Relevant bibliographies by topics / KCNA7 gene

Academic literature on the topic 'KCNA7 gene'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "KCNA7 gene"

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Angi, Beatrice, Silvia Muccioli, Ildikò Szabò, and Luigi Leanza. "A Meta-Analysis Study to Infer Voltage-Gated K+ Channels Prognostic Value in Different Cancer Types." Antioxidants 12, no. 3 (February 24, 2023): 573. http://dx.doi.org/10.3390/antiox12030573.

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Potassium channels are often highly expressed in cancer cells with respect to healthy ones, as they provide proliferative advantages through modulating membrane potential, calcium homeostasis, and various signaling pathways. Among potassium channels, Shaker type voltage-gated Kv channels are emerging as promising pharmacological targets in oncology. Here, we queried publicly available cancer patient databases to highlight if a correlation exists between Kv channel expression and survival rate in five different cancer types. By multiple gene comparison analysis, we found a predominant expression of KCNA2, KCNA3, and KCNA5 with respect to the other KCNA genes in skin cutaneous melanoma (SKCM), uterine corpus endometrial carcinoma (UCEC), stomach adenocarcinoma (STAD), lung adenocarcinoma (LUAD), and lung squamous cell carcinoma (LUSC). This analysis highlighted a prognostic role of KCNA3 and KCNA5 in SKCM, LUAD, LUSC, and STAD, respectively. Interestingly, KCNA3 was associated with a positive prognosis in SKCM and LUAD but not in LUSC. Results obtained by the analysis of KCNA3-related differentially expressed genes (DEGs); tumor immune cell infiltration highlighted differences that may account for such differential prognosis. A meta-analysis study was conducted to investigate the role of KCNA channels in cancer using cancer patients’ datasets. Our study underlines a promising correlation between Kv channel expression in tumor cells, in infiltrating immune cells, and survival rate.
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Kashuba, Vladimir I., Sergei M. Kvasha, Alexei I. Protopopov, Rinat Z. Gizatullin, Alla V. Rynditch, Claes Wahlestedt, Wyeth W. Wasserman, and Eugene R. Zabarovsky. "Initial isolation and analysis of the human Kv1.7 ( KCNA7 ) gene, a member of the voltage-gated potassium channel gene family." Gene 268, no. 1-2 (May 2001): 115–22. http://dx.doi.org/10.1016/s0378-1119(01)00423-1.

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AL-Eitan, Laith, Islam Al-Dalalah, Afrah Elshammari, Wael Khreisat, and Ayah Almasri. "The Impact of Potassium Channel Gene Polymorphisms on Antiepileptic Drug Responsiveness in Arab Patients with Epilepsy." Journal of Personalized Medicine 8, no. 4 (November 14, 2018): 37. http://dx.doi.org/10.3390/jpm8040037.

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This study aims to investigate the effects of the three potassium channel genes KCNA1, KCNA2, and KCNV2 on increased susceptibility to epilepsy as well as on responsiveness to antiepileptic drugs (AEDs). The pharmacogenetic and case-control cohort (n = 595) consisted of 296 epileptic patients and 299 healthy individuals. Epileptic patients were recruited from the Pediatric Neurology clinic at the Queen Rania Al Abdullah Hospital (QRAH) in Amman, Jordan. A custom platform array search for genetic association in Jordanian-Arab epileptic patients was undertaken. The MassARRAY system (iPLEX GOLD) was used to genotype seven single nucleotide polymorphisms (SNPs) within three candidate genes (KCNA1, KCNA2, and KCNV2). Only one SNP in KCNA2, rs3887820, showed significant association with increased risk of susceptibility to generalized myoclonic seizure (p-value < 0.001). Notably, the rs112561866 polymorphism of the KCNA1 gene was non-polymorphic, but no significant association was found between the KCNA1 (rs2227910, rs112561866, and rs7974459) and KCNV2 (rs7029012, rs10967705, and rs10967728) polymorphisms and disease susceptibility or drug responsiveness among Jordanian patients. This study suggests that a significant association exists between the KCNA2 SNP rs3887820 and increased susceptibility to generalized myoclonic seizure. However, the present findings indicate that the KCNA1 and KCNV2 SNPs do not influence disease susceptibility and drug responsiveness in epileptic patients. Pharmacogenetic and case-control studies involving a multicenter and multiethnic approach are needed to confirm our results. To improve the efficacy and safety of epilepsy treatment, further studies are required to identify other genetic factors that contribute to susceptibility and treatment outcome.
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Bardien-Kruger, Soraya, Heike Wulff, Zainu Arieff, Paul Brink, K. George Chandy, and Valerie Corfield. "Characterisation of the human voltage-gated potassium channel gene, KCNA7, a candidate gene for inherited cardiac disorders, and its exclusion as cause of progressive familial heart block I (PFHBI)." European Journal of Human Genetics 10, no. 1 (January 2002): 36–43. http://dx.doi.org/10.1038/sj.ejhg.5200739.

