| scholarly article | Q13442814 |
| P6179 | Dimensions Publication ID | 1020351722 |
| P356 | DOI | 10.1007/S00424-006-0112-3 |
| P3181 | OpenCitations bibliographic resource ID | 3302685 |
| P698 | PubMed publication ID | 17021801 |
| P5875 | ResearchGate publication ID | 6772841 |
| P50 | author | Frances Ashcroft | Q5478504 |
| Guiomar Perez de Nanclares | Q51014984 | ||
| Christophe Girard | Q73661941 | ||
| Luis Castaño | Q42278338 | ||
| P2093 | author name string | Kenju Shimomura | |
| Peter Proks | |||
| Nathan Absalom | |||
| P2860 | cites work | Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches | Q22337395 |
| Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor | Q24304448 | ||
| Molecular mechanism for ATP-dependent closure of the K+ channel Kir6.2 | Q24308180 | ||
| Involvement of the N-terminus of Kir6.2 in the inhibition of the KATP channel by ATP. | Q50741434 | ||
| KCNJ11 activating mutations in Italian patients with permanent neonatal diabetes | Q52085176 | ||
| The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus | Q53863141 | ||
| Transient neonatal diabetes: widening the understanding of the etiopathogenesis of diabetes | Q74102330 | ||
| Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features | Q24320031 | ||
| Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes | Q24338339 | ||
| Crystal structure of the potassium channel KirBac1.1 in the closed state | Q27641201 | ||
| A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes | Q27863920 | ||
| Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor | Q28237709 | ||
| Electrophysiology of the pancreatic beta-cell | Q28240546 | ||
| Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells | Q28259615 | ||
| ATP interaction with the open state of the K(ATP) channel | Q28346280 | ||
| Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions | Q28565185 | ||
| Targeted Overactivity of β Cell KATP Channels Induces Profound Neonatal Diabetes | Q29027344 | ||
| ATP-sensitive potassium channelopathies: focus on insulin secretion | Q33905803 | ||
| Neonatal diabetes: new insights into aetiology and implications | Q33968569 | ||
| A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome | Q34166805 | ||
| 3-D structural and functional characterization of the purified KATP channel complex Kir6.2-SUR1. | Q34324901 | ||
| Adenosine diphosphate as an intracellular regulator of insulin secretion. | Q34382672 | ||
| Sulphonylurea action revisited: the post-cloning era. | Q35159821 | ||
| Type 2 diabetes mellitus: not quite exciting enough? | Q35634223 | ||
| Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy | Q36241098 | ||
| From molecule to malady | Q36428969 | ||
| Octameric Stoichiometry of the KATP Channel Complex | Q36436003 | ||
| Molecular analysis of ATP-sensitive K channel gating and implications for channel inhibition by ATP. | Q36436065 | ||
| Stabilization of the activity of ATP-sensitive potassium channels by ion pairs formed between adjacent Kir6.2 subunits | Q36436497 | ||
| MgATP activates the beta cell KATP channel by interaction with its SUR1 subunit. | Q36515292 | ||
| Cloning and functional expression of the cDNA encoding a novel ATP-sensitive potassium channel subunit expressed in pancreatic beta-cells, brain, heart and skeletal muscle | Q36789864 | ||
| ATP sensitivity of ATP-sensitive K+ channels: role of the gamma phosphate group of ATP and the R50 residue of mouse Kir6.2. | Q40372990 | ||
| Functional analysis of a structural model of the ATP-binding site of the KATP channel Kir6.2 subunit. | Q40949543 | ||
| Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2: patient characteristics and initial response to sulfonylurea therapy | Q45077978 | ||
| Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2. | Q45142819 | ||
| Relapsing diabetes can result from moderately activating mutations in KCNJ11. | Q45271611 | ||
| Cytoplasmic domain structures of Kir2.1 and Kir3.1 show sites for modulating gating and rectification | Q46536039 | ||
| Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP. | Q46640868 | ||
| Kir6.2 mutations are a common cause of permanent neonatal diabetes in a large cohort of French patients | Q47306165 | ||
| Properties of cloned ATP-sensitive K+ currents expressed in Xenopus oocytes | Q48968120 | ||
| Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations | Q50646471 | ||
| Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy | Q50648710 | ||
| Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects | Q50648718 | ||
| P433 | issue | 3 | |
| P407 | language of work or name | English | Q1860 |
| P921 | main subject | clinical chemistry | Q849994 |
| P304 | page(s) | 323-332 | |
| P577 | publication date | 2006-09-22 | |
| P1433 | published in | Pfluegers Archiv | Q1091689 |
| P1476 | title | Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes | |
| P478 | volume | 453 |
| Q107514451 | Inward rectifying potassium channel complex, Kir6.2-SUR1 |
| Q107602501 | Inward rectifying potassium channel complex, Kir6.2-SUR1 |
| Q42599483 | A conserved tryptophan at the membrane-water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated. |
| Q47629498 | A novel KCNJ11 mutation associated with transient neonatal diabetes |
| Q36042053 | Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism |
| Q41466635 | Ankyrin regulates KATP channel membrane trafficking and gating in excitable cells |
| Q58590946 | Cognitive, Neurological, and Behavioral Features in Adults With Neonatal Diabetes |
| Q36957386 | DEND mutation in Kir6.2 (KCNJ11) reveals a flexible N-terminal region critical for ATP-sensing of the KATP channel |
| Q36146862 | Decreases in Gap Junction Coupling Recovers Ca2+ and Insulin Secretion in Neonatal Diabetes Mellitus, Dependent on Beta Cell Heterogeneity and Noise |
| Q39261263 | Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism |
| Q83797707 | Detection of KCNJ11 gene mutations in a family with neonatal diabetes mellitus: implications for therapeutic management of family members with long-standing disease |
| Q36953066 | Diagnosis and treatment of neonatal diabetes: a United States experience |
| Q46964176 | Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes |
| Q34718408 | Functional characterization of a novel KCNJ11 in frame mutation-deletion associated with infancy-onset diabetes and a mild form of intermediate DEND: a battle between K(ATP) gain of channel activity and loss of channel expression. |
| Q37634376 | K(ATP) channelopathies in the pancreas |
| Q42378734 | KATP Channel Mutations and Neonatal Diabetes |
| Q28238720 | Molecular cell biology of KATP channels: implications for neonatal diabetes |
| Q90540588 | Monogenic Forms of Diabetes Mellitus |
| Q37677448 | Mutations in KCNJ11 are associated with the development of autosomal dominant, early-onset type 2 diabetes |
| Q81152665 | Neonatal diabetes mellitus |
| Q94592225 | New insights into KATP channel gene mutations and neonatal diabetes mellitus |
| Q26744692 | Running out of time: the decline of channel activity and nucleotide activation in adenosine triphosphate-sensitive K-channels |
| Q36908155 | Successful transfer to sulfonylureas in KCNJ11 neonatal diabetes is determined by the mutation and duration of diabetes. |
| Q37022565 | Switching to sulphonylureas in children with iDEND syndrome caused by KCNJ11 mutations results in improved cerebellar perfusion |
| Q48555497 | The Walter B. Cannon Physiology in Perspective Lecture, 2007. ATP-sensitive K+ channels and disease: from molecule to malady |
| Q34316689 | The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes |
| Q37259401 | 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 |
| Q30466668 | Whole-exome sequencing and high throughput genotyping identified KCNJ11 as the thirteenth MODY gene |
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