ArticleFrontiers in molecular neuroscience2012
Increased expression of stefin B in the nucleus of T98G astrocytoma cells delays caspase activation.
Article in Frontiers in molecular neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Characterization of Cystatin B Interactome in Saliva from Healthy Elderly and Alzheimer's Disease Patients.Life (Basel, Switzerland) · 2023Article
- Berberine Photo-Activation Potentiates Cytotoxicity in Human Astrocytoma Cells through Apoptosis Induction.Journal of personalized medicine · 2021Article
- Top-Down Proteomics of Human Saliva Highlights Anti-inflammatory, Antioxidant, and Antimicrobial Defense Responses in Alzheimer Disease.Frontiers in neuroscience · 2021Article
- Characterization of a rare Unverricht-Lundborg disease mutation.Molecular genetics and metabolism reports · 2015Article
- The Role of Stefin B in Neuro-inflammation.Frontiers in cellular neuroscience · 2015Review
- Innate Immune Response in Brain, NF-Kappa B Signaling and Cystatins.Frontiers in molecular neuroscience · 2015Review
- Proteomic analysis of saliva from patients with oral chronic graft-versus-host disease.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2014Article
- Expression analysis of all protease genes reveals cathepsin K to be overexpressed in glioblastoma.PloS one · 2014Article
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stefin B (cystatin B) is an endogenous inhibitor of cysteine proteinases localized in the nucleus and the cytosol. Loss-of-function mutations in the stefin B gene (CSTB) gene were reported in patients with Unverricht-Lundborg disease (EPM1). Our previous results showed that thymocytes isolated from stefin B-deficient mice are more sensitive to apoptosis induced by the protein kinase C (PKC) inhibitor staurosporin (STS) than the wild-type control cells. We have also shown that the increased expression of stefin B in the nucleus of T98G astrocytoma cells delayed cell cycle progression through the S phase. In the present study we examined if the nuclear or cytosolic functions of stefin B are responsible for the accelerated induction of apoptosis observed in the cells from stefin B-deficient mice. We have shown that the overexpression of stefin B in the nucleus, but not in the cytosol of astrocytoma T98G cells, delayed caspase-3 and -7 activation. Pretreatment of cells with the pan-caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone completely inhibited caspase activation, while treatment with the inhibitor of calpains- and papain-like cathepsins (2S,3S)-trans-epoxysuccinyl-leucylamido-3-methyl-butane ethyl ester did not prevent caspase activation. We concluded that the delay of caspase activation in T98G cells overexpressing stefin B in the nucleus is independent of cathepsin inhibition.
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