linkage analysis, Sanger sequencing, heterologous expression in Xenopus oocytes (two-electrode voltage clamp), Kcnj10 knockout mouse The New England journal of medicine High 19420365
2010 EAST syndrome mutations (R65P, G77R, R175Q, R199X) in KCNJ10 expressed in CHO and HEK293 cells cause marked impairment of channel function with strongly reduced mean open time; R65P and R175Q shift pH sensitivity to alkaline range; R199X causes complete loss of function; KCNJ10 and KCNJ16 co-localize in basolateral membranes of mouse distal convoluted tubule. Heterologous expression in CHO/HEK293 cells, single-channel patch clamp, immunostaining, electron microscopy of patient kidney Proceedings of the National Academy of Sciences of the United States of America High 20651251
2010 EAST/SeSAME mutations in Kir4.1 compromise channel function via distinct mechanisms: R65P, T164I, R297C cause alkaline shift in pH sensitivity (indicating roles in pH sensing/pore gating); C140R breaks a Cys108-Cys140 disulfide bond essential for protein folding; R199X causes dramatic decrease in surface expression; A167V may reduce surface expression; G77R may affect channel structure via charge introduction in the bilayer. Radiotracer efflux assay, inside-out patch clamp in COSm6 cells, co-expression with Kir5.1 The Journal of biological chemistry High 20807765
2010 Glial-conditional Kir4.1 knockout mice (driven by gfa2/GFAP promoter) show slower recovery of extracellular K+ after low-level stimulation, more depolarized glial membrane potentials, and loss of glial membrane potential tracking of [K+]o changes, confirming Kir4.1's role in setting glial membrane potential and K+ spatial buffering in vivo. In vivo K+-sensitive microelectrode recording, sharp electrode glial recordings, glial-conditional knockout mouse The Journal of neuroscience High 21106816
2011 Glia-specific deletion of Kcnj10 delays K+ clearance after synaptic activation in hippocampal slices without altering activity-dependent extracellular space volume changes, indicating that Kir4.1 mediates osmotically neutral K+ spatial buffering and that compromised spatial buffering underlies the epilepsy phenotype in KCNJ10 mutations. K+-sensitive electrode recording and extracellular space volume measurement in hippocampal slices from glia-specific Kcnj10 knockout mice Glia High 21748805
2004 Brain astrocytes express at least two subsets of Kir channels: heteromeric Kir4.1/Kir5.1 (assembled in region-specific fashion in neocortex and olfactory bulb glomeruli) and homomeric Kir4.1 (confined to hippocampus and thalamus); both can associate with PDZ domain-containing syntrophins involved in subcellular targeting. Immunoprecipitation, immunolabeling with subunit-specific antibodies, regional brain dissection The Journal of biological chemistry Medium 15310750
2000 Kir4.1 channels are inhibited by intracellular acidification (pKa ~6.03); co-expression with Kir5.1 increases pH sensitivity by 1.4 pH units (pKa ~7.45); a lysine residue at position 67 (K67) in the N-terminus of Kir4.1 is critical—K67M mutation completely eliminates CO2/pH sensitivity of both homomeric Kir4.1 and heteromeric Kir4.1-Kir5.1. Two-electrode voltage clamp in Xenopus oocytes, excised inside-out patches, site-directed mutagenesis The Journal of physiology High 10790154
2000 Glu158 in the M2 transmembrane domain of Kir4.1 controls rectification, single-channel conductance, and pH sensitivity; E158N mutation shifts unitary conductance to ~35 pS and pKa to ~6.72, closely matching Kir1.1 properties; additional pore residues (Val140, Gly210) contribute to these biophysical differences. Site-directed mutagenesis, single-channel and whole-cell patch clamp in Xenopus oocytes The Journal of physiology High 11034617
2000 Lys53 in the N-terminus of Kir4.1 is a key determinant of its low pH sensitivity (pKa ~6.0); K53V mutation markedly increases sensitivity to CO2/pH; additional COOH-terminal histidine residues further contribute to pH sensitivity differences between Kir4.1 and Kir1.1. Site-directed mutagenesis, two-electrode voltage clamp in Xenopus oocytes American journal of physiology. Cell physiology High 11029294
2001 Kir5.1 forms functional channels only by co-expression with Kir4.1 or Kir4.2; heteromeric Kir5.1-Kir4.1 channels are significantly more sensitive to intracellular acidification than Kir4.1 homomers, due to modulation of intrinsic Kir4.1 pH sensitivity by Kir5.1; Kir4.2 has intrinsically higher pH sensitivity (pKa 7.1) than Kir4.1 (pKa 5.99). Heterologous co-expression in Xenopus oocytes, cell-attached single-channel analysis, immunolocalization in pancreas The Journal of physiology High 11306656
