Affinage

Showing ABCC8 — SUR1 is a alias.

ABCC8

ATP-binding cassette sub-family C member 8 · UniProt Q09428

Length
1581 aa
Mass
177.0 kDa
Annotated
2026-06-09
100 papers in source corpus 33 papers cited in narrative 33 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

ABCC8 encodes SUR1, the regulatory subunit of the pancreatic KATP channel, which couples cellular metabolic state to membrane excitability and insulin secretion by forming a direct physical complex with the Kir6.2 pore-forming subunit (PMID:9488482, PMID:29594720). SUR1 senses adenine nucleotides at two nucleotide-binding folds: NBF1 binds ATP with high affinity in a Mg2+-independent manner, while NBF2 binds MgADP and exhibits ATP hydrolysis, with cooperative communication between the two domains (PMID:9287292, PMID:15893323). Mg-nucleotide binding and hydrolysis at the SUR1 NBDs generate a stimulatory action that activates the Kir6.2 pore, counterbalancing the inhibitory ATP binding at Kir6.2 (PMID:9618560, PMID:20876358). This activation depends on functional coupling between the subunits, mediated by SUR1 TMD0 and by specific inter-subunit contacts including SUR1-E203 with Kir6.2-Q52 and the Kir6.2 N-terminus, contacts that are also required for sulfonylurea and potassium-channel-opener pharmacology (PMID:10435998, PMID:16613899, PMID:22802363, PMID:29594720). Disease mutations partition along this mechanism: activating ABCC8 mutations that elevate basal Mg-nucleotide stimulation cause neonatal diabetes and DEND syndrome, whereas loss-of-function mutations that impair MgADP/diazoxide responsiveness or surface trafficking cause hyperinsulinemic hypoglycemia (PMID:16885549, PMID:16613899, PMID:21199866, PMID:21536946). Beyond the channel, SUR1-dependent KATP activity regulates beta-cell proliferation during islet development and is required for cAMP/incretin potentiation of insulin secretion (PMID:12453898, PMID:33404684). In a distinct pathological program, SUR1 is transcriptionally upregulated de novo after CNS ischemia and injury through sequential HIF1α→Sp1 activation, and co-assembles with TRPM4 to form non-selective cation channels—and with AQP4 as a tripartite complex—that drive Na+ and water influx, cytotoxic edema, and tissue swelling (PMID:16550187, PMID:22086197, PMID:23255597, PMID:28906027, PMID:37279286).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 1997 High

    Established that SUR1 is a bona fide nucleotide sensor with two functionally distinct binding sites, defining the biochemical basis for how metabolic nucleotides act on the channel.

    Evidence Photoaffinity labeling with azido-ATP and Walker A/B mutagenesis of NBF1 and NBF2

    PMID:9287292

    Open questions at the time
    • Did not establish how nucleotide binding translates into pore gating
    • Stoichiometry within the assembled channel not resolved
  2. 1998 High

    Demonstrated that SUR1 physically associates with Kir6.2 and that this association alters single-channel kinetics and trafficking, identifying the molecular partnership underlying the KATP channel.

    Evidence Reciprocal co-immunoprecipitation from in vitro translation and COS cells, confocal imaging, single-channel patch-clamp

    PMID:9488482

    Open questions at the time
    • Subunit stoichiometry not defined
    • Structural interface unresolved
  3. 1998 High

    Showed that Mg-nucleotide stimulation requires intact SUR1 NBDs, separating the SUR1-mediated activating input from the Kir6.2-intrinsic inhibitory ATP site.

    Evidence Inside-out patch-clamp of reconstituted Kir6.2/SUR1 with NBD mutations and SUR1-free truncated Kir6.2

    PMID:9618560

    Open questions at the time
    • Conformational mechanism linking NBD to pore not visualized
  4. 1999 High

    Defined the requirement for functional Kir6.2-SUR1 coupling for both drug action and MgADP stimulation, showing PIP2 and pore open-state stability gate the channel's responsiveness to SUR1.

    Evidence Inside-out patch-clamp with PIP2 and Kir6.2 open-state mutants (ΔN30, L164A) plus NBF2 ATPase comparison of SUR1 vs SUR2A

    PMID:10435998 PMID:15893323

    Open questions at the time
    • Physical path of coupling between subunits not mapped
    • Isoform ATPase difference correlated but not structurally explained
  5. 2000 High

    Linked a hyperinsulinism mutation to disrupted NBF1-NBF2 cooperativity, providing the first mutation-level mechanism for loss of MgADP activation in disease.

    Evidence Domain-specific photolabeling with tryptic digestion plus patch-clamp of R1420C with ATP-insensitive Kir6.2-R50G

    PMID:10993895

    Open questions at the time
    • Does not generalize to all hyperinsulinism mutations
    • In vivo beta-cell consequences inferred, not measured
  6. 2001 High

    Identified Kir6.2 residues R176/R177 as required for transmitting SUR1 regulatory input, localizing the coupling interface on the pore subunit.

    Evidence Inside-out patch-clamp of Kir6.2 point mutants co-expressed with SUR1

    PMID:11585851

    Open questions at the time
    • Reciprocal SUR1 contact residues not yet identified
    • Structural proximity inferred functionally
  7. 2002 High

    Established SUR1 as required for cAMP/incretin potentiation of insulin secretion beyond its electrical role, and identified SUR1-selective pharmacology determinants in transmembrane domains 8-11.

    Evidence Pharmacology in Sur1 knockout islets; chimera and Walker A mutagenesis with radioligand binding for NNC 55-9216

    PMID:12031979 PMID:12453898

    Open questions at the time
    • Molecular intermediary of cAMP sensing not yet identified
    • Drug binding pose not structurally resolved at this stage
  8. 2004 High

    Mapped extracellular SUR1 histidines as the basis for isoform-specific zinc activation, demonstrating SUR1-specific extracellular regulatory sites.

    Evidence Site-directed mutagenesis of His-326/His-332 with patch-clamp and SUR1/SUR2A comparison

    PMID:15613469

    Open questions at the time
    • Physiological relevance of zinc gating not established
  9. 2006 High

    Defined the gain-of-function disease mechanism whereby activating SUR1 mutations elevate basal Mg-nucleotide stimulation, causing neonatal diabetes and DEND syndrome, and implicated TMD0 in setting Kir6.2 ATP sensitivity.

