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Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events

ABSTRACT: Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events

PROVIDER: PRJNA611588 | ENA |

REPOSITORIES: ENA

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Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

Project description:Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

| PRJNA611596 | ENA

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

Project description:Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

| PRJNA611595 | ENA

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

Project description:Analysis of rhythmonome gene expression in cardiac myocytes derived from human induced pluripotent stem cells Cardiac electrical activity is controlled by the carefully orchestrated activity of more than a dozen different ion conductances. Yet, there is considerable variability in cardiac ion channel expression levels both within and between subjects. In this study we tested the hypothesis that variations in ion channel expression between individuals are not random but rather there are modules of co-expressed genes and that these modules make electrical signaling in the heart more robust. Meta-analysis of 3653 public RNA-Seq datasets identified a strong correlation between expression of CACNA1C (L-type calcium current, ICaL) and KCNH2 (rapid delayed rectifier K+ current, IKr), which was verified in mRNA extracted from human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM). In silico modeling, validated with functional measurements in hiPSC-CM, indicates that the co-expression of CACNA1C and KCNH2 limits the variability in action potential duration and reduces susceptibility to early afterdepolarizations, a surrogate marker for pro-arrhythmia.

2020-03-10 | GSE146665 | GEO

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

2020-03-10 | GSE146664 | GEO

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-10 | GSE146667 | GEO

Confirmation of recombinant Calcium-activated potassium channel from Leishmania donovani

Project description:Calcium-activated potassium channels are important membrane proteins that help in maintaining the cellular physiology and cell signalling. Till date no Calcium-activated potassium channels have been identified in Leishmania donovani. It’s gene was cloned into pET vector and expressed in E. coli BL21 (DE3). The recombinant protein was purified using nickel affinity chromatography.

2021-05-11 | PXD019577 | Pride

KCNQ POTASSIUM CHANNELS MODULATE WNT ACTIVITY IN GASTRO-OESOPHAGEAL ADENOCARCINOMAS

Project description:Voltage sensitive potassium channels play an important role in controlling membrane potential and ionic homeostasis in the gut and have been implicated in gastrointestinal (GI) cancers. Through large scale analysis of 897 patients with Gastro-oesophageal adenocarcincomas (GOA) coupled with in vitro models, we find KCNQ family genes are mutated in ~30% of patients, and play therapeutically targetable roles in GOA cancer growth. KCNQ1 and KCNQ3 mediate the WNT pathway and MYC to increase proliferation through resultant effects on cadherins junctions. This also highlights novel roles for KCNQ3 in non-excitable tissues. We additionally discover that activity of KCNQ3 sensitises cancer cells to existing potassium channel inhibitors, and that inhibition of KCNQ activity reduces proliferation of GOA cancer cells. These findings reveal a novel and exploitable role for potassium channels in the advancement of human cancer, and highlight that supplemental treatments for GOAs may exist through KCNQ inhibitors.

2023-09-13 | GSE242782 | GEO

Pro-inflammatory cytokines drive functional deregulation of potassium channels in primary synovial fibroblasts

Project description:The synovium secretes synovial fluid but is also richly innervated with nociceptors and acts as a gateway between avascular joint tissues and the circulatory system. Resident fibroblast-like synoviocytes’ (FLS) calcium-activated potassium channels (KCa) change in activity in arthritis models and this correlates with FLS activation. To deepen our understanding of the synovium in the context of synovial joint health and disease, the electrophysiological profile of FLS cells needs to be characterised, along with the ion channels that are present. Ion channels are an essential component of any cell membrane that controls ion movement in and out of the cell and play an important role in a multitude of cell regulating processes, typically by modulating the membrane potential To this end, we chose to perform an UNBIASED screen to identify/screen the ion channels that are transcribed in these cells and determine if this "channelome" changes with cytokine exposure. PCR/Westerns naturally bias toward the known proteins and transcripts and so we used Next Generation sequencing to scan the entire transcriptome. Objective: To determine the mechanism of this activation in an in vitro model of inflammatory arthritis; 72hr treatment with the cytokines TNFa and IL1b.

2020-03-06 | E-MTAB-7798 | biostudies-arrayexpress

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Project description:Kv1.2 is a prominent voltage-gated potassium channel that influences action potential generation and propagation in the central nervous system. We explored multi-protein complexes containing Kv1.2 using mass spectrometry of immunoprecipitated samples. Proteins identified as candidate interactors were prioritized based on abundance, and were screened for functional effects on Kv1.2 channels using electrophysiology.

2018-11-04 | PXD011010 | Pride

Mechanism of pharmacochaperoning in ATP-sensitive potassium channels revealed by cryo-EM

Project description:ATP-sensitive potassium (K-ATP) channels composed of a pore-forming Kir6.2 potassium channel and a regulatory ABC transporter sulfonylurea receptor 1 (SUR1) regulate insulin secretion in pancreatic beta-cells to maintain glucose homeostasis. Mutations that impair channel folding or assembly prevent cell surface expression and cause congenital hyperinsulinism. Structurally diverse K-ATP inhibitors have been shown to act as pharmacochaperones to correct mutant channel expression, but the mechanism is unknown. Here, we compare cryoEM structures of K-ATP channels bound to pharmacochaperones glibenclamide, repaglinide, and carbamazepine. CyanurBiotinDimercaptoPropionylSuccinimide (CBDPS) cross-linking mass spectrometry was used to partially confirm cryoEM structures.

2019-08-12 | PXD014498 | Pride

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