1997 KCNJ10 (Kir1.2) encodes a K+-selective inwardly rectifying channel expressed in brain and kidney; expression in Xenopus oocytes generates inwardly rectifying current inhibited by Ba2+ and Cs+; channel is inhibited by intracellular protons (IC50 pH 6.2, Hill coefficient ~2) but not extracellular acidification. cDNA cloning, Northern blot, Xenopus oocyte expression, two-electrode voltage clamp, pH manipulation The Journal of biological chemistry High 8995301
2014 KCNJ10 (Kir4.1) is the dominant contributor to basolateral K+ conductance in early distal convoluted tubule (DCT1); a 40-pS K+ channel in DCT1 basolateral membrane is absent in Kcnj10 knockout mice; disruption of Kcnj10 abolishes basolateral K+ conductance, depolarizes DCT1 membrane potential, decreases basolateral Cl- conductance, inhibits SPAK expression, and reduces apical NCC expression. Patch clamp of DCT1 in knockout and wild-type mice, immunostaining, Western blot Proceedings of the National Academy of Sciences of the United States of America High 25071208
2013 Src family protein tyrosine kinase (SFK) phosphorylates KCNJ10 at Tyr8 and Tyr9; SFK inhibition reversibly reduces basolateral 40-pS K+ channel activity in DCT1 and shifts K+ reversal potential; Tyr9 mutation decreases whole-cell K+ currents, probability of finding K+ channels, and surface expression of KCNJ10. Single-channel patch clamp, whole-cell recording, LC/MS phosphoproteomics, site-directed mutagenesis, surface biotinylation, Western blot The Journal of biological chemistry High 23873931
2006 The Ca2+-sensing receptor (CaR) physically interacts with Kir4.1 (reciprocal co-immunoprecipitation from HEK-293 cells and rat kidney extracts); co-expression of CaR with Kir4.1 in Xenopus oocytes inactivates Kir4.1 whole-cell current; a non-functional CaR mutant that does not co-immunoprecipitate with Kir4.1 has no effect; Kir4.1 and CaR co-localize in basolateral membrane of distal nephron. Yeast two-hybrid screen, reciprocal co-immunoprecipitation, two-electrode voltage clamp in Xenopus oocytes, immunolocalization American journal of physiology. Renal physiology High 17122384
2010 CaR decreases cell surface expression of Kir4.1 via a mechanism involving Gαq and caveolin-1 (not clathrin-mediated endocytosis); activated Gαq reduces Kir4.1 surface expression and current density; RGS4 blocks this effect; knockdown of caveolin-1 but not clathrin heavy chain abolishes the Gαq effect on Kir4.1; CaR, Kir4.1, and caveolin-1 physically associate by co-immunoprecipitation. Co-immunoprecipitation, cell surface biotinylation, siRNA knockdown, patch clamp, dominant-active/negative constructs in HEK-293 cells The Journal of biological chemistry High 21084311
2005 The C-terminal PDZ-binding motif (Ser377) and di-hydrophobic array (Val333/Val334) of Kir4.1 regulate its subcellular distribution; disruption of the PDZ-binding motif causes clustered rather than linear surface expression; disruption of the di-hydrophobic array causes diffuse cytoplasmic distribution and diminishes channel activity; both motifs participate in basolateral localization of Kir4.1 and Kir5.1/Kir4.1 heteromers in MDCK cells. Site-directed mutagenesis, heterologous expression in HEK293T and MDCK cells, confocal microscopy, electrophysiology Journal of the American Society of Nephrology Medium 16033858
2005 Laminin-1 induces clustering of alpha-dystroglycan (DG), syntrophin, and Kir4.1 in Müller cell cultures; deletion of the PDZ-ligand domain of Kir4.1 prevents laminin-induced clustering; both laminin-1 and alpha-DG are involved in polarized distribution of Kir4.1 to specific Müller cell membrane domains via a PDZ-domain-mediated interaction. Cell culture, recombinant C-agrin treatment, immunocytochemistry, PDZ-domain deletion constructs in Müller cell cultures Journal of neurochemistry Medium 16033419
2007 Kir4.1 expression in glioma cells confers K+ conductance, hyperpolarizes resting membrane potential from -50 to -80 mV, and impairs cell growth by shifting cells from G2/M into G0/G1 phase; this growth arrest is abolished by pharmacological Kir4.1 blockade (BaCl2) or chronic membrane depolarization (KCl), demonstrating that Kir4.1-mediated hyperpolarization is sufficient for growth attenuation. Stable Kir4.1 expression in glioma cell lines, whole-cell patch clamp, cell cycle analysis (flow cytometry), pharmacological blockade Glia High 17876807