    Evidence Patch-clamp of mutant channels in intact cells/excised patches with ABCC8 sequencing of patients (incl. F132L TMD0)

    PMID:16613899 PMID:16885549

    Open questions at the time
    • Full spectrum of mutation severity-to-phenotype not enumerated
    • Structural basis of TMD0 effect not yet resolved
  10. 2006 High

    Revealed a KATP-independent role for SUR1 by showing de novo SUR1 expression after ischemia forms non-selective cation channels driving edema, opening a CNS injury axis distinct from beta-cell biology.

    Evidence Western blot, in situ hybridization, electrophysiology and glibenclamide rescue in rodent stroke models

    PMID:16550187

    Open questions at the time
    • Identity of the partner pore subunit not yet defined at this point
    • Transcriptional trigger only partially characterized
  11. 2008 High

    Extended the activating-mutation mechanism to an allosteric reduction of Kir6.2 ATP sensitivity independent of Mg2+, broadening the molecular spectrum of ABCC8 diabetes.

    Evidence Multiple patch-clamp configurations plus Ca2+ imaging of SUR1-Y356C in INS1 cells

    PMID:18346985

    Open questions at the time
    • Structural path of TMD1-to-pore allostery not resolved
  12. 2010 High

    Isolated the SUR1 activating action using an inhibition-insensitive pore and showed both MgATP and MgADP act through SUR1 NBDs to drive identical high-Po gating, with hydrolysis-competent nucleotide required; in parallel established the spinal cord injury phenotype of Abcc8 loss.

    Evidence Inside-out patch-clamp of Kir6.2-G334D/SUR1 with NBD mutants and nucleotide analogues; Abcc8 KO and antisense in SCI models with human tissue

    PMID:20410530 PMID:20876358

    Open questions at the time
    • Conformational coupling still inferred kinetically
    • Endothelial oncosis mechanism downstream of SUR1 channels not fully detailed
  13. 2011 High

    Defined the injury-induced transcriptional program (sequential HIF1α→Sp1) driving SUR1 upregulation and a disulfide-dependent trafficking requirement whose disruption causes hyperinsulinism, plus the functional distinction between diazoxide-responsive and -unresponsive dominant mutations.

    Evidence Reporter assays with promoter deletion and in vivo ChIP; cysteine mutagenesis/glycosylation/MG132 rescue; Rb+ efflux across 13 mutations in 15 families

    PMID:21199866 PMID:21536946 PMID:22086197

    Open questions at the time
    • Upstream signals initiating HIF1α in injury not fully mapped
    • Why some trafficking-normal mutants lose only MgADP response not structurally explained
  14. 2012 High

    Identified TRPM4 as the SUR1 partner pore in CNS injury and resolved an inter-subunit contact (SUR1-E203/Kir6.2-Q52) governing ATP sensitivity, while a contradictory study failed to detect SUR1-TRPM4 association.

    Evidence FRET, co-IP, electrophysiology and calmodulin assay for SUR1-TRPM4 (positive); charge-swap and cysteine cross-linking for E203/Q52; contrasting negative FRET/electrophysiology in COSm6

    PMID:22291026 PMID:22802363 PMID:23255597

    Open questions at the time
    • SUR1-TRPM4 association reported negative in one system (idx 30), reflecting genuine controversy in heterologous reconstitution
    • Stoichiometry of SUR1-TRPM4 heteromer undefined
  15. 2013 Medium

    Identified EPAC as a direct intracellular regulator binding SUR1 to close KATP channels, linking cAMP signaling to channel state and seizure vulnerability.

    Evidence Direct peptide binding (SUR1 859-881), patch-clamp, glutamate release and in vivo seizure model in EPAC KO mice

    PMID:23678128

    Open questions at the time
    • Single lab; structural basis of EPAC-SUR1 interaction not resolved
    • Relationship to the incretin/cAMP secretion pathway not integrated
  16. 2016 High

    Showed Sur1-Trpm4 channels regulate inflammatory gene transcription (NOS2 via Ca2+/CaMKII/calcineurin/NFAT) in activated microglia, extending the injury channel into immune signaling.

    Evidence Electrophysiology, Ca2+ imaging, ChIP and Abcc8-/-/Trpm4-/- mice with pharmacology

    PMID:27246103

    Open questions at the time
    • Whether this pathway operates in non-microglial cell types unclear
  17. 2017 High

    Defined the tripartite SUR1-TRPM4-AQP4 complex as a high-capacity water-transport unit, mechanistically linking the injury cation channel to astrocyte swelling.

    Evidence Co-IP, FRET, calcein swelling assay and in vivo genetic pore inactivation in a cold-injury edema model

    PMID:28906027

    Open questions at the time
    • Stoichiometry and structure of the tripartite complex unresolved
  18. 2018 High

    Provided cryo-EM structures resolving the glibenclamide site, Kir6.2 N-terminus coupling, and Mg-nucleotide binding mode, structurally validating decades of functional inference about SUR1-pore coupling.

    Evidence Cryo-EM of pancreatic KATP channel at 4.1–4.5 Å in multiple states; NF-κB/tPA-PAR1 induction of SUR1-TRPM4 MMP-9 secretion in brain endothelium

    PMID:29594720 PMID:29617457

    Open questions at the time
    • Structures of injury-related SUR1-TRPM4/AQP4 complexes not determined
    • Higher-resolution catalytic intermediates not captured
  19. 2019 High

    Dissected channel subunits genetically in vivo to show post-ischemic brain swelling is mediated by SUR1-TRPM4, not KATP channels, cleanly separating the two SUR1 functional programs.

    Evidence Subunit-specific antisense ODNs (Abcc8, Trpm4, Kcnj8, Kcnj11) with MRI swelling, immuno-FRET and co-IP in rat pMCAo

    PMID:31899311

    Open questions at the time
    • Did not address mixed contributions in other injury contexts
  20. 2021 High

    Demonstrated using isogenic patient iPSC islets that SUR1-mediated KATP activity controls beta-cell proliferation during islet development, adding a developmental role to its secretory function.