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Si, Man, Krystle Trosclair, Kathryn A. Hamilton, and Edward Glasscock. "Genetic ablation or pharmacological inhibition of Kv1.1 potassium channel subunits impairs atrial repolarization in mice." American Journal of Physiology-Cell Physiology 316, no. 2 (February 1, 2019): C154—C161. http://dx.doi.org/10.1152/ajpcell.00335.2018.

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Voltage-gated Kv1.1 potassium channel α-subunits, encoded by the Kcna1 gene, have traditionally been regarded as neural-specific with no expression or function in the heart. However, recent data revealed that Kv1.1 subunits are expressed in atria where they may have an overlooked role in controlling repolarization and arrhythmia susceptibility independent of the nervous system. To explore this concept in more detail and to identify functional and molecular effects of Kv1.1 channel impairment in the heart, atrial cardiomyocyte patch-clamp electrophysiology and gene expression analyses were performed using Kcna1 knockout ( Kcna1−/−) mice. Specifically, we hypothesized that Kv1.1 subunits contribute to outward repolarizing K+ currents in mouse atria and that their absence prolongs cardiac action potentials. In voltage-clamp experiments, dendrotoxin-K (DTX-K), a Kv1.1-specific inhibitor, significantly reduced peak outward K+ currents in wild-type (WT) atrial cells but not Kcna1−/− cells, demonstrating an important contribution by Kv1.1-containing channels to mouse atrial repolarizing currents. In current-clamp recordings, Kcna1−/− atrial myocytes exhibited significant action potential prolongation which was exacerbated in right atria, effects that were partially recapitulated in WT cells by application of DTX-K. Quantitative RT-PCR measurements showed mRNA expression remodeling in Kcna1−/− atria for several ion channel genes that contribute to the atrial action potential including the Kcna5, Kcnh2, and Kcnj2 potassium channel genes and the Scn5a sodium channel gene. This study demonstrates a previously undescribed heart-intrinsic role for Kv1.1 subunits in mediating atrial repolarization, thereby adding a new member to the already diverse collection of known K+ channels in the heart.
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Brevnova, Elena E., Oleksandr Platoshyn, Shen Zhang, and Jason X. J. Yuan. "Overexpression of human KCNA5 increases IK(V) and enhances apoptosis." American Journal of Physiology-Cell Physiology 287, no. 3 (September 2004): C715—C722. http://dx.doi.org/10.1152/ajpcell.00050.2004.

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Apoptotic cell shrinkage, an early hallmark of apoptosis, is regulated by K+ efflux and K+ channel activity. Inhibited apoptosis and downregulated K+ channels in pulmonary artery smooth muscle cells (PASMC) have been implicated in development of pulmonary vascular medial hypertrophy and pulmonary hypertension. The objective of this study was to test the hypothesis that overexpression of KCNA5, which encodes a delayed-rectifier voltage-gated K+ (Kv) channel, increases K+ currents and enhances apoptosis. Transient transfection of KCNA5 caused 25- to 34-fold increase in KCNA5 channel protein level and 24- to 29-fold increase in Kv channel current ( IK(V)) at +60 mV in COS-7 and rat PASMC, respectively. In KCNA5-transfected COS-7 cells, staurosporine (ST)-mediated increases in caspase-3 activity and the percentage of cells undergoing apoptosis were both enhanced, whereas basal apoptosis (without ST stimulation) was unchanged compared with cells transfected with an empty vector. In rat PASMC, however, transfection of KCNA5 alone caused marked increase in basal apoptosis, in addition to enhancing ST-mediated apoptosis. Furthermore, ST-induced apoptotic cell shrinkage was significantly accelerated in COS-7 cells and rat PASMC transfected with KCNA5, and blockade of KCNA5 channels with 4-aminopyridine (4-AP) reduced K+ currents through KCNA5 channels and inhibited ST-induced apoptosis in KCNA5-transfected COS-7 cells. Overexpression of the human KCNA5 gene increases K+ currents (i.e., K+ efflux or loss), accelerates apoptotic volume decrease (AVD), increases caspase-3 activity, and induces apoptosis. Induction of apoptosis in PASMC by KCNA5 gene transfer may serve as an important strategy for preventing the progression of pulmonary vascular wall thickening and for treating patients with idiopathic pulmonary arterial hypertension (IPAH).
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Fountain, Samuel J., Alex Cheong, Jing Li, Naciye Y. Dondas, Fanning Zeng, Ian C. Wood, and David J. Beech. "Kv1.5 potassium channel gene regulation by Sp1 transcription factor and oxidative stress." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 5 (November 2007): H2719—H2725. http://dx.doi.org/10.1152/ajpheart.00637.2007.