2007 Fluoxetine (SSRI) selectively inhibits Kir4.1 channel currents (IC50 ~15.2 μM) in a reversible, voltage-independent manner with little effect on Kir1.1 or Kir2.1; sertraline and fluvoxamine also inhibit Kir4.1; tetracyclic (mianserin) and 5-HT1A-related (buspirone) antidepressants do not. Whole-cell patch clamp in HEK293T cells expressing Kir4.1, Kir1.1, or Kir2.1; pharmacological dose-response Brain research Medium 17920044
2009 Antidepressants (fluoxetine, nortriptyline) interact with Kir4.1 channel pore residues Thr128 and Glu158 on transmembrane domain 2; mutagenesis of these residues eliminates drug inhibition; 3D QSAR modeling indicates antidepressants share a hydrogen bond acceptor and positively charged moiety that interact with these pore residues by hydrogen bond and ionic interactions. Chimeric and site-directed mutagenesis of Kir4.1, two-electrode voltage clamp in Xenopus oocytes, 3D QSAR modeling Molecular pharmacology High 19264848
1999 Kir4.1 is expressed specifically on the apical membrane processes of retinal pigment epithelial (RPE) cells (not basolateral), with developmental onset ~10 days postnatal parallel to retinal activity maturation; single-channel recordings from apical RPE membrane match Kir4.1 biophysical properties, establishing Kir4.1 as the RPE apical Kir channel for K+ transport in the subretinal space. Single-channel patch clamp, RT-PCR, in situ hybridization, immunohistochemistry, developmental series The Journal of physiology High 10523406
2008 The Kir4.1/Kir5.1 heteromeric channel is the major K+ conductance in the basolateral membrane of mouse cortical collecting duct (CCD) principal cells; the intermediate-conductance (40 pS) channel shows pH-dependence (pK 7.24) and spermine sensitivity; dietary K+ does not affect channel properties but Na+-depleted diet increases open probability by ~25%. Patch clamp (cell-attached and inside-out), real-time PCR, immunohistochemistry with AQP2 co-localization, dietary manipulation American journal of physiology. Renal physiology High 18367659
2014 Kir4.1 in hippocampal slices mediates spatial K+ buffering only during local increases in extracellular K+; Na+/K+-ATPase (especially the astrocyte-characteristic α2β2 subunit composition) is the dominant mechanism for post-stimulus K+ clearance; NKCC1 plays no role in activity-induced extracellular K+ recovery in native hippocampal tissue. K+-sensitive electrode recordings in hippocampal slices, Ba2+ blockade, pharmacological inhibition, Xenopus oocyte expression of ATPase subunits Glia High 24482245
2018 Upregulation of astroglial Kir4.1 in the lateral habenula (LHb) in rat depression models drives neuronal bursting; Kir4.1 is expressed on astrocytic membrane processes wrapping tightly around LHb neuronal somata; astrocyte-specific gain of Kir4.1 increases neuronal bursting and depression-like symptoms, while loss of Kir4.1 reduces them (bidirectional regulation). Quantitative proteomics screen, electrophysiology, computational modelling, astrocyte-specific viral Kir4.1 gain/loss of function, behavioral tests Nature High 29446379
2018 Loss of astrocyte-encoded Kir4.1 selectively alters fast α-motor neuron (FαMN) size and function, reducing peak grip strength; overexpression of Kir4.1 in astrocytes increases MN size through activation of the PI3K/mTOR/pS6 pathway; Kir4.1 expression around MNs depends on VGLUT1; Kir4.1 is cell-autonomously downregulated in ALS patient astrocytes with SOD1 mutation. Conditional knockout mouse, viral overexpression in astrocytes, electrophysiology, behavioral grip strength testing, PI3K/mTOR pathway analysis, iPSC-derived ALS astrocytes Neuron High 29606582
2014 DNA methylation is a critical epigenetic regulator of KCNJ10 expression during CNS development; developmental upregulation of Kir4.1 in rat is coincident with reduction in KCNJ10 DNA methylation; chromatin immunoprecipitation reveals dynamic interaction between KCNJ10 promoter and DNA methyltransferase 1 during development; demethylation of the KCNJ10 promoter is necessary for transcription. ChIP analysis, bisulfite sequencing, DNA methylation inhibitor treatment, quantitative PCR, Western blot across developmental time points Glia Medium 24415225