    Evidence iPSC-derived SC-islets with CRISPR correction, secretion and proliferation assays, pharmacological KATP inactivation and xenografts

    PMID:33404684

    Open questions at the time
    • Molecular link between channel activity and proliferation signaling not defined
  21. 2023 High

    Resolved the downstream effector chain by which astrocytic SUR1-TRPM4 drives edema: Na+ influx→reverse-mode NCX1 Ca2+ entry→calmodulin-dependent AQP4 surface translocation→water influx.

    Evidence Astrocyte-specific Abcc8 conditional KO, pharmacology, Ca2+ imaging and AQP4 surface assays in mouse pMCAo

    PMID:37279286

    Open questions at the time
    • Quantitative contribution of this pathway vs other edema mechanisms not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single SUR1 protein is partitioned between KATP and SUR1-TRPM4/AQP4 assemblies, and the structural basis of the injury-induced complexes, remain unresolved.
  • No structure of SUR1-TRPM4 or the tripartite SUR1-TRPM4-AQP4 complex
  • Conflicting reconstitution data on SUR1-TRPM4 association (idx 18 vs idx 30) not reconciled structurally
  • Switch governing partner-subunit choice after injury unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0140657 ATP-dependent activity 4 GO:0005215 transporter activity 3 GO:0016787 hydrolase activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-382551 Transport of small molecules 3
Partners
AQP4EPACKCNJ11TRPM4
Complex memberships
KATP channel (SUR1/Kir6.2)SUR1-TRPM4 channelSUR1-TRPM4-AQP4 tripartite complex

