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c-Abl activates RIPK3 signaling in Gaucher disease

Journal
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
ISSN
0925-4439
Date Issued
2021
Author(s)
M.J. Yañez
F. Campos
T. Marín
A.D. Klein
A.H. Futerman
A.R. Alvarez
S. Zanlungo
Type
Resource Types::text::journal::journal article
Scopus ID
2-s2.0-85100642771
WoS ID
WOS:000632563900014
DOI
URL
URL Institutional Repository
Cite this document
Yañez, 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.2021.166089
Project(s)
Subjects
tyrosine kinase c-abl

; 

receptor interacting serine/threonine kinase 3 (ripk3)

; 

gaucher disease (gd)

; 

lysosomal storage disorders (lsd)

; 

necroptosis

; 

death

; 

animals

; 

apoptosis

; 

gaucher disease

; 

glucosylceramidase

; 

male

; 

mice

; 

mice, inbred c57bl

; 

mice, knockout

; 

necroptosis

; 

neurons

; 

phosphorylation

; 

proto-oncogene proteins c-abl

; 

receptor-interacting protein serine-threonine kinases

; 

signal transduction

; 

abelson kinase

; 

cd68 antigen

; 

genomic dna

; 

glucosylceramide

; 

imatinib

; 

mixed lineage leukemia protein

; 

receptor interacting protein serine threonine kinase

; 

receptor interacting serine threonine kinase 3

; 

tyrosine

; 

unclassified drug

; 

abelson kinase

; 

glucosylceramidase

; 

receptor interacting protein serine threonine kinase

; 

ripk3 protein, mouse

; 

adult

; 

animal experiment

; 

animal model

; 

animal tissue

; 

article

; 

brain cell

; 

brain cell culture

; 

brain tissue

; 

c57bl 6 mouse

; 

cell damage

; 

controlled study

; 

embryo

; 

enzyme activation

; 

enzyme activity

; 

enzyme phosphorylation

; 

female

; 

food and drug administration

; 

gaucher disease

; 

hela cell line

; 

hippocampus

; 

human

; 

human cell

; 

mouse

; 

nerve cell

; 

nervous system inflammation

; 

neuroapoptosis

; 

nonhuman

; 

primary culture

; 

priority journal

; 

protein phosphorylation

; 

protein protein interaction

; 

sh-sy5y cell line

; 

signal transduction

; 

transgenic organism

; 

animal

; 

apoptosis

; 

c57bl mouse

; 

gaucher disease

; 

genetics

; 

knockout mouse

; 

male

; 

metabolism

; 

necroptosis

; 

pathology

; 

phosphorylation

; 

physiology

; 

signal transduction