2018 MeCP2 directly binds the KCNJ10 promoter (shown by ChIP); Mecp2-deficient mice show significantly reduced Kir4.1 mRNA and protein in astrocytes, translating to >50% reduction in Ba2+-sensitive Kir4.1 currents and impaired extracellular K+ dynamics; loss of Kir4.1 is cell-autonomous in astrocytes. Chromatin immunoprecipitation, whole-cell patch clamp, immunostaining, qPCR, Western blot in Mecp2 knockout mice eNeuro High 29464197
2018 Kir4.1 mRNA is a direct binding target of FMRP; FMRP loss in Fmr1 knockout mice leads to impaired Kir4.1 expression and function in astrocytes with abnormal extracellular K+ homeostasis; viral delivery of Kir4.1 specifically to hippocampal astrocytes of Fmr1 knockout mice rescues normal astrocyte K+ uptake, neuronal excitability, and cognitive/social performance. FMRP RNA binding assay, patch clamp, viral Kir4.1 rescue, behavioral testing in Fmr1 knockout mice Nature communications High 38678030
2018 Nedd4-2 binds to Kir5.1 at the COOH-terminal phosphothreonine motif (TPVT, AA249-252) and facilitates ubiquitination of Kir4.1 in Kir4.1/Kir5.1 heterotetramer; Nedd4-2 fails to ubiquitinate Kir4.1 alone or in the absence of Kir5.1; Kir5.1 T249A mutation abolishes Nedd4-2 association and its inhibitory effect; kidney-specific Nedd4-2 or Kir5.1 knockout mice show increased Kir4.1 expression and DCT K+ conductance. Co-immunoprecipitation, GST pull-down, ubiquitination assay, patch clamp, Western blot, conditional knockout mice American journal of physiology. Renal physiology High 29897283
2015 Insulin and IGF-1 activate Kir4.1/Kir5.1 channel activity and open probability in CCD principal cells via a phosphatidylinositol 3-kinase (PI3K)-dependent mechanism, leading to hyperpolarization of the basolateral membrane; nortriptyline (Kir4.1 inhibitor) but not fluoxetine virtually abolishes whole-cell K+ conductance. Patch clamp in freshly isolated murine CCD (single-channel and whole-cell), pharmacological inhibition of PI3K (LY294002), amiloride/TPNQ/ouabain controls American journal of physiology. Renal physiology Medium 26632606
2019 Norepinephrine stimulates the basolateral Kir4.1/Kir5.1 heterotetramer (40 pS channel) in DCT via β-adrenergic receptor → cAMP → PKA signaling; this stimulation is required for norepinephrine-induced NCC activation, as demonstrated by the absence of this effect in kidney-specific Kir4.1 knockout mice. Single-channel and whole-cell patch clamp in DCT, adrenergic agonist/antagonist pharmacology, renal clearance in Kir4.1 kidney-specific knockout mice Hypertension High 30571558
2018 Dietary K+ intake regulates Kir4.1/Kir5.1 activity in the DCT (low K+ stimulates, high K+ inhibits); this regulation is essential for dietary K+-induced modulation of NCC, as deletion of renal Kir4.1 abolished the effect of dietary K+ intake on NCC expression/activity. Electrophysiology (patch clamp), immunoblotting, renal clearance in wild-type and kidney-specific Kir4.1 knockout mice on varying K+ diets Journal of the American Society of Nephrology High 30559144
2007 Protein kinase C (PKC) activation by PMA inhibits the heteromeric Kir4.1-Kir5.1 channel (but not homomeric Kir4.1) by reducing channel open probability; this inhibition is dependent on PKC activity (blocked by PKC inhibitors) and is independent of PIP2 depletion and clathrin-mediated internalization; C-terminal peptides of both subunits are phosphorylated by PKC in vitro. Two-electrode voltage clamp in Xenopus oocytes expressing tandem Kir4.1-Kir5.1 dimer, PKC activators/inhibitors, in vitro kinase assay, site-directed mutagenesis Biochimica et biophysica acta Medium 17585871
2013 The KCNJ10 A167V mutation alone shows residual channel function in homomeric expression, but co-expression with KCNJ16 (Kir5.1) in Xenopus oocytes abolishes function almost completely, providing explanation for its pathogenicity in EAST syndrome; this demonstrates functional cooperation between KCNJ10 and KCNJ16. Two-electrode voltage clamp in Xenopus oocytes, co-expression of mutant KCNJ10 with KCNJ16, Ba2+ inhibition assays, Western blotting Nephron. Physiology Medium 24193250
2011 Kir4.1 is expressed in parietal cells co-localizing with H+/K+-ATPase; Kir4.1-null mice secrete significantly more gastric acid faster, with upregulation of H+/K+-ATPase gene and protein expression, and show fully fused canalicular membranes lacking tubulovesicles at rest, suggesting Kir4.1 balances K+ loss/reabsorption and may affect secretory membrane recycling. Kir4.1 knockout mouse, acid secretion measurements, electron microscopy, qPCR, Western blot, immunolocalization The Journal of biological chemistry Medium 21367857