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 SUR1 (ABCC8) binds ATP at NBF1 in a Mg2+-independent manner with high affinity, while MgADP binds at NBF2 and antagonizes ATP binding at NBF1 through cooperative inter-domain communication; NBF1 Walker A/B mutations impaired ATP binding, NBF2 mutations reduced MgADP antagonism. Photoaffinity labeling with 8-azido-[α-32P]ATP and 8-azido-[γ-32P]ATP; site-directed mutagenesis of Walker A and B motifs in NBF1 and NBF2 The Journal of biological chemistry High 9287292
1998 MgATP (like MgADP) stimulates KATP channel activity through interaction with the nucleotide-binding domains (NBDs) of SUR1; mutations abolishing MgATP binding/hydrolysis (D853N, D1505N, K719A, K1384M) in SUR1 NBDs eliminated the stimulatory effect of MgATP, while ATP sensitivity of truncated Kir6.2 expressed without SUR1 was unaffected by Mg2+. Inside-out patch-clamp recordings of reconstituted Kir6.2/SUR1 channels with NBD mutations in Xenopus oocytes Proceedings of the National Academy of Sciences of the United States of America High 9618560
1998 SUR1 and Kir6.2 form a direct physical complex, as demonstrated by co-immunoprecipitation from in vitro translated proteins and co-transfected COS cells; physical association alters cellular distribution (from honeycomb to diffuse pattern) and single-channel kinetic behavior (extended burst duration), and the distal C-terminus of Kir6.2 is not required for subunit association. Co-immunoprecipitation using Kir6.2-specific antibody from in vitro translated proteins and COS cell lysates; confocal microscopy; single-channel patch-clamp electrophysiology Molecular and cellular biology High 9488482
1998 The SUR1 and Kir6.2 gene promoters are G+C rich with no TATA box; the SUR1 promoter is active in beta-cell lines (HIT T15, MIN6) and inactive in fibroblasts (COS7), with a short 173 bp fragment sufficient for maximal SUR1 promoter activity; Kir6.2 promoter requires >900 bp for high-level expression. Genomic library screening, luciferase reporter transient transfection assays, deletion analysis in multiple cell lines Diabetes Medium 9703328
1999 Sulfonylurea high-affinity block and potassium channel opener (PCO)/MgADP stimulation of KATP channels require functional coupling between Kir6.2 and SUR1; PIP2 stabilizes the channel open state and abolishes high-affinity tolbutamide sensitivity by driving the channel away from closed states preferentially affected by tolbutamide; mutations in Kir6.2 (ΔN30 or L164A) that increase open-state stability similarly uncouple the channel from SUR1 regulatory input. Inside-out patch-clamp recordings with PIP2 application and Kir6.2 point mutations (ΔN30, L164A, R176A) co-expressed with SUR1 in Xenopus oocytes The Journal of general physiology High 10435998
1999 SUR1 NBF1 binds ATP strongly even without Mg2+, while NBF2 binds ADP; NBF2 of SUR1 exhibits greater in vitro ATP hydrolysis than NBF2 of SUR2A, which may underlie the greater MgADP stimulation of SUR1-containing KATP channels versus SUR2A-containing channels. In vitro ATP hydrolysis assay with affinity-purified NBF2 constructs; electrophysiology comparison of Kir6.2/SUR1 versus Kir6.2/SUR2A channels with PIP2 Journal of molecular and cellular cardiology Medium 15893323
2000 The PHHI missense mutation R1420C in SUR1 NBF2 reduces MgATP and MgADP affinity at NBF2 ~5-fold and abolishes cooperative nucleotide binding between NBF1 and NBF2; it increases the EC50 for MgADP activation from 74 to 197 μM when assessed with ATP-insensitive Kir6.2-R50G, while channel expression is reduced but ATP inhibition, tolbutamide block, and diazoxide activation are unaffected. Photoaffinity labeling with mild tryptic digestion to distinguish NBF1/NBF2; inside-out patch-clamp of reconstituted channels in Xenopus oocytes The Journal of biological chemistry High 10993895
2001 Positively charged residues R176 and R177 in Kir6.2 are required for functional coupling to SUR1, conferring MgADP stimulation and sulfonylurea sensitivity; R176C and R177C mutants are not reactivated by MgADP after ATP inhibition and are insensitive to glyburide, whereas R301C and R314C mutants retain MgADP and glyburide sensitivity. Inside-out patch-clamp recordings of Kir6.2 point mutants (R176C, R177C, R301C, R314C) co-expressed with SUR1 in Xenopus oocytes The Journal of general physiology High 11585851
2002 Loss of SUR1 in Sur1 knockout mice impairs PKA-independent cAMP potentiation of insulin secretion by incretins (GLP-1, GIP), establishing that SUR1 is required for the cAMP-sensing mechanism downstream of incretin receptors in pancreatic beta-cells; this effect is specific, as other modulators (mastoparan, PKC activators) remain functional in Sur1KO islets. Pharmacological experiments in isolated islets from Sur1 knockout mice; cAMP measurement; PKA inhibitor treatment (H-89, KT5720); insulin secretion assays Diabetes High 12453898
2004 Zinc activates KATP channels through binding to two SUR1-specific extracellular histidine residues, His-326 and His-332; site-directed mutagenesis of these residues individually and in combination (H326A/H332A) abolished zinc-induced activation, while SUR2A-containing channels showed inhibition by zinc, demonstrating SUR1 isoform specificity. Inside-out and whole-cell patch-clamp with site-directed mutagenesis of SUR1 histidine residues in insulinoma cells and transfected cells The Journal of biological chemistry High 15613469
2006 Activating missense mutations in ABCC8 (encoding SUR1) cause neonatal diabetes by elevating the basal Mg-nucleotide-dependent stimulatory action of SUR1 on the Kir6.2 pore, resulting in markedly higher channel open probability (Po) at physiologic MgATP concentrations in intact cells; mutant channels retain sulfonylurea sensitivity. Electrophysiological assay of mutant KATP channels expressed in intact cells and excised patches; ABCC8 sequencing in 34 neonatal diabetes patients The New England journal of medicine High 16885549
2006 A heterozygous de novo F132L mutation in SUR1 TMD0 (first set of transmembrane helices), proposed to interact with Kir6.2, markedly reduces KATP channel sensitivity to MgATP inhibition and increases whole-cell KATP current, causing DEND syndrome; this establishes TMD0 of SUR1 as a region affecting Kir6.2 ATP sensitivity. ABCC8 sequencing; whole-cell and inside-out patch-clamp electrophysiology of recombinant F132L channels in Xenopus oocytes Human molecular genetics High 16613899
