Last update 01 Nov 2024

KCa2.3

Last update 01 Nov 2024

Basic Info

Synonyms

hSK3, K3, KCa2.3

+ [9]

Introduction

Forms a voltage-independent potassium channel activated by intracellular calcium (PubMed:31155282, PubMed:20562108). Activation is followed by membrane hyperpolarization (By similarity). Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization (By similarity).

Drugs associated with KCa2.3

NSD-8011

Target

KCNN2 x KCa2.3

Mechanism

KCNN2 inhibitors [+1]

Active Org.

Cadent Therapeutics, Inc.

Originator Org.

NTG Nordic Transport Group A/S

Active Indication

Ataxia

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with KCa2.3

100 Translational Medicine associated with KCa2.3

0 Patents (Medical) associated with KCa2.3

571

Literatures (Medical) associated with KCa2.3

01 Dec 2024·Reproductive BioMedicine Online

The relationship between Sjögren's syndrome and recurrent pregnancy loss: a bioinformatics analysis

Article

Author: Liu, Cai ; Wang, Fang ; Huo, Huyan ; Zeng, Xianghui ; Mu, Fangxiang

RESEARCH QUESTIONAs Sjögren's syndrome is an autoimmune disease and an essential factor in recurrent pregnancy loss (RPL), are there gene-related relationships between the pathogenesis of Sjögren's syndrome and RPL?DESIGNThe gene datasets for Sjögren's syndrome and RPL were obtained from the Gene Expression Omnibus database, and the co-expression modules and shared differentially expressed genes were identified through weighted gene co-expression network analysis (WGCNA) and limma analysis based on sample size. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes analyses were applied to reveal the hidden biological pathways. Additionally, shared hub gene identification, gene set enrichment analysis, association of the hub gene with ferroptosis and immunity, drug sensitivity analysis, single-cell RNA sequencing analysis, and construction of the competing endogenous RNA (ceRNA) network were conducted.RESULTSBy intersecting the genes from WGCNA and limma analysis, one shared hub gene (KCNN3) was derived, exhibiting up-regulation in Sjögren's syndrome and RPL. There was a positive relationship between KCNN3 and the immune-related gene TLR2. The ceRNA network revealed that XIST was the most shared long non-coding RNA, which may bind competitively with eight microRNA to regulate the expression of KCNN3. Forty-eight drugs were found to be strongly associated with KCNN3 expression, including estramustine and cyclosporine. Moreover, KCNN3 exhibited high expression in RPL endothelial cells of villous tissue.CONCLUSIONSThis is one of the first studies to reveal that Sjögren's syndrome shares common biological pathways with RPL. KCNN3 was identified as the hub gene associated with Sjögren's syndrome and RPL, and may be a new target for mechanistic studies on Sjögren's syndrome and RPL.

01 Sep 2024·American Journal of Physiology-Gastrointestinal and Liver Physiology

Modulation of intracellular calcium activity in interstitial cells of Cajal by inhibitory neural pathways within the internal anal sphincter

Article

Author: Ni Bhraonain, Emer P ; Gould, Thomas W. ; Hannigan, Karen I. ; Hannigan, Karen I ; Keef, Kathleen D. ; Gould, Thomas W ; Cobine, Caroline A. ; Keef, Kathleen D ; Ni Bhraonain, Emer P. ; Cobine, Caroline A

Two intramuscular interstitial cells of Cajal (ICC-IM) subtypes exist within the internal anal sphincter (IAS). This study provides the first evidence for direct coupling between nitrergic motor neurons and both ICC-IM subtypes as well as indirect coupling between purinergic inputs and Type II ICC-IM. The spatiotemporal properties of whole cell Ca2+ transients in Type II ICC-IM mimic those of smooth muscle cells (SMCs), suggesting that ICC-IM modulate the activity of SMCs via their joint participation in a SIP syncytium (SMCs, ICC, and PDGFRα+ cells).

01 Sep 2024·JAMA Psychiatry

Key Roles of CACNA1C/Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders

Article

Author: Krienen, Fenna M ; Datta, Dibyadeep ; Rakic, Pasko ; Lewis, David A ; Arnsten, Amy F T ; Uchendu, Stacy ; Wang, Min ; Berretta, Sabina ; Perone, Isabella ; Woo, Elizabeth ; Goldman, Melissa ; Arellano, Jon ; Morozov, Yury ; McCarroll, Steven A ; Duque, Alvaro ; Yang, Shengtao ; Gonzalez-Burgos, Guillermo ; Ling, Emi ; van Dyck, Christopher H ; O'Dell, Ryan ; Joyce, Mary Kate P ; Murray, John

ImportanceThe risk of mental disorders is consistently associated with variants in CACNA1C (L-type calcium channel Cav1.2) but it is not known why these channels are critical to cognition, and whether they affect the layer III pyramidal cells in the dorsolateral prefrontal cortex that are especially vulnerable in cognitive disorders.ObjectiveTo examine the molecular mechanisms expressed in layer III pyramidal cells in primate dorsolateral prefrontal cortices.Design, Setting, and ParticipantsThe design included transcriptomic analyses from human and macaque dorsolateral prefrontal cortex, and connectivity, protein expression, physiology, and cognitive behavior in macaques. The research was performed in academic laboratories at Yale, Harvard, Princeton, and the University of Pittsburgh. As dorsolateral prefrontal cortex only exists in primates, the work evaluated humans and macaques.Main Outcomes and MeasuresOutcome measures included transcriptomic signatures of human and macaque pyramidal cells, protein expression and interactions in layer III macaque pyramidal cells using light and electron microscopy, changes in neuronal firing during spatial working memory, and working memory performance following pharmacological treatments.ResultsLayer III pyramidal cells in dorsolateral prefrontal cortex coexpress a constellation of calcium-related proteins, delineated by CALB1 (calbindin), and high levels of CACNA1C (Cav1.2), GRIN2B (NMDA receptor GluN2B), and KCNN3 (SK3 potassium channel), concentrated in dendritic spines near the calcium-storing smooth endoplasmic reticulum. L-type calcium channels influenced neuronal firing needed for working memory, where either blockade or increased drive by β1-adrenoceptors, reduced neuronal firing by a mean (SD) 37.3% (5.5%) or 40% (6.3%), respectively, the latter via SK potassium channel opening. An L-type calcium channel blocker or β1-adrenoceptor antagonist protected working memory from stress.Conclusions and RelevanceThe layer III pyramidal cells in the dorsolateral prefrontal cortex especially vulnerable in cognitive disorders differentially express calbindin and a constellation of calcium-related proteins including L-type calcium channels Cav1.2 (CACNA1C), GluN2B-NMDA receptors (GRIN2B), and SK3 potassium channels (KCNN3), which influence memory-related neuronal firing. The finding that either inadequate or excessive L-type calcium channel activation reduced neuronal firing explains why either loss- or gain-of-function variants in CACNA1C were associated with increased risk of cognitive disorders. The selective expression of calbindin in these pyramidal cells highlights the importance of regulatory mechanisms in neurons with high calcium signaling, consistent with Alzheimer tau pathology emerging when calbindin is lost with age and/or inflammation.

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KCa2.3

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