2007 Kir4.1 channels expressed in COS-1 cells or found in wild-type astrocyte brain slices mediate Ca2+ influx when extracellular K+ is lowered to ≤2 mM; this Ca2+ response is blocked by Ba2+ and is dramatically reduced in Kir4.1 knockout mice, identifying Kir4.1 as the molecular substrate for astrocyte-specific low-K+-induced Ca2+ transients. Heterologous expression in COS-1 cells, Ca2+ imaging in acute brain stem slices from WT and Kir4.1 knockout mice, Ba2+ pharmacology Cell calcium Medium 17284334
2013 miR-205 targets the 3' UTR of KCNJ10 to suppress Kir4.1 expression; scratch injury increases miR-205 and decreases KCNJ10 expression in corneal epithelial cells; inhibition of KCNJ10 partially rescues the wound-healing delay caused by miR-205 antagomer; this pathway promotes wound healing by suppressing Kir4.1. Dual luciferase reporter assay (3' UTR targeting), miRNA mimic/antagomer, patch clamp, BrdU proliferation assay, wound scratch assay, Western blot Investigative ophthalmology & visual science Medium 23950153
2009 Kir4.1 channels are regulated by external K+ through interactions with specific sites in the selectivity filter; increased [K+]o slowly increases whole-cell Kir4.1 currents; K+ removal causes slow current decrease; voltage-dependent blockers Cs+ and Ba2+ substitute for K+ preventing deactivation; NH4+ permeates but does not regulate the channel, unlike Rb+. Two-electrode voltage clamp in Xenopus oocytes, kinetic modeling, pharmacological ion substitution Channels Medium 21532341
2016 Disruption of Kir4.1 in the collecting duct/connecting tubule significantly increases expression of ENaCβ and ENaCγ subunits and aquaporin-2 in medullary CD, identified as a compensatory response to impaired Na+ transport in the DCT; Kir4.1 forms the 40-pS K+ channel in CNT/CCD basolateral membrane and partially contributes to membrane potential there. Patch clamp in CNT/CCD in Kcnj10 knockout mice, Western blotting, immunostaining American journal of physiology. Renal physiology Medium 26887833
2012 IgG antibodies against Kir4.1 in multiple sclerosis patients bind specifically to the first extracellular loop of Kir4.1; injection of KIR4.1 serum IgG into mouse cisternae magnae causes profound loss of Kir4.1 expression, altered GFAP expression in astrocytes, and complement cascade activation at Kir4.1 expression sites. Proteomic identification, ELISA, immunofluorescence on brain tissue, intracisternal injection in mice, complement pathway analysis The New England journal of medicine High 22784115
2023 In spinal cord astrocytes, MeCP2 regulates Kir4.1 expression after chronic constriction injury (CCI); conditional knockout of Kir4.1 in spinal astrocytes produces hyperalgesia; overexpression in spinal cord relieves CCI-induced hyperalgesia; Kir4.1 knockdown increases astrocyte excitability and alters neuronal firing patterns in dorsal spinal cord. scRNA-seq, conditional knockout, viral overexpression, electrophysiological recording in spinal slices, behavioral pain testing Progress in neurobiology Medium 36931588

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Astroglial Kir4.1 in the lateral habenula drives neuronal bursts in depression. Nature 488 29446379
2009 Epilepsy, ataxia, sensorineural deafness, tubulopathy, and KCNJ10 mutations. The New England journal of medicine 450 19420365
2004 Aquaporin-4 in the central nervous system: cellular and subcellular distribution and coexpression with KIR4.1. Neuroscience 408 15561407
2012 Potassium channel KIR4.1 as an immune target in multiple sclerosis. The New England journal of medicine 265 22784115
2008 Functional implications for Kir4.1 channels in glial biology: from K+ buffering to cell differentiation. Journal of neurochemistry 253 18691387
2002 KCNJ10 (Kir4.1) potassium channel knockout abolishes endocochlear potential. American journal of physiology. Cell physiology 253 11788352
2001 Kir4.1 potassium channel subunit is crucial for oligodendrocyte development and in vivo myelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 238 11466414
2014 Contributions of the Na⁺/K⁺-ATPase, NKCC1, and Kir4.1 to hippocampal K⁺ clearance and volume responses. Glia 222 24482245