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KV1.5, a voltage-gated potassium channel, has functional importance in regulating blood vessel tone and cardiac action potentials and is a target for numerous therapeutic drug development programs. Despite the importance of KV1.5, there is little knowledge of the mechanisms controlling expression of its underlying gene, Kcna5. We identified a 5′ flanking region of the murine Kcna5 gene that drives expression of a luciferase reporter gene in primary smooth muscle cells and a smooth muscle cell line. The promoter contained CACCC nucleotide motifs, which we have shown to bind the Sp1 transcription factor in the aorta under physiological conditions in vivo. Inhibition of Sp1- Kcna5 promoter interactions using mithramycin A, a dominant-negative Sp1 mutant, or disruption of the CACCC boxes by mutagenesis inhibited promoter activity. Conversely, expression of exogenous Sp1 augmented promoter activity. Sp1 has known sensitivity to oxidative stress and, consistent with this property, Kcna5 promoter activity was suppressed by hydrogen peroxide-induced oxidative stress. Our results show that Kcna5 promoter activity in vascular smooth muscle is critically dependent on Sp1 regulation via CACCC box motifs and identify mechanisms that potentially influence the expression of KV1.5 channel expression in physiological or pathological conditions.
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Paulhus, Kelsey, Lauren Ammerman, and Edward Glasscock. "Clinical Spectrum of KCNA1 Mutations: New Insights into Episodic Ataxia and Epilepsy Comorbidity." International Journal of Molecular Sciences 21, no. 8 (April 17, 2020): 2802. http://dx.doi.org/10.3390/ijms21082802.

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Mutations in the KCNA1 gene, which encodes voltage-gated Kv1.1 potassium channel α-subunits, cause a variety of human diseases, complicating simple genotype–phenotype correlations in patients. KCNA1 mutations are primarily associated with a rare neurological movement disorder known as episodic ataxia type 1 (EA1). However, some patients have EA1 in combination with epilepsy, whereas others have epilepsy alone. KCNA1 mutations can also cause hypomagnesemia and paroxysmal dyskinesia in rare cases. Why KCNA1 variants are associated with such phenotypic heterogeneity in patients is not yet understood. In this review, literature databases (PubMed) and public genetic archives (dbSNP and ClinVar) were mined for known pathogenic or likely pathogenic mutations in KCNA1 to examine whether patterns exist between mutation type and disease manifestation. Analyses of the 47 deleterious KCNA1 mutations that were identified revealed that epilepsy or seizure-related variants tend to cluster in the S1/S2 transmembrane domains and in the pore region of Kv1.1, whereas EA1-associated variants occur along the whole length of the protein. In addition, insights from animal models of KCNA1 channelopathy were considered, as well as the possible influence of genetic modifiers on disease expressivity and severity. Elucidation of the complex relationship between KCNA1 variants and disease will enable better diagnostic risk assessment and more personalized therapeutic strategies for KCNA1 channelopathy.
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Ślęczkowska, Milena, Rowida Almomani, Margherita Marchi, Erika Salvi, Bianca T. A. de Greef, Maurice Sopacua, Janneke G. J. Hoeijmakers, et al. "Peripheral Ion Channel Genes Screening in Painful Small Fiber Neuropathy." International Journal of Molecular Sciences 23, no. 22 (November 15, 2022): 14095. http://dx.doi.org/10.3390/ijms232214095.

