ArticleCell death & disease2020
Sorcin is an early marker of neurodegeneration, Ca
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- First-in-human controlled inhalation of thin graphene oxide nanosheets to study acute cardiorespiratory responses.Nature nanotechnology · 2024Trial
- The Senescent Phenotype of Cultured Hypothalamic Astrocytes from Rats with Streptozotocin-Induced Dementia.Neurochemical research · 2026Article
- Revealing the Mechanisms of Alzheimer's, Parkinson's and Huntington's Diseases Through Invertebrate Models.Biology · 2026Review
- Long-Timescale Molecular Dynamics Reveal a Coordination-Biased Conformational Selection Mechanism for Sorcin Activation.bioRxiv : the preprint server for biology · 2026Article
- Guardians of T-Cell CaCells · 2026Review
- The ATC12 small molecule inhibits the Aurora-A/TPX2 interaction and impairs the proliferation of breast cancer cells.Cell death & disease · 2026Article
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Epithelial cell-based multi-omics integration identifies SPINK5 and SRI as novel diagnostic biomarkers for ulcerative colitis.Frontiers in pharmacology · 2026Article
- Mitochondrial Calcium Channels and MAM Interaction in Calcium Homeostasis Dysregulation in Parkinson's Disease.Neurochemical research · 2025Review
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Kinetic investigation of calcium-induced Sorcin aggregation by stopped-flow light scattering.The Biochemical journal · 2025Article
- Sorcin regulates alveolarization and airway tissue remodeling during lung morphogenesis.Cellular and molecular life sciences : CMLS · 2025Article
- Sex-Dependent Changes in the Gene Expression of UPR-Associated Calcium-Binding Proteins in the STZ-Induced Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- A preliminary bioinformatic screen to identify SRI SMC2 PSIP1 TLE4 and MSX1 as potential diagnostic and prognostic markers of osteoarthritis.Scientific reports · 2025Article
- Pharmacological and Pathological Implications of Sigma-1 Receptor in Neurodegenerative Diseases.Biomedicines · 2025Review
- Development of an Adaptive, Economical, and Easy-to-Use SP3-TMT Automated Sample Preparation Workflow for Quantitative Proteomics.Journal of proteome research · 2025Article
- EGF receptor in organ development, tissue homeostasis and regeneration.Journal of biomedical science · 2025Review
- Potential of extracellular vesicle cargo as molecular signals in Schizophrenia: a scoping review.Schizophrenia (Heidelberg, Germany) · 2025Review
- Genetic and neuro-epigenetic effects of divergent artificial selection for feather pecking behaviour in chickens.BMC genomics · 2024Article
- Sorcin: mechanisms of action in cancer hallmarks, drug resistance and opportunities in therapeutics.Medical oncology (Northwood, London, England) · 2024Review
Corrections and comments
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Authors and funding
23 authors.
Funding
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Abstract
Dysregulation of calcium signaling is emerging as a key feature in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD), and targeting this process may be therapeutically beneficial. Under this perspective, it is important to study proteins that regulate calcium homeostasis in the cell. Sorcin is one of the most expressed calcium-binding proteins in the human brain; its overexpression increases endoplasmic reticulum (ER) calcium concentration and decreases ER stress in the heart and in other cellular types. Sorcin has been hypothesized to be involved in neurodegenerative diseases, since it may counteract the increased cytosolic calcium levels associated with neurodegeneration. In the present work, we show that Sorcin expression levels are strongly increased in cellular, animal, and human models of AD, PD, and HD, vs. normal cells. Sorcin partially colocalizes with RyRs in neurons and microglia cells; functional experiments with microsomes containing high amounts of RyR2 and RyR3, respectively, show that Sorcin is able to regulate these ER calcium channels. The molecular basis of the interaction of Sorcin with RyR2 and RyR3 is demonstrated by SPR. Sorcin also interacts with other ER proteins as SERCA2 and Sigma-1 receptor in a calcium-dependent fashion. We also show that Sorcin regulates ER calcium transients: Sorcin increases the velocity of ER calcium uptake (increasing SERCA activity). The data presented here demonstrate that Sorcin may represent both a novel early marker of neurodegenerative diseases and a response to cellular stress dependent on neurodegeneration.
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