2016 The role of glial-specific Kir4.1 in normal and pathological states of the CNS. Acta neuropathologica 208 26961251
2010 Implication of Kir4.1 channel in excess potassium clearance: an in vivo study on anesthetized glial-conditional Kir4.1 knock-out mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 190 21106816
2010 KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function. Proceedings of the National Academy of Sciences of the United States of America 176 20651251
2004 Differential assembly of inwardly rectifying K+ channel subunits, Kir4.1 and Kir5.1, in brain astrocytes. The Journal of biological chemistry 142 15310750
2014 KCNJ10 determines the expression of the apical Na-Cl cotransporter (NCC) in the early distal convoluted tubule (DCT1). Proceedings of the National Academy of Sciences of the United States of America 129 25071208
2011 Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human Kir4.1 gene (KCNJ10). Glia 129 21748805
2004 Association between variation in the human KCNJ10 potassium ion channel gene and seizure susceptibility. Epilepsy research 122 15120748
2004 Fine mapping of a seizure susceptibility locus on mouse Chromosome 1: nomination of Kcnj10 as a causative gene. Mammalian genome : official journal of the International Mammalian Genome Society 120 15112102
2001 Differential pH sensitivity of Kir4.1 and Kir4.2 potassium channels and their modulation by heteropolymerisation with Kir5.1. The Journal of physiology 120 11306656
2000 Modulation of kir4.1 and kir5.1 by hypercapnia and intracellular acidosis. The Journal of physiology 110 10790154
2008 Kir4.1/Kir5.1 channel forms the major K+ channel in the basolateral membrane of mouse renal collecting duct principal cells. American journal of physiology. Renal physiology 103 18367659
2018 Kir4.1-Dependent Astrocyte-Fast Motor Neuron Interactions Are Required for Peak Strength. Neuron 101 29606582
2006 Functional expression of Kir4.1 channels in spinal cord astrocytes. Glia 97 16369934
1997 Cloning and characterization of two K+ inward rectifier (Kir) 1.1 potassium channel homologs from human kidney (Kir1.2 and Kir1.3). The Journal of biological chemistry 95 8995301
2007 Role of Kir4.1 channels in growth control of glia. Glia 91 17876807
2010 Molecular mechanisms of EAST/SeSAME syndrome mutations in Kir4.1 (KCNJ10). The Journal of biological chemistry 88 20807765
2007 Inhibition of astroglial Kir4.1 channels by selective serotonin reuptake inhibitors. Brain research 87 17920044
2007 Aquaporin-4 independent Kir4.1 K+ channel function in brain glial cells. Molecular and cellular neurosciences 84 17869537
2006 Interaction of the Ca2+-sensing receptor with the inwardly rectifying potassium channels Kir4.1 and Kir4.2 results in inhibition of channel function. American journal of physiology. Renal physiology 74 17122384
2004 Kir4.1 expression by astrocytes and oligodendrocytes in CNS white matter: a developmental study in the rat optic nerve. Journal of anatomy 74 15198689
2018 Inwardly Rectifying Potassium Channel Kir4.1 as a Novel Modulator of BDNF Expression in Astrocytes. International journal of molecular sciences 70 30356026
2014 The role of an inwardly rectifying K(+) channel (Kir4.1) in the inner ear and hearing loss. Neuroscience 70 24480364
2011 Altered electroretinograms in patients with KCNJ10 mutations and EAST syndrome. The Journal of physiology 65 21300747
2003 Differential expression and distribution of Kir5.1 and Kir4.1 inwardly rectifying K+ channels in retina. American journal of physiology. Cell physiology 64 12686518
2010 Molecular basis of decreased Kir4.1 function in SeSAME/EAST syndrome. Journal of the American Society of Nephrology : JASN 59 21088294
2016 Expression of Kir4.1 and Kir5.1 inwardly rectifying potassium channels in oligodendrocytes, the myelinating cells of the CNS. Brain structure & function 58 26879293
2009 Mutational and in silico analyses for antidepressant block of astroglial inward-rectifier Kir4.1 channel. Molecular pharmacology 58 19264848
2009 Heterogeneity of Kir4.1 channel expression in glia revealed by mouse transgenesis. Glia 57 19382212
2014 DNA methylation functions as a critical regulator of Kir4.1 expression during CNS development. Glia 54 24415225
2014 A homozygous KCNJ10 mutation in Jack Russell Terriers and related breeds with spinocerebellar ataxia with myokymia, seizures, or both. Journal of veterinary internal medicine 53 24708069
