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Erythrocytes from hereditary xerocytosis patients heterozygous for KCNN4 V282M exhibit increased spontaneous Gardos channel-like activity inhibited by senicapoc.

作者信息

Rivera Alicia, Vandorpe David H, Shmukler Boris E, Gallagher Denis R, Fikry Christopher C, Kuypers Frans A, Brugnara Carlo, Snyder L Michael, Alper Seth L

机构信息

Division of Nephrology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Am J Hematol. 2017 Jun;92(6):E108-E110. doi: 10.1002/ajh.24716. Epub 2017 Apr 29.

DOI:10.1002/ajh.24716
PMID:28295477
Abstract
摘要

相似文献

1
Erythrocytes from hereditary xerocytosis patients heterozygous for KCNN4 V282M exhibit increased spontaneous Gardos channel-like activity inhibited by senicapoc.对于KCNN4 V282M杂合的遗传性口形红细胞增多症患者，其红细胞表现出自发性加尔多斯通道样活性增加，且该活性受到司尼可泊抑制。
Am J Hematol. 2017 Jun;92(6):E108-E110. doi: 10.1002/ajh.24716. Epub 2017 Apr 29.
2
Erythrocyte ion content and dehydration modulate maximal Gardos channel activity in KCNN4 V282M/+ hereditary xerocytosis red cells.红细胞离子含量和脱水调节 KCNN4 V282M/+遗传性非球形细胞增多症红细胞中最大 Gardos 通道活性。
Am J Physiol Cell Physiol. 2019 Aug 1;317(2):C287-C302. doi: 10.1152/ajpcell.00074.2019. Epub 2019 May 15.
3
Senicapoc: a potent candidate for the treatment of a subset of hereditary xerocytosis caused by mutations in the Gardos channel.司尼卡波：一种治疗由加尔杜斯通道突变引起的遗传性口形红细胞增多症亚型的有力候选药物。
Haematologica. 2016 Nov;101(11):e431-e435. doi: 10.3324/haematol.2016.149104. Epub 2016 Jul 21.
4
A mutation in the Gardos channel is associated with hereditary xerocytosis.Gardos 通道突变与遗传性血影红细胞增多症有关。
Blood. 2015 Sep 10;126(11):1273-80. doi: 10.1182/blood-2015-04-642496. Epub 2015 Jul 6.
5
Mutations in the Gardos channel (KCNN4) are associated with hereditary xerocytosis.加尔杜斯通道（KCNN4）的突变与遗传性口形红细胞增多症相关。
Blood. 2015 Sep 10;126(11):1281-4. doi: 10.1182/blood-2015-07-657957. Epub 2015 Jul 21.
6
Red blood cell Gardos channel (KCNN4): the essential determinant of erythrocyte dehydration in hereditary xerocytosis.红细胞加尔多斯通道（KCNN4）：遗传性干燥细胞增多症中红细胞脱水的关键决定因素。
Haematologica. 2017 Oct;102(10):e415-e418. doi: 10.3324/haematol.2017.171389. Epub 2017 Jun 15.
7
Characterisation of Asp669Tyr Piezo1 cation channel activity in red blood cells: an unexpected phenotype.红细胞中Asp669Tyr Piezo1阳离子通道活性的表征：一种意外的表型。
Br J Haematol. 2021 Jul;194(1):e51-e55. doi: 10.1111/bjh.17467. Epub 2021 May 11.
8
Inhibition of the potassium channel K3.1 by senicapoc reverses tactile allodynia in rats with peripheral nerve injury.塞尼卡波对钾通道K3.1的抑制作用可逆转周围神经损伤大鼠的触觉异常性疼痛。
Eur J Pharmacol. 2017 Jan 15;795:1-7. doi: 10.1016/j.ejphar.2016.11.031. Epub 2016 Nov 19.
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Novel Gardos channel mutations linked to dehydrated hereditary stomatocytosis (xerocytosis).与干燥遗传性口形红细胞增多症（干血质）相关的新型 Gardos 通道突变。
Am J Hematol. 2015 Oct;90(10):921-6. doi: 10.1002/ajh.24117.
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The Clinically Tested Gardos Channel Inhibitor Senicapoc Exhibits Antimalarial Activity.经临床测试的加尔杜斯通道抑制剂司尼卡波具有抗疟活性。
Antimicrob Agents Chemother. 2015 Oct 12;60(1):613-6. doi: 10.1128/AAC.01668-15. Print 2016 Jan.

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New KCNN4 Variants Associated With Anemia: Stomatocytosis Without Erythrocyte Dehydration.与贫血相关的新型KCNN4变体：无红细胞脱水的口形细胞增多症
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The Gardos effect drives erythrocyte senescence and leads to Lu/BCAM and CD44 adhesion molecule activation.加德索斯效应驱动红细胞衰老，并导致 Lu/BCAM 和 CD44 黏附分子的激活。
Blood Adv. 2020 Dec 22;4(24):6218-6229. doi: 10.1182/bloodadvances.2020003077.
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Red cell membrane disorders: structure meets function.红细胞膜疾病：结构与功能的相遇。
Blood. 2020 Sep 10;136(11):1250-1261. doi: 10.1182/blood.2019000946.
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Pharmacology of Small- and Intermediate-Conductance Calcium-Activated Potassium Channels.小电导和中等电导钙激活钾通道的药理学。
Annu Rev Pharmacol Toxicol. 2020 Jan 6;60:219-240. doi: 10.1146/annurev-pharmtox-010919-023420. Epub 2019 Jul 23.
8
Dehydrated hereditary stomatocytosis: clinical perspectives.脱水遗传性口形红细胞增多症：临床视角
J Blood Med. 2019 Jul 4;10:183-191. doi: 10.2147/JBM.S179764. eCollection 2019.
9
Activation mechanism of a human SK-calmodulin channel complex elucidated by cryo-EM structures.冷冻电镜结构解析人源 SK 钙调蛋白通道复合物的激活机制。
Science. 2018 May 4;360(6388):508-513. doi: 10.1126/science.aas9466.
10
On the Mechanism of Human Red Blood Cell Longevity: Roles of Calcium, the Sodium Pump, PIEZO1, and Gardos Channels.论人类红细胞寿命的机制：钙、钠泵、PIEZO1和加尔多斯通道的作用
Front Physiol. 2017 Dec 12;8:977. doi: 10.3389/fphys.2017.00977. eCollection 2017.