M.J. YañezF. CamposT. MarínA.D. KleinA.H. FutermanA.R. AlvarezS. Zanlungo2023-02-062023-02-062021Yañez, M. J., Campos, F., Marín, T., Klein, A. D., Futerman, A. H., Alvarez, A. R., & Zanlungo, S. (2021). C-abl activates ripk3 signaling in gaucher disease. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1867(5), 166089. https://doi.org/10.1016/j.bbadis.2021.166089http://hdl.handle.net/11447/6031https://investigadores.udd.cl/handle/123456789/577410.1016/j.bbadis.2021.1660892-s2.0-85100642771WOS:000632563900014tyrosine kinase c-ablreceptor interacting serine/threonine kinase 3 (ripk3)gaucher disease (gd)lysosomal storage disorders (lsd)necroptosisdeathanimalsapoptosisgaucher diseaseglucosylceramidasemalemicemice, inbred c57blmice, knockoutnecroptosisneuronsphosphorylationproto-oncogene proteins c-ablreceptor-interacting protein serine-threonine kinasessignal transductionabelson kinasecd68 antigengenomic dnaglucosylceramideimatinibmixed lineage leukemia proteinreceptor interacting protein serine threonine kinasereceptor interacting serine threonine kinase 3tyrosineunclassified drugabelson kinaseglucosylceramidasereceptor interacting protein serine threonine kinaseripk3 protein, mouseadultanimal experimentanimal modelanimal tissuearticlebrain cellbrain cell culturebrain tissuec57bl 6 mousecell damagecontrolled studyembryoenzyme activationenzyme activityenzyme phosphorylationfemalefood and drug administrationgaucher diseasehela cell linehippocampushumanhuman cellmousenerve cellnervous system inflammationneuroapoptosisnonhumanprimary culturepriority journalprotein phosphorylationprotein protein interactionsh-sy5y cell linesignal transductiontransgenic organismanimalapoptosisc57bl mousegaucher diseasegeneticsknockout mousemalemetabolismnecroptosispathologyphosphorylationphysiologysignal transductionResource Types::text::journal::journal article