ArticleThe Biochemical journal2007
Fortilin binds Ca2+ and blocks Ca2+-dependent apoptosis in vivo.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- Fortilin binds and stabilizes MEF2C, activates it through phosphorylation, and drives transcription of the cell structural and survival protein CTNNA3.The Journal of biological chemistry · 2026Article
- Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.Communications biology · 2025Article
- High plasma levels of fortilin are associated with cardiovascular events in patients undergoing coronary angiography.Heart and vessels · 2025Article
- Fortilin binds CTNNA3 and protects it against phosphorylation, ubiquitination, and proteasomal degradation to guard cells against apoptosis.Communications biology · 2025Article
- Biological Activities of Glass Ionomer Cement Supplemented with Fortilin on Human Dental Pulp Stem Cells.Journal of functional biomaterials · 2022Article
- Long-Term Effect of Modified Glass Ionomer Cement with Mimicked Biological Property of Recombinant Translationally Controlled Protein.Polymers · 2022Article
- High Plasma Levels of Fortilin in Patients with Coronary Artery Disease.International journal of molecular sciences · 2022Article
- Fortilin interacts with TGF-β1 and prevents TGF-β receptor activation.Communications biology · 2022Article
- Expression and purification of a cleavable recombinant fortilin from Escherichia coli for structure activity studies.Protein expression and purification · 2022Article
- Fortilin inhibits p53, halts cardiomyocyte apoptosis, and protects the heart against heart failure.Cell death discovery · 2021Article
- Investigating the Role of Translationally Control Tumor Protein in Growth, Development and Differentiation ofFrontiers in cell and developmental biology · 2020Article
- Upregulation of TCTP is associated with cholangiocarcinoma progression and metastasis.Oncology letters · 2017Article
- Fortilin binds IRE1α and prevents ER stress from signaling apoptotic cell death.Nature communications · 2017Article
- Clearing the outer mitochondrial membrane from harmful proteins via lipid droplets.Cell death discovery · 2017Article
- Interaction of antihistaminic drugs with human translationally controlled tumor protein (TCTP) as novel approach for differentiation therapy.Oncotarget · 2016Article
- Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice.Scientific reports · 2016Article
- Expression and clinical role of TCTP in epithelial ovarian cancer.Journal of molecular histology · 2015Article
- Translationally controlled tumor protein induces epithelial to mesenchymal transition and promotes cell migration, invasion and metastasis.Scientific reports · 2015Article
- Elevation of serum fortilin levels is specific for apoptosis and signifies cell death in vivo.BBA clinical · 2014Article
- Interaction of translationally controlled tumor protein with Apaf-1 is involved in the development of chemoresistance in HeLa cells.BMC cancer · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Fortilin, a 172-amino-acid polypeptide present both in the cytosol and nucleus, possesses potent anti-apoptotic activity. Although fortilin is known to bind Ca2+, the biochemistry and biological significance of such an interaction remains unknown. In the present study we report that fortilin must bind Ca2+ in order to protect cells against Ca2+-dependent apoptosis. Using a standard Ca2+-overlay assay, we first validated that full-length fortilin binds Ca2+ and showed that the N-terminus (amino acids 1-72) is required for its Ca2+-binding. We then used flow dialysis and CD spectropolarimetry assays to demonstrate that fortilin binds Ca2+ with a dissociation constant (Kd) of approx. 10 mM and that the binding of fortilin to Ca2+ induces a significant change in the secondary structure of fortilin. In order to evaluate the impact of the binding of fortilin to Ca2+ in vivo, we measured intracellular Ca2+ levels upon thapsigargin challenge and found that the lack of fortilin in the cell results in the exaggerated elevation of intracellular Ca2+ in the cell. We then tested various point mutants of fortilin for their Ca2+ binding and identified fortilin(E58A/E60A) to be a double-point mutant of fortilin lacking the ability of Ca2+-binding. We then found that wild-type fortilin, but not fortilin(E58A/E60A), protected cells against thapsigargin-induced apoptosis, suggesting that the binding of fortilin to Ca2+ is required for fortilin to protect cells against Ca2+-dependent apoptosis. Together, these results suggest that fortilin is an intracellular Ca2+ scavenger, protecting cells against Ca2+-dependent apoptosis by binding and sequestering Ca2+ from the downstream Ca2+-dependent apoptotic pathways.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.