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c-Abl activates RIPK3 signaling in Gaucher disease
M J Yañez
, F Campos
, T Marín
, A D Klein
,
A H Futerman
, A R Alvarez
, S Zanlungo
Department of Biomolecular Sciences
Weizmann Institute of Science
Research output
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peer-review
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Keyphrases
Gaucher Disease
100%
Receptor-interacting Protein Kinase 3 (RIPK3)
100%
C-Abl
100%
Disease Model
16%
Imatinib
8%
Phosphorylation
8%
Tyrosine
8%
Parkinson's Disease
8%
Mouse Model
8%
Cell Death
8%
Therapeutic Approaches
8%
Patient Fibroblasts
8%
Neurological Symptoms
8%
Pharmacological Inhibitors
8%
Null Mice
8%
Homozygous mutation
8%
Genetic Risk
8%
Necrosis
8%
Phosphorylated Forms
8%
Necroptosis
8%
FDA-approved Drugs
8%
Genetic Ablation
8%
Downstream Signaling
8%
GBA1 Gene
8%
α-glucosidase
8%
Direct Induction
8%
Abl Tyrosine Kinase
8%
Indirect Function
8%
Visceral Symptoms
8%
Biochemistry, Genetics and Molecular Biology
Gaucher's Disease
100%
RIPK3
100%
Enzyme
8%
Kinase
8%
Phosphotransferase
8%
Tyrosine
8%
Fibroblast
8%
Mouse Model
8%
Cell Death
8%
Imatinib
8%
Receptor Tyrosine Kinase
8%
Tyrosine Kinase
8%
Knockout Mouse
8%
Genetic Risk
8%
Necroptosis
8%
Genetic Ablation
8%
Glucosidase
8%