Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/41346
DC FieldValueLanguage
dc.contributor.authorMani, Thangaduraien_US
dc.contributor.authorBourguinat, Catherineen_US
dc.contributor.authorKeller, Kathyen_US
dc.contributor.authorCarreton, Elenaen_US
dc.contributor.authorPeregrine, Andrewen_US
dc.contributor.authorPrichard, Roger K.en_US
dc.date.accessioned2018-06-21T08:27:41Z-
dc.date.available2018-06-21T08:27:41Z-
dc.date.issued2016en_US
dc.identifier.issn2211-3207en_US
dc.identifier.urihttp://hdl.handle.net/10553/41346-
dc.description.abstractDirofilaria immitis, a filarial parasite, causes cardiopulmonary dirofilariasis in dogs, cats and wild canids. The macrocyclic lactone (ML) class of drugs has been used to prevent heartworm infection. There is confirmed ML resistance in D. immitis and thus there is an urgent need to find new anthelmintics that could prevent and/or control the disease. Targeting ion channels of D. immitis for drug design has obvious advantages. These channels, present in the nematode nervous system, control movement, feeding, mating and respond to environmental cues which are necessary for survival of the parasite. Any new drug that targets these ion channels is likely to have a motility phenotype and should act to clear the worms from the host. Many of the successful anthelmintics in the past have targeted these ion channels and receptors. Knowledge about genetic variability of the ion channel and receptor genes should be useful information for drug design as receptor polymorphism may affect responses to a drug. Such information may also be useful for anticipation of possible resistance development. A total of 224 ion channel genes/subunits have been identified in the genome of D. immitis. Whole genome sequencing data of parasites from eight different geographical locations, four from ML-susceptible populations and the other four from ML-loss of efficacy (LOE) populations, were used for polymorphism analysis. We identified 1762 single nucleotide polymorphic (SNP) sites (1508 intronic and 126 exonic) in these 224 ion channel genes/subunits with an overall polymorphic rate of 0.18\%. Of the SNPs found in the exon regions, 129 of them caused a non-synonymous type of polymorphism. Fourteen of the exonic SNPs caused a change in predicted secondary structure. A few of the SNPs identified may have an effect on gene expression, function of the protein and resistance selection processes.en_US
dc.languageengen_US
dc.relation.ispartofInternational Journal for Parasitology: Drugs and Drug Resistanceen_US
dc.sourceInternational Journal for Parasitology: Drugs and Drug Resistance [ISSN 2211-3207], v. 6, p. 343-355en_US
dc.subject3109 Ciencias veterinariasen_US
dc.subject.otherDirofilaria immitisen_US
dc.subject.otherIon channelsen_US
dc.subject.otherMacrocyclic lactonesen_US
dc.subject.otherLoss of efficacyen_US
dc.subject.otherNeuromuscular systemen_US
dc.subject.otherSingle nucleotide polymorphismen_US
dc.subject.otherDrug targetsen_US
dc.titlePolymorphism in ion channel genes of Dirofilaria immitis: Relevant knowledge for future anthelmintic drug designen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.ijpddr.2016.06.003en_US
dc.identifier.scopus84992738228-
dc.identifier.isi000393046300023-
dc.contributor.authorscopusid56779771600-
dc.contributor.authorscopusid12242061100-
dc.contributor.authorscopusid35582703800-
dc.contributor.authorscopusid57212666993-
dc.contributor.authorscopusid36143929200-
dc.contributor.authorscopusid7005370261-
dc.contributor.authorscopusid23055977100-
dc.description.lastpage355en_US
dc.identifier.issue3-
dc.description.firstpage343en_US
dc.relation.volume6en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000393046300023-
dc.contributor.daisngid5593284-
dc.contributor.daisngid1558628-
dc.contributor.daisngid1930033-
dc.contributor.daisngid1038823-
dc.contributor.daisngid168685-
dc.contributor.daisngid52000-
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Mani, T-
dc.contributor.wosstandardWOS:Bourguinat, C-
dc.contributor.wosstandardWOS:Keller, K-
dc.contributor.wosstandardWOS:Carreton, E-
dc.contributor.wosstandardWOS:Peregrine, A-
dc.contributor.wosstandardWOS:Prichard, RK-
dc.date.coverdateDiciembre 2016en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-VETen_US
dc.description.sjr1,791
dc.description.jcr4,809
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptGIR IUIBS: Medicina Veterinaria e Investigación Terapéutica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Patología Animal, Producción Animal, Bromatología y Tecnología de Los Alimentos-
crisitem.author.orcid0000-0001-6509-910X-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameCarretón Gómez, Elena-
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