2006 SUR1 protein and mRNA are newly expressed (de novo) after ischemia in neurons, astrocytes, and capillaries in rodent stroke models; upregulation is linked to activation of transcription factor Sp1; newly expressed SUR1 forms functional NC(Ca-ATP) (non-selective cation) channels rather than KATP channels, and block with glibenclamide reduces cerebral edema and infarct volume by ~50%. Western blot, in situ hybridization, immunofluorescence, electrophysiology in rodent stroke models; pharmacological block with glibenclamide Nature medicine High 16550187
2008 An activating Y356C mutation in SUR1 transmembrane helix 7 (TMD1) reduces KATP channel sensitivity to MgATP inhibition via an allosteric effect on Kir6.2 (IC50 increased from 24 to 95 μM, even in absence of Mg2+), impairs glucose-induced cell depolarization and Ca2+ responses in INS1 cells, and causes adult-onset diabetes. Inside-out patch-clamp recordings; perforated whole-cell patch recordings; confocal microscopy; Ca2+ imaging with Fura-Red in INS1(832/13) cells overexpressing SUR1-Y356C Diabetes High 18346985
2010 KATP channel activation by MgADP and MgATP operates through SUR1 NBDs; using Kir6.2-G334D (ATP-inhibition-insensitive) channels, MgATP and MgADP activated channels with EC50 of 112 and 8 μM respectively; activation was suppressed by Walker A lysine mutations in either NBD of SUR1; MgATPγS activated channels; AMPPCP did not activate; both nucleotides produced identical single-channel kinetic effects (elevated Po>0.8, increased open time, reduced interburst closures). Inside-out patch-clamp of Kir6.2-G334D/SUR1 channels with NBD Walker A mutations in Xenopus oocytes The Journal of general physiology High 20876358
2011 Hypoxia stimulates transcription of Abcc8 (SUR1) sequentially through HIF1α binding to HIF-binding sites on the Sp1 promoter, which then drives Sp1 expression; Sp1 in turn binds to the Abcc8 promoter to stimulate SUR1 transcription. HIF-binding sites on the Abcc8 promoter itself are not required; chromatin immunoprecipitation confirmed HIF binding to the Sp1 promoter after cerebral ischemia in vivo. Luciferase reporter assays with promoter deletions; chromatin immunoprecipitation (ChIP) in ischemic rat brain; co-expression of HIF1α; brain microvascular endothelial cell culture Journal of cerebral blood flow and metabolism High 22086197
2011 A conserved intramolecular disulfide bond formed between two N-terminal cysteines in SUR1 (ABCC8) is critical for ER exit and cell surface trafficking; a disease-causing mutation in a conserved N-terminal cysteine of SUR1 prevents the protein from reaching the cell surface, causing hyperinsulinemic hypoglycemia. Mutagenesis of conserved cysteines; glycosylation analysis; immunoblot; proteasome inhibitor MG132 rescue experiments in multiple cell types The Journal of biological chemistry High 21199866
2011 Dominant loss-of-function ABCC8 mutations causing diazoxide-unresponsive diffuse hyperinsulinism produce SUR1 channels with normal plasma membrane trafficking but severely impaired responses to diazoxide or MgADP, contrasting with dominant mutations causing diazoxide-responsive disease; the degree of impairment of diazoxide/MgADP response distinguishes diazoxide-responsive from diazoxide-unresponsive dominant mutations. Expression in COSm6 cells; Rb+ efflux assay; ABCC8 sequencing in 15 families Diabetes High 21536946
2012 SUR1 co-assembles with TRPM4 (transient receptor potential melastatin 4) to form Sur1-TRPM4 heteromers that constitute the NC(Ca-ATP) non-selective cation channel in CNS injury; co-expression yields channels with biophysical properties of TRPM4 and pharmacological properties of SUR1; co-assembly with SUR1 doubles TRPM4 affinity for calmodulin and doubles its Ca2+ sensitivity; Sur1-TRPM4 heteromers appear de novo after spinal cord injury. FRET (Förster resonance energy transfer); co-immunoprecipitation; patch-clamp electrophysiology; calmodulin binding assay; rat spinal cord injury model The Journal of biological chemistry High 23255597
2012 E203 in SUR1 and Q52 in Kir6.2 are in close proximity and their interaction dynamically regulates KATP channel ATP sensitivity; E203K/Q52E double mutant channels exhibit ~100-fold higher ATP sensitivity than wild-type; cross-linking of E203C and Q52C locks the channel in a closed state reversible by reducing agents. Site-directed mutagenesis (E203K in SUR1, Q52E in Kir6.2); cysteine cross-linking with oxidizing/reducing agents; inside-out patch-clamp in Xenopus oocytes The Journal of general physiology High 22802363
2013 EPAC (Exchange Protein Activated by cAMP) binds directly to an intracellular loop of SUR1 (amino acids 859-881); this binding closes KATP channels; ablation of EPAC or expression of the competing SUR1(859-881) peptide increases KATP channel open probability, inhibits glutamate release, and reduces seizure vulnerability in mice. Direct binding assay (EPAC to SUR1(859-881) peptide); patch-clamp electrophysiology; glutamate release assay; in vivo seizure model in adult mice with EPAC knockout The Journal of neuroscience Medium 23678128
2017 SUR1-TRPM4 co-assembles with AQP4 to form a heteromultimeric water/ion channel complex (SUR1-TRPM4-AQP4); the full tripartite complex is required for fast, high-capacity transmembrane water transport driving cell swelling; co-assembly confirmed by co-IP and FRET; genetic inactivation of the SUR1-TRPM4 solute pore blocked in vivo astrocyte swelling in a brain edema model. Co-immunoprecipitation; FRET; calcein fluorescence cell-swelling assay in COS-7 cells; diolistic labeling for in vivo astrocyte volume measurement; cold-injury mouse brain edema model Glia High 28906027
2018 Cryo-EM structures of pancreatic KATP channels reveal the glibenclamide binding site on SUR1, show how the Kir6.2 N-terminus couples the peripheral SUR1 subunit to the central Kir6.2 pore, reveal the binding mode of activating Mg-nucleotides at SUR1 NBDs, and suggest the mechanism by which Mg-ADP binding drives conformational change of SUR1. Cryo-electron microscopy at 4.1–4.5 Å resolution Protein & cell High 29594720
