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Palabras clave – provistas por la editorial

deubiquitinase; degradation; therapeutic target; cancer; hematopoiesis; hematopoietic stem cells; immune response; regulation of gene expression; ubiquitin system; genetic diseases; ubiquitin ligase; deubiquitinases; monoubiquitin signaling; vesicular trafficking; protein complex formation; inflammation; inhibitor; innate immune; interferon; LUBAC; NF-κB; ubiquitin; Parkinson’s disease; dopa-responsive dystonia; tyrosine hydroxylase; α-synuclein; fatty acid-binding protein 3; ubiquitination; proteasomal degradation; ubiquitin-proteasome system; mitochondria; E3 ubiquitin ligase; MITOL/MARCH5; salt-sensitive hypertension; Nedd4L/Nedd4-2; epithelial sodium channel; aldosterone sensitive distal nephron; excitation-transcription coupling; RNF183; RNF186; RNF182; RNF152; RING finger; mTOR; endoplasmic reticulum stress; osmotic stress; ubiquitin code; virus infection; virus-host interaction; tau protein; semisynthesis; disulfide-coupling; polyubiquitin; fibrils; aggregation; neurodegeneration; deubiquitination; inhibitors; protein quality control; proteolysis; protein stabilization; regulatory T cells; mesenchymal stem cell; cortical bone derived stem cell; myocardial infarction; blood pressure; renal salt reabsorption; vascular function; ubiquitin proteasome system; ubiquitin–proteasome pathway; cilia; ciliogenesis; differentiation; proliferation; ciliopathy; E3s; DUBs; UPS; neurodegenerative disease; immune-related diseases