Please use this identifier to cite or link to this item: http://repositorio.ugto.mx/handle/20.500.12059/5747
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dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0es_MX
dc.contributorVICTOR HUGO HERNANDEZ GONZALEZes_MX
dc.creatorCARLA MARIA JARAMILLO RESTREPOes_MX
dc.date.accessioned2022-03-08T19:41:47Z-
dc.date.available2022-03-08T19:41:47Z-
dc.date.issued2021-12-
dc.identifier.urihttp://repositorio.ugto.mx/handle/20.500.12059/5747-
dc.language.isoengen
dc.publisherUniversidad de Guanajuatoes_MX
dc.rightsinfo:eu-repo/semantics/openAccesses_MX
dc.subject.classificationCLE- Maestría en Ciencias Aplicadases_MX
dc.titleBiophotonic and molecular analysis of tubulinopathiesen
dc.typeinfo:eu-repo/semantics/masterThesises_MX
dc.subject.ctiinfo:eu-repo/classification/cti/3es_MX
dc.subject.ctiinfo:eu-repo/classification/cti/32es_MX
dc.subject.ctiinfo:eu-repo/classification/cti/3208es_MX
dc.subject.keywordsCytoskeleton - Alterationsen
dc.subject.keywordsTubulinopathies - Biophotonic and molecular analysisen
dc.subject.keywordsHypo-demyelination - Pathophysiological processesen
dc.subject.keywordsH-ABC (Hypomyelination with Atrophy of the Basal Ganglia and Cerebellum)en
dc.subject.keywordsTUBB4A (Tubulin Beta 4A) – Mutationsen
dc.subject.keywordsDrugs - Pharmacological modelsen
dc.contributor.idinfo:eu-repo/dai/mx/cvu/91295es_MX
dc.contributor.roledirectores_MX
dc.type.versioninfo:eu-repo/semantics/publishedVersiones_MX
dc.contributor.twoSILVIA ALEJANDRA LOPEZ JUAREZes_MX
dc.contributor.idtwoinfo:eu-repo/dai/mx/cvu/161743es_MX
dc.contributor.roletwodirectoren
dc.description.abstractEnglishIn this work, we analyze the changes in the cytoskeleton produced by drugs that affect microtubular dynamics on three cultured human cell lines to generate molecular models to explain the pathophysiological processes that give rise to hypo-demyelination and central malformations of the H-ABC tubulinopathy. Tubulinopathies are diseases characterized by mutations in the genes that code for tubulin; specifically, mutations in TUBB4A produce hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC). Clinically, it is characterized by spasticity, extrapyramidal movements, ataxia, and cognitive and sensory deficits. Morphologically it has been observed that oligodendrocytes (OL) present an abnormal abundance of microtubules (MTs). The molecular mechanisms that trigger these cytoskeletal alterations are unknown, so their study will allow us to understand the pathophysiological processes that give rise to hypo-demyelination and the characteristic central malformations of H-ABC. We found that paclitaxel and epothilone B (Epo B) induced a higher tubulin density, thus suggesting that treatment with these drugs could generate microtubular behavior, similar to that observed in OL from patients with H-ABC. These results lead us to have a better understanding of H-ABC disease, since the changes that these drugs produce in MTs can be used as pharmacological models to study the structural modifications that occur in the cytoskeleton of patients with this disease. As future work, OLs with and without the mutation will expose to different drugs that affect the dynamics of MTs. These experiments will allow mimicking the microtubular defect observed in H-ABC, which will be analyzed later using other microscopy techniques, such as electron microscopy, following the MTs in detail.en
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