2018 NF-κB activation of brain endothelial cells (BEC) causes de novo expression of SUR1-TRPM4 channels; tPA induces PAR1-mediated opening of SUR1-TRPM4 channels in a plasmin-, TRPC3-, and Ca2+-dependent manner; functional SUR1-TRPM4 channels are required for tPA-induced phasic (but not tonic) secretion of MMP-9 from BEC; SUR1 inhibition decreases tPA-induced MMP-9 secretion. Patch-clamp electrophysiology; ELISA and zymography for MMP-9; calcium imaging; genetic and pharmacological manipulation of SUR1, TRPM4, PAR1, TRPC3; NF-κB activation in murine and human BEC PloS one High 29617457
2019 SUR1-TRPM4 channels (not KATP channels) mediate post-ischemic brain swelling; antisense oligodeoxynucleotides against Abcc8/SUR1 or Trpm4/TRPM4 each reduced hemispheric swelling by ~50% in rat permanent MCA occlusion, whereas AS-ODNs against Kcnj8/KIR6.1 or Kcnj11/KIR6.2 had no significant effect on swelling; SUR1-TRPM4 heteromers were confirmed by immuno-FRET and co-IP in post-ischemic tissue. Antisense oligodeoxynucleotides (molecularly targeted knockdown); MRI-based hemispheric swelling measurement; immuno-FRET; co-immunoprecipitation in rat pMCAo model Neuroscience letters High 31899311
2021 Loss of SUR1 function in iPSC-derived islets (homozygous ABCC8-V187D) causes excess insulin secretion at low glucose, beta-cell proliferation, and nucleomegaly; pharmacological KATP channel inactivation in corrected cells recapitulates the proliferation phenotype, establishing that SUR1-mediated KATP channel activity regulates beta-cell proliferation during islet development. iPSC differentiation to SC-islets; CRISPR-Cas9 correction; static and dynamic insulin secretion assays; BrdU proliferation assay; pharmacological KATP inactivation; xenograft in NOD-SCID gamma mice Diabetologia High 33404684
2023 In ischemic stroke, SUR1-TRPM4 channels in perivascular astrocyte endfeet mediate Na+ influx that drives Ca2+ entry via NCX1 operating in reverse mode; elevated intra-endfoot Ca2+ triggers calmodulin-dependent AQP4 translocation to the plasma membrane, causing water influx and brain swelling; pharmacological inhibition or astrocyte-specific deletion of SUR1-TRPM4 or NCX1 reduced brain swelling and improved neurological function independently of infarct size. Mouse permanent MCA occlusion; astrocyte-specific Abcc8 conditional knockout (pGfap-cre); pharmacological inhibition; Ca2+ imaging; AQP4 surface localization assay; neurological function scoring Science signaling High 37279286
2016 Sur1-Trpm4 channels regulate NOS2 transcription in TLR4-activated microglia through a Ca2+-sensitive calcineurin/NFAT pathway; inhibition or gene silencing of Sur1 or Trpm4 paradoxically increases intracellular Ca2+ (by removing Na+ influx-driven Ca2+ suppression), yet decreases NFAT nuclear translocation via activation of CaMKII and calcineurin phosphorylation; chromatin immunoprecipitation confirmed NFAT binding to the Nos2 promoter. Patch-clamp electrophysiology; calcium imaging; qPCR; Griess assay; immunoblot; chromatin immunoprecipitation; Abcc8-/- and Trpm4-/- mice; pharmacological inhibition in vivo and in vitro Journal of neuroinflammation High 27246103
2002 Novel SUR1-selective KATP channel opener NNC 55-9216 activates Kir6.2/SUR1 but not Kir6.2/SUR2A or Kir6.2/SUR2B channels; activation requires intracellular MgATP and Walker A motif integrity in both NBDs of SUR1; chimera analysis identified transmembrane domains 8-11 of SUR1 as critical structural determinants for NNC 55-9216 action, with NBD2 providing additional contribution. Inside-out patch-clamp in Xenopus oocytes; SUR1/SUR2A chimeras; Walker A mutagenesis; [3H]glibenclamide competitive binding Diabetes High 12031979
2005 Glibenclamide-induced apoptosis is specifically enhanced by expression of SUR1 but not SUR2B; a single amino acid substitution M1289T in transmembrane helix 17 (TM17) of SUR1 abolishes the apoptotic enhancement; coexpression with Kir6.2 does not alter the apoptotic effect, indicating a Kir6.2/KATP channel-independent pro-apoptotic function of SUR1. Cell detachment, nuclear condensation, DNA fragmentation, caspase-3-like activity assays in HEK293 cells expressing SUR1, SUR2B, SUR1(M1289T), or SUR1+Kir6.2 The Journal of pharmacology and experimental therapeutics Medium 16306272
2012 TRPM4 currents expressed alone or with SUR1 in COSm6 cells are Ca2+-activated, voltage-dependent, ATP-inhibited, and insensitive to glibenclamide and tolbutamide; cotransfection of SUR1 did not alter TRPM4-mediated current properties; no detectable FRET was observed between fluorophore-tagged TRPM4 and SUR1, whereas robust FRET was detected between Kir6.2 and SUR1. This constitutes a negative finding: functional or structural association of TRPM4 and SUR1 was not detected in this experimental system. Patch-clamp electrophysiology; FRET in COSm6 cells co-expressing TRPM4 with or without SUR1 and/or Kir6.2 The Journal of biological chemistry Medium 22291026
2010 Abcc8 gene expression is upregulated after spinal cord injury in rodents and humans; elimination of SUR1 (Abcc8-/- mice) or antisense knockdown of Abcc8 prevents progressive hemorrhagic necrosis, reduces lesion size to one-quarter to one-third of controls, and improves neurological function; the protective effect is associated with prevention of oncotic death of capillary endothelial cells. Abcc8 knockout mice; antisense oligodeoxynucleotides in rats; histology; neurological scoring; immunohistochemistry for SUR1 in human and rodent SCI tissue Science translational medicine High 20410530
2012 Promoter CpG methylation differentially regulates SUR1 (Abcc8) and SUR2 (Abcc9) expression in cardiomyocytes; in HL-1 atrial cardiomyocytes, SUR2 promoter CpGs are 57.6% methylated versus 0.14% for SUR1, and 5-aza-2'-deoxycytidine treatment increases unmethylated SUR2 fraction and mRNA; SUR1 and SUR2 CpG islands are essentially unmethylated in native atrial and ventricular myocytes, indicating additional regulatory mechanisms exist. Bisulfite sequencing of genomic DNA; 5-aza-2'-deoxycytidine treatment; qRT-PCR for SUR1 and SUR2 mRNA in HL-1 cells and native myocytes PloS one Medium 22844491

