ArticlePloS one2014
Human stefin B role in cell's response to misfolded proteins and autophagy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Defective EV-mediated transport of SHH alters neural fate specification in EPM1 epilepsy.Science advances · 2026Article
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- Characterization of Cystatin B Interactome in Saliva from Healthy Elderly and Alzheimer's Disease Patients.Life (Basel, Switzerland) · 2023Article
- Progressive mitochondrial dysfunction in cerebellar synaptosomes of cystatin B-deficient mice.Frontiers in molecular neuroscience · 2023Article
- Disruption of the Ubiquitin-Proteasome System and Elevated Endoplasmic Reticulum Stress in Epilepsy.Biomedicines · 2022Review
- Human stefin B: from its structure, folding, and aggregation to its function in health and disease.Frontiers in molecular neuroscience · 2022Review
- Cystatin B is essential for proliferation and interneuron migration in individuals with EPM1 epilepsy.EMBO molecular medicine · 2020Article
- Review
- Cathepsin D regulates cathepsin B activation and disease severity predominantly in inflammatory cells during experimental pancreatitis.The Journal of biological chemistry · 2018Article
- Inhibition of Protein Aggregation by Several Antioxidants.Oxidative medicine and cellular longevity · 2018Article
- Co-chaperoning by amyloid-forming proteins: cystatins vs. crystallins.European biophysics journal : EBJ · 2017Article
- Proline Residues as Switches in Conformational Changes Leading to Amyloid Fibril Formation.International journal of molecular sciences · 2017Article
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- Proteolysis mediated by cysteine cathepsins and legumain-recent advances and cell biological challenges.Protoplasma · 2015Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative functions, apart from cathepsins inhibition, are being discovered for stefin B. Here, we investigate its role in vesicular trafficking and autophagy. Astrocytes isolated from stefin B knock-out (KO) mice exhibited an increased level of protein aggregates scattered throughout the cytoplasm. Addition of stefin B monomers or small oligomers to the cell medium reverted this phenotype, as imaged by confocal microscopy. To monitor the identity of proteins embedded within aggregates in wild type (wt) and KO cells, the insoluble cell lysate fractions were isolated and analyzed by mass spectrometry. Chaperones, tubulins, dyneins, and proteosomal components were detected in the insoluble fraction of wt cells but not in KO aggregates. In contrast, the insoluble fraction of KO cells exhibited increased levels of apolipoprotein E, fibronectin, clusterin, major prion protein, and serpins H1 and I2 and some proteins of lysosomal origin, such as cathepsin D and CD63, relative to wt astrocytes. Analysis of autophagy activity demonstrated that this pathway was less functional in KO astrocytes. In addition, synthetic dosage lethality (SDL) gene interactions analysis in Saccharomyces cerevisiae expressing human stefin B suggests a role in transport of vesicles and vacuoles These activities would contribute, directly or indirectly to completion of autophagy in wt astrocytes and would account for the accumulation of protein aggregates in KO cells, since autophagy is a key pathway for the clearance of intracellular protein aggregates.
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