KCNA3 Antibody / Kv1.3 (R32012)

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KCNA3 Antibody / Kv1.3 (R32012) Catalog No. Formulation Size R32012 0.5mg/ml if reconstituted with 0.2ml sterile DI water 100 ug Bulk quote request Availability 1-3 business days Species Reactivity Human, Mouse, Rat Format Antigen affinity purified Clonality Polyclonal (rabbit origin) Isotype Rabbit IgG Purity Antigen affinity Buffer Lyophilized from 1X PBS with 2.5% BSA and 0.025% sodium azide UniProt P22001 Applications Western blot : 0.1-0.5ug/ml Limitations This KCNA3 antibody is available for research use only. Western blot testing of 1) rat brain, 2) mouse brain, human 3) K562, 4) HeLa and 5) 22RV1 lysate with KCNA3 antibody. Expected molecular weight ~64 kDa, observed here at ~55 kDa. Description Potassium voltage-gated channel, shaker-related subfamily, member 3, also known as KCNA3 or Kv1.3, is a protein that in humans is encoded by the KCNA3 gene. This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily. This member contains six membrane-spanning domains with a shaker-type repeat in the fourth segment. It belongs to the delayed rectifier class, members of which allow nerve cells to efficiently repolarize following an action potential. It plays an essential role in T-cell proliferation and activation. This gene appears to be intronless and it is clustered together with KCNA2 and KCNA10 genes on chromosome 1. And Kv1.3 has been reported to be expressed in the inner mitochondrial membrane in lymphocytes. The apoptotic protein Bax has been suggested to insert into theouter mitochondrial membrane and occlude the pore of Kv1.3 via a lysine residue. Thus, Kv1.3 modulation may be one of many mechanisms that contribute to apoptosis. Application Notes Optimal dilution of the KCNA3 antibody should be determined by the researcher. Immunogen Amino acids EELRKARSNSTLSKSEYMVIEEGGMNHSAFPQ of human KCNA3 were used as the immunogen for the KCNA3 antibody. Storage After reconstitution, the KCNA3 antibody can be stored for up to one month at 4oC. For long-term, aliquot and store at -20oC. Avoid repeated freezing and thawing. Ordering: Phone:858.663.9055 | Fax:1.267.821.0800 | Email:[email protected] Copyright © NSJ Bioreagents. All rights reserved.

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Potassium Channels in Epilepsy
Downloaded from http://perspectivesinmedicine.cshlp.org/ on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Potassium Channels in Epilepsy Ru¨diger Ko¨hling and Jakob Wolfart Oscar Langendorff Institute of Physiology, University of Rostock, Rostock 18057, Germany Correspondence: [email protected] This review attempts to give a concise and up-to-date overview on the role of potassium channels in epilepsies. Their role can be defined from a genetic perspective, focusing on variants and de novo mutations identified in genetic studies or animal models with targeted, specific mutations in genes coding for a member of the large potassium channel family. In these genetic studies, a demonstrated functional link to hyperexcitability often remains elusive. However, their role can also be defined from a functional perspective, based on dy- namic, aggravating, or adaptive transcriptional and posttranslational alterations. In these cases, it often remains elusive whether the alteration is causal or merely incidental. With 80 potassium channel types, of which 10% are known to be associated with epilepsies (in humans) or a seizure phenotype (in animals), if genetically mutated, a comprehensive review is a challenging endeavor. This goal may seem all the more ambitious once the data on posttranslational alterations, found both in human tissue from epilepsy patients and in chronic or acute animal models, are included. We therefore summarize the literature, and expand only on key findings, particularly regarding functional alterations found in patient brain tissue and chronic animal models. INTRODUCTION TO POTASSIUM evolutionary appearance of voltage-gated so- CHANNELS dium (Nav)andcalcium (Cav)channels, Kchan- nels are further diversified in relation to their otassium (K) channels are related to epilepsy newer function, namely, keeping neuronal exci- Psyndromes on many different levels, ranging tation within limits (Anderson and Greenberg from direct control of neuronal excitability and 2001; Hille 2001).
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Supplementary Table 1
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S41598-019-42654-4.Pdf
www.nature.com/scientificreports OPEN Epigenome-wide Analysis Identifes Genes and Pathways Linked to Neurobehavioral Variation in Received: 22 November 2018 Accepted: 3 April 2019 Preterm Infants Published: xx xx xxxx Todd M. Everson1, Carmen J. Marsit1, T. Michael O’Shea2, Amber Burt 1, Karen Hermetz1, Brian S. Carter3, Jennifer Helderman4, Julie A. Hofeimer2, Elisabeth C. McGowan5, Charles R. Neal6, Steven L. Pastyrnak7, Lynne M. Smith8, Antoine Soliman 9, Sheri A. DellaGrotta10, Lynne M. Dansereau10, James F. Padbury5 & Barry M. Lester5,10,11 Neonatal molecular biomarkers of neurobehavioral responses (measures of brain-behavior relationships), when combined with neurobehavioral performance measures, could lead to better predictions of long-term developmental outcomes. To this end, we examined whether variability in buccal cell DNA methylation (DNAm) associated with neurobehavioral profles in a cohort of infants born less than 30 weeks postmenstrual age (PMA) and participating in the Neonatal Neurobehavior and Outcomes in Very Preterm Infants (NOVI) Study (N = 536). We tested whether epigenetic age, age acceleration, or DNAm levels at individual loci difered between infants based on their NICU Network Neurobehavioral Scale (NNNS) profle classifcations. We adjusted for recruitment site, infant sex, PMA, and tissue heterogeneity. Infants with an optimally well-regulated NNNS profle had older epigenetic age compared to other NOVI infants (β1 = 0.201, p-value = 0.026), but no signifcant diference in age acceleration. In contrast, infants with an atypical NNNS profle had diferential methylation at 29 CpG sites (FDR < 10%). Some of the genes annotated to these CpGs included PLA2G4E, TRIM9, GRIK3, and MACROD2, which have previously been associated with neurological structure and function, or with neurobehavioral disorders.
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1 1 2 3 Cell Type-Specific Transcriptomics of Hypothalamic
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Rabbit Anti-Human KCNA3 Polyclonal antibody (DPABH-02569) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Immunogen Kv1.3 fusion protein, sequence: MDERLSLLRSPPPPSARHRAHPPQRPASSGGAHTLVNHGYAEPAAGRELPPDMTVVPGDHLLE PEVADGGGAPPQGGCGGGGCDRYEPLPPSLPAAGEQDCCGERVVINISGLRFETQLKTLCQFP ETLLGDPKRRMRYFDPLRNEYFFDRNRPSFDAILYYYQSGGRIRRPVNVPIDIFSEEIRFYQLGEE AMEKFREDEGFLREEERPLPRRDFQRQVWLLFEY (N-term-226aa encoded by BC035059) Isotype IgG Source/Host Rabbit Species Reactivity Human, Mouse, Rat Purification Antigen affinity purification Conjugate Unconjugated Applications WB, ELISA Positive Control A549 cells, mouse thymus tissue Format Liquid Size 50 uL; 100 uL Buffer PBS with 0.1% sodium azide and 50% glycerol pH 7.3. Preservative 0.1% Sodium Azide Storage Store at -20°C. Aliquoting is unnecessary for -20°C storage. BACKGROUND Introduction Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily. This member contains six membrane-spanning domains with a shaker- type repeat in the fourth segment. It belongs to the delayed rectifier class, members of which allow nerve cells to efficiently repolarize following an action potential. It plays an essential role in T-cell proliferation and activation.
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