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Neuropathic pain is a characteristic feature of small fiber neuropathy (SFN), which in 18% of the cases is caused by genetic variants in voltage-gated sodium ion channels. In this study, we assessed the role of fifteen other ion channels in neuropathic pain. Patients with SFN (n = 414) were analyzed for ANO1, ANO3, HCN1, KCNA2, KCNA4, KCNK18, KCNN1, KCNQ3, KCNQ5, KCNS1, TRPA1, TRPM8, TRPV1, TRPV3 and TRPV4 variants by single-molecule molecular inversion probes–next-generation sequencing. These patients did not have genetic variants in SCN3A, SCN7A-SCN11A and SCN1B-SCN4B. In twenty patients (20/414, 4.8%), a potentially pathogenic heterozygous variant was identified in an ion-channel gene (ICG). Variants were present in seven genes, for two patients (0.5%) in ANO3, one (0.2%) in KCNK18, two (0.5%) in KCNQ3, seven (1.7%) in TRPA1, three (0.7%) in TRPM8, three (0.7%) in TRPV1 and two (0.5%) in TRPV3. Variants in the TRP genes were the most frequent (n = 15, 3.6%), partly in patients with high mean maximal pain scores VAS = 9.65 ± 0.7 (n = 4). Patients with ICG variants reported more severe pain compared to patients without such variants (VAS = 9.36 ± 0.72 vs. VAS = 7.47 ± 2.37). This cohort study identified ICG variants in neuropathic pain in SFN, complementing previous findings of ICG variants in diabetic neuropathy. These data show that ICG variants are central in neuropathic pain of different etiologies and provides promising gene candidates for future research.
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Platoshyn, Oleksandr, Elena E. Brevnova, Elyssa D. Burg, Ying Yu, Carmelle V. Remillard, and Jason X. J. Yuan. "Acute hypoxia selectively inhibits KCNA5 channels in pulmonary artery smooth muscle cells." American Journal of Physiology-Cell Physiology 290, no. 3 (March 2006): C907—C916. http://dx.doi.org/10.1152/ajpcell.00028.2005.

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Acute hypoxia causes pulmonary vasoconstriction in part by inhibiting voltage-gated K+ (Kv) channel activity in pulmonary artery smooth muscle cells (PASMC). The hypoxia-mediated decrease in Kv currents [ IK(V)] is selective to PASMC; hypoxia has little effect on IK(V) in mesenteric artery smooth muscle cells (MASMC). Functional Kv channels are homo- and/or heterotetramers of pore-forming α-subunits and regulatory β-subunits. KCNA5 is a Kv channel α-subunit that forms functional Kv channels in PASMC and regulates resting membrane potential. We have shown that acute hypoxia selectively inhibits IK(V) through KCNA5 channels in PASMC. Overexpression of the human KCNA5 gene increased IK(V) and caused membrane hyperpolarization in HEK-293, COS-7, and rat MASMC and PASMC. Acute hypoxia did not affect IK(V) in KCNA5-transfected HEK-293 and COS-7 cells. However, overexpression of KCNA5 in PASMC conferred its sensitivity to hypoxia. Reduction of Po2 from 145 to 35 mmHg reduced IK(V) by ∼40% in rat PASMC transfected with human KCNA5 but had no effect on IK(V) in KCNA5-transfected rat MASMC (or HEK and COS cells). These results indicate that KCNA5 is an important Kv channel that regulates resting membrane potential and that acute hypoxia selectively reduces KCNA5 channel activity in PASMC relative to MASMC and other cell types. Because Kv channels (including KCNA5) are ubiquitously expressed in PASMC and MASMC, the observation from this study indicates that a hypoxia-sensitive mechanism essential for inhibiting KCNA5 channel activity is exclusively present in PASMC. The divergent effect of hypoxia on IK(V) in PASMC and MASMC also may be due to different expression levels of KCNA5 channels.
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Dissertations / Theses on the topic "KCNA7 gene"

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Gittelman, Joshua X. "Genes and spike timing : how the Kcna1 gene helps limit action potential temporal variability /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/10663.

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FORTUNATO, ANGELO. "Identification and characterization of genes involved in the development and progression of colorectal and endometrial cancers." Doctoral thesis, 2012. http://hdl.handle.net/2158/794612.

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