2012 Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 β. Journal of neuroinflammation 53 23270518
2021 Emerging Roles of Astrocyte Kir4.1 Channels in the Pathogenesis and Treatment of Brain Diseases. International journal of molecular sciences 51 34638578
2011 The salt-wasting phenotype of EAST syndrome, a disease with multifaceted symptoms linked to the KCNJ10 K+ channel. Pflugers Archiv : European journal of physiology 51 21221631
2011 Expression of aquaporin 4 and Kir4.1 in diabetic rat retina: treatment with minocycline. The Journal of international medical research 50 21672350
2011 KCNJ10 mutations disrupt function in patients with EAST syndrome. Nephron. Physiology 50 21849804
2019 Kir4.1/Kir5.1 in the DCT plays a role in the regulation of renal K+ excretion. American journal of physiology. Renal physiology 49 30623727
2013 Src family protein tyrosine kinase regulates the basolateral K channel in the distal convoluted tubule (DCT) by phosphorylation of KCNJ10 protein. The Journal of biological chemistry 49 23873931
2015 KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb. American journal of physiology. Renal physiology 47 25834074
2014 Potassium channel KIR4.1-specific antibodies in children with acquired demyelinating CNS disease. Neurology 44 24415573
2010 Screening of SLC26A4, FOXI1 and KCNJ10 genes in unilateral hearing impairment with ipsilateral enlarged vestibular aqueduct. International journal of pediatric otorhinolaryngology 42 20621367
2010 Calcium-sensing receptor decreases cell surface expression of the inwardly rectifying K+ channel Kir4.1. The Journal of biological chemistry 42 21084311
2005 Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina. Neuroscience letters 42 16330144
2014 Differential loss of KIR4.1 immunoreactivity in multiple sclerosis lesions. Annals of neurology 41 24777949
2016 EAST syndrome: Clinical, pathophysiological, and genetic aspects of mutations in KCNJ10. Rare diseases (Austin, Tex.) 40 27500072
2013 Inhibition of miR-205 impairs the wound-healing process in human corneal epithelial cells by targeting KIR4.1 (KCNJ10). Investigative ophthalmology & visual science 40 23950153
2005 Dystroglycan and Kir4.1 coclustering in retinal Müller glia is regulated by laminin-1 and requires the PDZ-ligand domain of Kir4.1. Journal of neurochemistry 40 16033419
2010 Variable loss of Kir4.1 channel function in SeSAME syndrome mutations. Biochemical and biophysical research communications 38 20678478
2016 The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney. American journal of physiology. Renal physiology 36 27122539
2015 Hyperglycemia reduces functional expression of astrocytic Kir4.1 channels and glial glutamate uptake. Neuroscience 36 26404875
2015 Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage. American journal of physiology. Renal physiology 36 26632606
2013 Lack of significant association between mutations of KCNJ10 or FOXI1 and SLC26A4 mutations in Pendred syndrome/enlarged vestibular aqueducts. BMC medical genetics 36 23965030
2013 KCNJ10 mutations display differential sensitivity to heteromerisation with KCNJ16. Nephron. Physiology 36 24193250
2022 Kir4.1 channel activation in NG2 glia contributes to remyelination in ischemic stroke. EBioMedicine 35 36527899
2020 Metformin Corrects Abnormal Circadian Rhythm and Kir4.1 Channels in Diabetes. Investigative ophthalmology & visual science 35 32572457
2016 Disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct. American journal of physiology. Renal physiology 34 26887833
1999 Expression and polarized distribution of an inwardly rectifying K+ channel, Kir4.1, in rat retinal pigment epithelium. The Journal of physiology 34 10523406
2018 Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter. Journal of the American Society of Nephrology : JASN 33 30559144
2008 Localization of glial aquaporin-4 and Kir4.1 in the light-injured murine retina. Neuroscience letters 32 18328627
2007 Calcium influx mediated by the inwardly rectifying K+ channel Kir4.1 (KCNJ10) at low external K+ concentration. Cell calcium 32 17284334
2018 MeCP2 Deficiency Leads to Loss of Glial Kir4.1. eNeuro 31 29464197
2018 Kir5.1 regulates Nedd4-2-mediated ubiquitination of Kir4.1 in distal nephron. American journal of physiology. Renal physiology 30 29897283
2007 Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat. Molecular vision 30 17356517
