dc.contributorUniversidad Nacional de Asunción - Facultad Politécnica
dc.creatorFernández-Calleja, Vanessa
dc.creatorFernández Nestosa, María José
dc.creatorHernández, Pablo
dc.creatorSCHVARTZMAN, JORGE BERNARDO
dc.creatorKrimer, Dora
dc.date2022-05-02T18:48:43Z
dc.date2022-05-02T18:48:43Z
dc.date2019-01
dc.date.accessioned2023-09-25T13:31:50Z
dc.date.available2023-09-25T13:31:50Z
dc.identifierhttp://hdl.handle.net/20.500.14066/3848
dc.identifierhttp://doi.org/10.7717/peerj.6284
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8807656
dc.descriptionWiskott-Aldrich syndrome (WAS) is a recessive X-linked inmmunodeficiency caused by loss-of-function mutations in the gene encoding the WAS protein (WASp). WASp plays an important role in the polymerization of the actin cytoskeleton in hematopoietic cells through activation of the Arp2/3 complex. In a previous study, we found that actin cytoskeleton proteins, including WASp, were silenced in murine erythroleukemia cells defective in differentiation.
dc.descriptionCONACYT – Consejo Nacional de Ciencia y Tecnología
dc.descriptionPROCIENCIA
dc.languageeng
dc.relationPINV15-573
dc.rightsopen access
dc.rights© 2019 Fernández-Calleja et al.
dc.subject7 Salud
dc.subjectWISKOTT-ALDRICH
dc.subjectERYTHROLEUKEMIA CELLS
dc.subjectACTIN CYTOSKELETON
dc.subjectCRISPR/CAS9
dc.subjectBRUTON TYROSINE KINASE
dc.titleCRISPR/Cas9-mediated deletion of the Wiskott-Aldrich syndrome locus causes actin cytoskeleton disorganization in murine erythroleukemia cells
dc.typeresearch article


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