ArticleOncotarget2016
Roles of calpain-calpastatin system (CCS) in human T cell activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Bighorn sheep T2T genome assembly reveals differences in immune genes: a potential cause of high morbidity due to respiratory pathogens.bioRxiv : the preprint server for biology · 2025Article
- A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023Review
- Proteostasis in T cell aging.Seminars in immunology · 2023Review
- Longevity, Centenarians and Modified Cellular Proteodynamics.International journal of molecular sciences · 2023Review
- Immunosenescence and COVID-19.Mechanisms of ageing and development · 2022Review
- Proteolysis dysfunction in the process of aging and age-related diseases.Frontiers in aging · 2022Review
- Photoreceptor Cell Calcium Dysregulation and Calpain Activation Promote Pathogenic Photoreceptor Oxidative Stress and Inflammation in Prodromal Diabetic Retinopathy.The American journal of pathology · 2021Article
- Exercise triggers CAPN1-mediated AIF truncation, inducing myocyte cell death in arrhythmogenic cardiomyopathy.Science translational medicine · 2021Article
- Effects of functionally diverse calpain system on immune cells.Immunologic research · 2021Review
- Calpain in the cleavage of alpha-synuclein and the pathogenesis of Parkinson's disease.Progress in molecular biology and translational science · 2019Review
- Dysregulation of Calpain Proteolytic Systems Underlies Degenerative Vascular Disorders.Journal of atherosclerosis and thrombosis · 2018Review
- Calpain inhibition as a possible new therapeutic target in multiple sclerosis.AIMS molecular science · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune response is determined by the speed of the T cell reaction to antigens assured by a state of readiness for proliferation and cytokine secretion. Proliferation, apoptosis and motion of many cell types are controlled by cytoplasmic proteases - µ- and m-calpain - and their inhibitor calpastatin, together forming the "calpain-calpastatin system" (CCS), assumed to modify their targets only upon activation-dependent cytoplasmic Ca2+ increase. Contrastingly to this notion, using quantitative real time PCR and semiquantitative flow cytometry respectively, we show here that the CCS genes are constitutively expressed, and that both calpains are constitutively active in resting, circulating human CD4+ and CD8+ lymphocytes. Furthermore, we demonstrate that calpain inhibition in the resting T cells prevents them from proliferation in vitro and greatly reduces secretion of multiple cytokines. The mechanistic reason for these effects of calpain inhibition on T cell functions might be the demonstrated significant reduction of the expression of active (phosphorylated) upstream signalling molecules, including the phospholipase C gamma, p56Lck and NFκB, in the inhibitor-treated cells. Thus, we propose that the constitutive, self-regulatory calpain-calpastatin system activity in resting human T cells is a necessary, controlling element of their readiness for complex and effective response to antigenic challenge.
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Registered trials
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