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. The New England journal of medicine 469 16885549
2006 Newly expressed SUR1-regulated NC(Ca-ATP) channel mediates cerebral edema after ischemic stroke. Nature medicine 346 16550187
1998 Paternal mutation of the sulfonylurea receptor (SUR1) gene and maternal loss of 11p15 imprinted genes lead to persistent hyperinsulinism in focal adenomatous hyperplasia. The Journal of clinical investigation 234 9769320
1997 Overlapping distribution of K(ATP) channel-forming Kir6.2 subunit and the sulfonylurea receptor SUR1 in rodent brain. FEBS letters 195 9003806
2009 Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism. Human mutation 191 18767144
2006 A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes. Human molecular genetics 167 16613899
2012 The sulfonylurea receptor 1 (Sur1)-transient receptor potential melastatin 4 (Trpm4) channel. The Journal of biological chemistry 154 23255597
1997 MgADP antagonism to Mg2+-independent ATP binding of the sulfonylurea receptor SUR1. The Journal of biological chemistry 149 9287292
1998 MgATP activates the beta cell KATP channel by interaction with its SUR1 subunit. Proceedings of the National Academy of Sciences of the United States of America 144 9618560
2020 Update of variants identified in the pancreatic β-cell KATP channel genes KCNJ11 and ABCC8 in individuals with congenital hyperinsulinism and diabetes. Human mutation 131 32027066
2011 Heterozygous ABCC8 mutations are a cause of MODY. Diabetologia 125 21989597
2009 Review. SUR1: a unique ATP-binding cassette protein that functions as an ion channel regulator. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 120 18990670
2008 Ser1369Ala variant in sulfonylurea receptor gene ABCC8 is associated with antidiabetic efficacy of gliclazide in Chinese type 2 diabetic patients. Diabetes care 117 18599530
2017 SUR1-TRPM4 and AQP4 form a heteromultimeric complex that amplifies ion/water osmotic coupling and drives astrocyte swelling. Glia 113 28906027
2001 Unbalanced expression of 11p15 imprinted genes in focal forms of congenital hyperinsulinism: association with a reduction to homozygosity of a mutation in ABCC8 or KCNJ11. The American journal of pathology 96 11395395
2010 ABCC8 and KCNJ11 molecular spectrum of 109 patients with diazoxide-unresponsive congenital hyperinsulinism. Journal of medical genetics 92 20685672
2006 Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Human mutation 90 16416420
2018 Ligand binding and conformational changes of SUR1 subunit in pancreatic ATP-sensitive potassium channels. Protein & cell 89 29594720
2015 Sur1-Trpm4 Cation Channel Expression in Human Cerebral Infarcts. Journal of neuropathology and experimental neurology 83 26172285
2002 cAMP-activated protein kinase-independent potentiation of insulin secretion by cAMP is impaired in SUR1 null islets. Diabetes 82 12453898
1999 Sulfonylurea and K(+)-channel opener sensitivity of K(ATP) channels. Functional coupling of Kir6.2 and SUR1 subunits. The Journal of general physiology 82 10435998
2011 Hyperinsulinaemic hypoglycaemia and diabetes mellitus due to dominant ABCC8/KCNJ11 mutations. Diabetologia 76 21674179
2016 The Sur1-Trpm4 channel regulates NOS2 transcription in TLR4-activated microglia. Journal of neuroinflammation 72 27246103
2007 SNPs in the KCNJ11-ABCC8 gene locus are associated with type 2 diabetes and blood pressure levels in the Japanese population. Journal of human genetics 71 17823772
1998 Evidence for direct physical association between a K+ channel (Kir6.2) and an ATP-binding cassette protein (SUR1) which affects cellular distribution and kinetic behavior of an ATP-sensitive K+ channel. Molecular and cellular biology 71 9488482
2010 Brief suppression of Abcc8 prevents autodestruction of spinal cord after trauma. Science translational medicine 70 20410530
2011 Sequential activation of hypoxia-inducible factor 1 and specificity protein 1 is required for hypoxia-induced transcriptional stimulation of Abcc8. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 68 22086197
2018 Loss-of-Function ABCC8 Mutations in Pulmonary Arterial Hypertension. Circulation. Genomic and precision medicine 66 30354297
2004 Hyperinsulinism of infancy: novel ABCC8 and KCNJ11 mutations and evidence for additional locus heterogeneity. The Journal of clinical endocrinology and metabolism 66 15579781
2010 Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11. Reviews in endocrine & metabolic disorders 65 20922570
2005 Differential nucleotide regulation of KATP channels by SUR1 and SUR2A. Journal of molecular and cellular cardiology 64 15893323
2004 Induction of beta-cell rest by a Kir6.2/SUR1-selective K(ATP)-channel opener preserves beta-cell insulin stores and insulin secretion in human islets cultured at high (11 mM) glucose. The Journal of clinical endocrinology and metabolism 64 14764798
2007 New ABCC8 mutations in relapsing neonatal diabetes and clinical features. Diabetes 63 17389331
2007 Mutations in the ABCC8 gene encoding the SUR1 subunit of the KATP channel cause transient neonatal diabetes, permanent neonatal diabetes or permanent diabetes diagnosed outside the neonatal period. Diabetes, obesity & metabolism 62 17919176
2005 Common variants in the ATP-sensitive K+ channel genes KCNJ11 (Kir6.2) and ABCC8 (SUR1) in relation to glucose intolerance: population-based studies and meta-analyses. Diabetic medicine : a journal of the British Diabetic Association 62 15842514
2011 Diazoxide-unresponsive congenital hyperinsulinism in children with dominant mutations of the β-cell sulfonylurea receptor SUR1. Diabetes 61 21536946
2004 Polymorphisms of the SUR1 (ABCC8) and Kir6.2 (KCNJ11) genes predict the conversion from impaired glucose tolerance to type 2 diabetes. The Finnish Diabetes Prevention Study. The Journal of clinical endocrinology and metabolism 58 15579791
2015 Silencing of Abcc8 or inhibition of newly upregulated Sur1-Trpm4 reduce inflammation and disease progression in experimental autoimmune encephalomyelitis. Journal of neuroinflammation 57 26581714
2008 A rare mutation in ABCC8/SUR1 leading to altered ATP-sensitive K+ channel activity and beta-cell glucose sensing is associated with type 2 diabetes in adults. Diabetes 52 18346985
2014 Ghrelin inhibits BSCB disruption/hemorrhage by attenuating MMP-9 and SUR1/TrpM4 expression and activation after spinal cord injury. Biochimica et biophysica acta 51 25261791
2008 Association of KCNJ11 and ABCC8 genetic polymorphisms with response to repaglinide in Chinese diabetic patients. Acta pharmacologica Sinica 51 18664331
2007 Co-localisation of the Kir6.2/SUR1 channel complex with glucagon-like peptide-1 and glucose-dependent insulinotrophic polypeptide expression in human ileal cells and implications for glycaemic control in new onset type 1 diabetes. European journal of endocrinology 51 17535866
1999 Comparative aspects of the function and mechanism of SUR1 and MDR1 proteins. Biochimica et biophysica acta 51 10581363
2006 Mutation spectra of ABCC8 gene in Spanish patients with Hyperinsulinism of Infancy (HI). Human mutation 50 16429405
2012 Does inhibiting Sur1 complement rt-PA in cerebral ischemia? Annals of the New York Academy of Sciences 49 22994227
2007 An ABCC8 gene mutation and mosaic uniparental isodisomy resulting in atypical diffuse congenital hyperinsulinism. Diabetes 49 17942822
2018 SUR1-TRPM4 channel activation and phasic secretion of MMP-9 induced by tPA in brain endothelial cells. PloS one 46 29617457
2013 Inhibition of SUR1 decreases the vascular permeability of cerebral metastases. Neoplasia (New York, N.Y.) 44 23633925
2023 Cation flux through SUR1-TRPM4 and NCX1 in astrocyte endfeet induces water influx through AQP4 and brain swelling after ischemic stroke. Science signaling 42 37279286
2015 17β-estradiol inhibits MMP-9 and SUR1/TrpM4 expression and activation and thereby attenuates BSCB disruption/hemorrhage after spinal cord injury in male rats. Endocrinology 42 25763638
