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Literature DB >> 27540685

Styrax blocks inward and outward current of Kir2.1 channel.

Shuxi Ren¹, Chunli Pang¹, Junwei Li¹, Yayue Huang¹, Suhua Zhang¹, Yong Zhan¹, Hailong An¹.

Abstract

Kir2.1 plays key roles in setting rest membrane potential and modulation of cell excitability. Mutations of Kir2.1, such as D172N or E299V, inducing gain-of-function, can cause type3 short QT syndrome (SQT3) due to the enlarged outward currents. So far, there is no clinical drug target to block the currents of Kir2.1. Here, we identified a novel blocker of Kir2.1, styrax, which is a kind of natural compound selected from traditional Chinese medicine. Our data show that styrax can abolish the inward and outward currents of Kir2.1. The IC50 of styrax for WT, D172N and E299V are 0.0113 ± 0.00075, 0.0204 ± 0.0048 and 0.0122 ± 0.0012 (in volume), respectively. The results indicate that styrax can serve as a novel blocker for Kir2.1.

Entities: Disease Gene Mutation

Keywords: Kir2.1; SQT3; bloker; fluxOR™; ion channel; patch clamp; styrax

Mesh：

Substances：

Year: 2016 PMID： 27540685 PMCID： PMC5279881 DOI： 10.1080/19336950.2016.1207022

Source DB: PubMed Journal: Channels (Austin) ISSN： 1933-6950 Impact factor: 2.581

39 in total

Review 1. Short QT syndrome.

Authors: Ramon Brugada; Kui Hong; Jonathan M Cordeiro; Robert Dumaine
Journal: CMAJ Date: 2005-11-22 Impact factor: 8.262

2. Cytoplasmic domain structures of Kir2.1 and Kir3.1 show sites for modulating gating and rectification.

Authors: Scott Pegan; Christine Arrabit; Wei Zhou; Witek Kwiatkowski; Anthony Collins; Paul A Slesinger; Senyon Choe
Journal: Nat Neurosci Date: 2005-02-20 Impact factor: 24.884

3. Structural bases for the different anti-fibrillatory effects of chloroquine and quinidine.

Authors: Sami F Noujaim; Jeanne A Stuckey; Daniela Ponce-Balbuena; Tania Ferrer-Villada; Angelica López-Izquierdo; Sandeep V Pandit; José A Sánchez-Chapula; José Jalife
Journal: Cardiovasc Res Date: 2011-01-13 Impact factor: 10.787

4. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome.

Authors: N M Plaster; R Tawil; M Tristani-Firouzi; S Canún; S Bendahhou; A Tsunoda; M R Donaldson; S T Iannaccone; E Brunt; R Barohn; J Clark; F Deymeer; A L George; F A Fish; A Hahn; A Nitu; C Ozdemir; P Serdaroglu; S H Subramony; G Wolfe; Y H Fu; L J Ptácek
Journal: Cell Date: 2001-05-18 Impact factor: 41.582

5. A novel neuropsychiatric phenotype of KCNJ2 mutation in one Taiwanese family with Andersen-Tawil syndrome.

Authors: Hoi-Fong Chan; Meng-Ling Chen; Jen-Jen Su; Li-Chin Ko; Chin-Hsien Lin; Ruey-Meei Wu
Journal: J Hum Genet Date: 2010-01-29 Impact factor: 3.172

6. Distant cytosolic residues mediate a two-way molecular switch that controls the modulation of inwardly rectifying potassium (Kir) channels by cholesterol and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)).

Authors: Avia Rosenhouse-Dantsker; Sergei Noskov; Huazhi Han; Scott K Adney; Qiong-Yao Tang; Aldo A Rodríguez-Menchaca; Gregory B Kowalsky; Vasileios I Petrou; Catherine V Osborn; Diomedes E Logothetis; Irena Levitan
Journal: J Biol Chem Date: 2012-09-20 Impact factor: 5.157

7. Spermine and spermidine as gating molecules for inward rectifier K+ channels.

Authors: E Ficker; M Taglialatela; B A Wible; C M Henley; A M Brown
Journal: Science Date: 1994-11-11 Impact factor: 47.728

8. Tamoxifen inhibits inward rectifier K+ 2.x family of inward rectifier channels by interfering with phosphatidylinositol 4,5-bisphosphate-channel interactions.

Authors: Daniela Ponce-Balbuena; Angélica López-Izquierdo; Tania Ferrer; Aldo A Rodríguez-Menchaca; Iván A Aréchiga-Figueroa; José A Sánchez-Chapula
Journal: J Pharmacol Exp Ther Date: 2009-08-04 Impact factor: 4.030

Styrax blocks inward and outward current of Kir2.1 channel.

Review 1. Short QT syndrome.

2. Cytoplasmic domain structures of Kir2.1 and Kir3.1 show sites for modulating gating and rectification.

3. Structural bases for the different anti-fibrillatory effects of chloroquine and quinidine.

4. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome.

5. A novel neuropsychiatric phenotype of KCNJ2 mutation in one Taiwanese family with Andersen-Tawil syndrome.

6. Distant cytosolic residues mediate a two-way molecular switch that controls the modulation of inwardly rectifying potassium (Kir) channels by cholesterol and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)).

7. Spermine and spermidine as gating molecules for inward rectifier K+ channels.

8. Tamoxifen inhibits inward rectifier K+ 2.x family of inward rectifier channels by interfering with phosphatidylinositol 4,5-bisphosphate-channel interactions.

9. Scanning the topography of polyamine blocker binding in an inwardly rectifying potassium channel.

10. PIP(2)-binding site in Kir channels: definition by multiscale biomolecular simulations.

1. Hydrocinnamic Acid Inhibits the Currents of WT and SQT3 Syndrome-Related Mutants of Kir2.1 Channel.

Review 2. Storax, A Promising Botanical Medicine for Treating Cardio-Cerebrovascular Diseases: A Review.