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CRISPR/Cas9-mediated deletion of the Wiskott-Aldrich syndrome locus causes actin cytoskeleton disorganization in murine erythroleukemia cells

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URI
http://hdl.handle.net/20.500.14066/3848
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Author(s)
Fernández-Calleja, Vanessa; Fernández Nestosa, María José; Hernández, Pablo; SCHVARTZMAN, JORGE BERNARDOCONACYT Authority; Krimer, Dora
Date of publishing
2019-01
Type of publication
research article
Subject(s)
WISKOTT-ALDRICH
ERYTHROLEUKEMIA CELLS
ACTIN CYTOSKELETON
CRISPR/CAS9
BRUTON TYROSINE KINASE
 
Abstract
Wiskott-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.
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