2000 Association of a variant in exon 31 of the sulfonylurea receptor 1 (SUR1) gene with type 2 diabetes mellitus in French Caucasians. Human genetics 42 11030411
2017 ABCC8 Single Nucleotide Polymorphisms are Associated with Cerebral Edema in Severe TBI. Neurocritical care 41 27677908
2016 ABCC8-Related Maturity-Onset Diabetes of the Young (MODY12): Clinical Features and Treatment Perspective. Diabetes therapy : research, treatment and education of diabetes and related disorders 41 27538677
2011 Clinical and metabolic features of adult-onset diabetes caused by ABCC8 mutations. Diabetes care 41 22210575
2010 Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1. The Journal of general physiology 40 20876358
2000 Functional analysis of a mutant sulfonylurea receptor, SUR1-R1420C, that is responsible for persistent hyperinsulinemic hypoglycemia of infancy. The Journal of biological chemistry 38 10993895
2019 SUR1-TRPM4 channels, not KATP, mediate brain swelling following cerebral ischemia. Neuroscience letters 37 31899311
2011 Conserved intramolecular disulfide bond is critical to trafficking and fate of ATP-binding cassette (ABC) transporters ABCB6 and sulfonylurea receptor 1 (SUR1)/ABCC8. The Journal of biological chemistry 37 21199866
2020 Resveratrol reduces cerebral edema through inhibition of de novo SUR1 expression induced after focal ischemia. Experimental neurology 34 32380020
2015 High Incidence of Heterozygous ABCC8 and HNF1A Mutations in Czech Patients With Congenital Hyperinsulinism. The Journal of clinical endocrinology and metabolism 34 26431509
1998 Cloning of the promoters for the beta-cell ATP-sensitive K-channel subunits Kir6.2 and SUR1. Diabetes 34 9703328
2020 HIV-1 Vpr-Induced Proinflammatory Response and Apoptosis Are Mediated through the Sur1-Trpm4 Channel in Astrocytes. mBio 32 33293383
2011 Characterization of ABCC8 and KCNJ11 gene mutations and phenotypes in Korean patients with congenital hyperinsulinism. European journal of endocrinology 32 21422196
2005 Glibenclamide-induced apoptosis is specifically enhanced by expression of the sulfonylurea receptor isoform SUR1 but not by expression of SUR2B or the mutant SUR1(M1289T). The Journal of pharmacology and experimental therapeutics 32 16306272
2002 The novel diazoxide analog 3-isopropylamino-7-methoxy-4H-1,2,4-benzothiadiazine 1,1-dioxide is a selective Kir6.2/SUR1 channel opener. Diabetes 32 12031979
2002 ABCC8 (SUR1) and KCNJ11 (KIR6.2) mutations in persistent hyperinsulinemic hypoglycemia of infancy and evaluation of different therapeutic measures. Journal of pediatric endocrinology & metabolism : JPEM 31 12199344
2000 Pharmacology of human sulphonylurea receptor SUR1 and inward rectifier K(+) channel Kir6.2 combination expressed in HEK-293 cells. British journal of pharmacology 29 10742287
2013 Association of adiponectin (AdipoQ) and sulphonylurea receptor (ABCC8) gene polymorphisms with Type 2 Diabetes in North Indian population of Punjab. Gene 28 23764562
2012 Engineered interaction between SUR1 and Kir6.2 that enhances ATP sensitivity in KATP channels. The Journal of general physiology 28 22802363
2008 Mutations in the ABCC8 (SUR1 subunit of the K(ATP) channel) gene are associated with a variable clinical phenotype. Clinical endocrinology 28 19021632
2002 Functional expression of Kir 6.1/SUR1-K(ATP) channels in frog retinal Müller glial cells. Glia 28 11968063
2022 Glibenclamide Directly Prevents Neuroinflammation by Targeting SUR1-TRPM4-Mediated NLRP3 Inflammasome Activation In Microglia. Molecular neurobiology 27 35972671
2021 SUR1-mutant iPS cell-derived islets recapitulate the pathophysiology of congenital hyperinsulinism. Diabetologia 27 33404684
2014 ABCC8 genetic variants and risk of diabetes mellitus. Gene 27 24768178
2011 ABCC8 mutation allele frequency in the Ashkenazi Jewish population and risk of focal hyperinsulinemic hypoglycemia. Genetics in medicine : official journal of the American College of Medical Genetics 27 21716120
2015 The Nucleotide-Binding Sites of SUR1: A Mechanistic Model. Biophysical journal 26 26682803
2004 Two SUR1-specific histidine residues mandatory for zinc-induced activation of the rat KATP channel. The Journal of biological chemistry 26 15613469
2012 On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1. The Journal of biological chemistry 24 22291026
2020 Characterization of rare ABCC8 variants identified in Spanish pulmonary arterial hypertension patients. Scientific reports 23 32934261
2019 Morphine Efficacy, Tolerance, and Hypersensitivity Are Altered After Modulation of SUR1 Subtype KATP Channel Activity in Mice. Frontiers in neuroscience 23 31695594
2017 KCNJ11, ABCC8 and TCF7L2 polymorphisms and the response to sulfonylurea treatment in patients with type 2 diabetes: a bioinformatics assessment. BMC medical genetics 23 28587604
2007 Arrhythmia susceptibility and premature death in transgenic mice overexpressing both SUR1 and Kir6.2[DeltaN30,K185Q] in the heart. American journal of physiology. Heart and circulatory physiology 23 17449558
2002 Sulfonylurea receptor -1 (SUR1): genetic and metabolic evidences for a role in the susceptibility to type 2 diabetes mellitus. Diabetes & metabolism 23 11938023
2001 Regulation of cloned ATP-sensitive K channels by adenine nucleotides and sulfonylureas: interactions between SUR1 and positively charged domains on Kir6.2. The Journal of general physiology 23 11585851
2017 Expression of JAZF1, ABCC8, KCNJ11and Notch2 genes and vitamin D receptor polymorphisms in type 2 diabetes, and their association with microvascular complications. Therapeutic advances in endocrinology and metabolism 22 28794851
2012 Promoter DNA methylation regulates murine SUR1 (Abcc8) and SUR2 (Abcc9) expression in HL-1 cardiomyocytes. PloS one 22 22844491
2016 SUR1 Receptor Interaction with Hesperidin and Linarin Predicts Possible Mechanisms of Action of Valeriana officinalis in Parkinson. Frontiers in aging neuroscience 21 27199743
2021 SUR1, newly expressed in astrocytes, mediates neuropathic pain in a mouse model of peripheral nerve injury. Molecular pain 20 33788643
2022 SUR1 As a New Therapeutic Target for Pulmonary Arterial Hypertension. American journal of respiratory cell and molecular biology 19 35175177
2019 Glibenclamide, a Sur1-Trpm4 antagonist, does not improve outcome after collagenase-induced intracerebral hemorrhage. PloS one 19 31042750
2019 Structure-Activity Relationships, Pharmacokinetics, and Pharmacodynamics of the Kir6.2/SUR1-Specific Channel Opener VU0071063. The Journal of pharmacology and experimental therapeutics 19 31201216
2015 Replication of KCNJ11 (p.E23K) and ABCC8 (p.S1369A) Association in Russian Diabetes Mellitus 2 Type Cohort and Meta-Analysis. PloS one 19 25955821
2013 EPAC inhibition of SUR1 receptor increases glutamate release and seizure vulnerability. The Journal of neuroscience : the official journal of the Society for Neuroscience 19 23678128
2007 Complex ABCC8 DNA variations in congenital hyperinsulinism: lessons from functional studies. Clinical endocrinology 19 17466004
2018 Deletion of Kir6.2/SUR1 potassium channels rescues diminishing of DA neurons via decreasing iron accumulation in PD. Molecular and cellular neurosciences 18 30171894
2022 Role of upregulation of the KATP channel subunit SUR1 in dopaminergic neuron degeneration in Parkinson's disease. Aging cell 17 35441806
2008 A novel ABCC8 (SUR1)-dependent mechanism of metabolism-excitation uncoupling. The Journal of biological chemistry 17 18281290
2017 Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9. Scientific reports 16 28600547
2022 Association of KCNJ11 and ABCC8 single-nucleotide polymorphisms with type 2 diabetes mellitus in a Kinh Vietnamese population. Medicine 15 36401380
2019 Aβ1-42 increases the expression of neural KATP subunits Kir6.2/SUR1 via the NF-κB, p38 MAPK and PKC signal pathways in rat primary cholinergic neurons. Human & experimental toxicology 15 30868916

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