2000 Molecular determinants for the distinct pH sensitivity of Kir1.1 and Kir4.1 channels. American journal of physiology. Cell physiology 30 11029294
2024 Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model. Nature communications 29 38678030
2015 Developmental expression of Kir4.1 in astrocytes and oligodendrocytes of rat somatosensory cortex and hippocampus. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 29 26427731
2021 Astrocytic Kir4.1 regulates NMDAR/calpain signaling axis in lipopolysaccharide-induced depression-like behaviors in mice. Toxicology and applied pharmacology 28 34474083
2012 Screening of SLC26A4, FOXI1, KCNJ10, and GJB2 in bilateral deafness patients with inner ear malformation. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery 28 22412181
2007 Polyamine permeation and rectification of Kir4.1 channels. Channels (Austin, Tex.) 28 18690029
2023 Spinal astrocytic MeCP2 regulates Kir4.1 for the maintenance of chronic hyperalgesia in neuropathic pain. Progress in neurobiology 27 36931588
2018 Increased expression of inwardly rectifying Kir4.1 channel in the parietal cortex from patients with major depressive disorder. Journal of affective disorders 27 30419525
2011 Kir4.1 channel expression is essential for parietal cell control of acid secretion. The Journal of biological chemistry 27 21367857
2000 A single residue contributes to the difference between Kir4.1 and Kir1.1 channels in pH sensitivity, rectification and single channel conductance. The Journal of physiology 27 11034617
2018 Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss. Communications biology 26 30271961
2014 Mutation analysis of the SLC26A4, FOXI1 and KCNJ10 genes in individuals with congenital hearing loss. PeerJ 26 24860705
2009 Modulation of Kir4.1 and Kir4.1-Kir5.1 channels by small changes in cell volume. Neuroscience letters 26 19429167
2005 PDZ-binding and di-hydrophobic motifs regulate distribution of Kir4.1 channels in renal cells. Journal of the American Society of Nephrology : JASN 25 16033858
2019 Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule. Hypertension (Dallas, Tex. : 1979) 23 30571558
2018 It's All about Timing: The Involvement of Kir4.1 Channel Regulation in Acute Ischemic Stroke Pathology. Frontiers in cellular neuroscience 23 29503609
2014 KCNJ10 may not be a contributor to nonsyndromic enlargement of vestibular aqueduct (NSEVA) in Chinese subjects. PloS one 23 25372295
2020 Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule. Journal of the American Society of Nephrology : JASN 22 32295826
2020 Deeper and Deeper on the Role of BK and Kir4.1 Channels in Glioblastoma Invasiveness: A Novel Summative Mechanism? Frontiers in neuroscience 22 33328867
2019 Age-dependent alterations of Kir4.1 expression in neural crest-derived cells of the mouse and human cochlea. Neurobiology of aging 22 31220650
2018 Antiepileptic Drugs Elevate Astrocytic Kir4.1 Expression in the Rat Limbic Region. Frontiers in pharmacology 21 30127740
2022 Inwardly rectifying K+ channels 4.1 and 5.1 (Kir4.1/Kir5.1) in the renal distal nephron. American journal of physiology. Cell physiology 20 35759440
2019 Astroglial Mechanisms of Ketamine Action Include Reduced Mobility of Kir4.1-Carrying Vesicles. Neurochemical research 20 30793220
2018 Potassium conservation is impaired in mice with reduced renal expression of Kir4.1. American journal of physiology. Renal physiology 20 30110571
2007 Protein kinase C dependent inhibition of the heteromeric Kir4.1-Kir5.1 channel. Biochimica et biophysica acta 20 17585871
2016 Novel KCNJ10 Gene Variations Compromise Function of Inwardly Rectifying Potassium Channel 4.1. The Journal of biological chemistry 19 26867573
2015 A KCNJ10 mutation previously identified in the Russell group of terriers also occurs in Smooth-Haired Fox Terriers with hereditary ataxia and in related breeds. Acta veterinaria Scandinavica 19 25998802
2023 Dystrophin Short Product, Dp71, Interacts with AQP4 and Kir4.1 Channels in the Mouse Cerebellar Glial Cells in Contrast to Dp427 at Inhibitory Postsynapses in the Purkinje Neurons. Molecular neurobiology 17 36918517
2011 Kir4.1 K+ channels are regulated by external cations. Channels (Austin, Tex.) 17 21532341
2022 EAST/SeSAME Syndrome and Beyond: The Spectrum of Kir4.1- and Kir5.1-Associated Channelopathies. Frontiers in physiology 16 35370765

Missed literature

Know a paper Affinage missed for KCNJ10? Flag it for the maintainers and the community.

No submissions yet.