ArticleThe Journal of biological chemistry2011
Physical and functional antagonism between tumor suppressor protein p53 and fortilin, an anti-apoptotic protein.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 37 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
- Fortilin binds CTNNA3 and protects it against phosphorylation, ubiquitination, and proteasomal degradation to guard cells against apoptosis.Communications biology · 2025Article
- Translationally controlled tumor protein interacts with connexin 43 and facilitates intercellular coupling between cardiomyocytes.Frontiers in cell and developmental biology · 2025Article
- Deubiquitylase OTUD3 Mediates Endoplasmic Reticulum Stress through Regulating Fortilin Stability to Restrain Dopaminergic Neurons Apoptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Fortilin interacts with TGF-β1 and prevents TGF-β receptor activation.Communications biology · 2022Article
- Fortilin inhibits p53, halts cardiomyocyte apoptosis, and protects the heart against heart failure.Cell death discovery · 2021Article
- Article
- Translationally controlled tumor protein (TCTP) plays a pivotal role in cardiomyocyte survival through a Bnip3-dependent mechanism.Cell death & disease · 2019Article
- Ticagrelor induces paraoxonase-1 (PON1) and better protects hypercholesterolemic mice against atherosclerosis compared to clopidogrel.PloS one · 2019Article
- Some Biological Consequences of the Inhibition of Na,K-ATPase by Translationally Controlled Tumor Protein (TCTP).International journal of molecular sciences · 2018Review
- Fortilin binds IRE1α and prevents ER stress from signaling apoptotic cell death.Nature communications · 2017Article
- Translationally controlled tumour protein TCTP is induced early in human colorectal tumours and contributes to the resistance of HCT116 colon cancer cells to 5-FU and oxaliplatin.Cell communication and signaling : CCS · 2017Article
- Function of translationally controlled tumor protein (TCTP) in Eudrilus eugeniae regeneration.PloS one · 2017Article
- Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice.Scientific reports · 2016Article
- FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53.Journal of virology · 2015Article
- Evolutionarily conserved binding of translationally controlled tumor protein to eukaryotic elongation factor 1B.The Journal of biological chemistry · 2015Article
- Fuse binding protein antagonizes the transcription activity of tumor suppressor protein p53.BMC cancer · 2014Article
- Elevation of serum fortilin levels is specific for apoptosis and signifies cell death in vivo.BBA clinical · 2014Article
- Self-aggregating TIAF1 in lung cancer progression.Translational respiratory medicine · 2013Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Tumor suppressor protein p53, our most critical defense against tumorigenesis, can be made powerless by mechanisms such as mutations and inhibitors. Fortilin, a 172-amino acid polypeptide with potent anti-apoptotic activity, is up-regulated in many human malignancies. However, the exact mechanism by which fortilin exerts its anti-apoptotic activity remains unknown. Here we present significant insight. Fortilin binds specifically to the sequence-specific DNA binding domain of p53. The interaction of fortilin with p53 blocks p53-induced transcriptional activation of Bax. In addition, fortilin, but not a double point mutant of fortilin lacking p53 binding, inhibits p53-dependent apoptosis. Furthermore, cells with wild-type p53 and fortilin, but not cells with wild-type p53 and the double point mutant of fortilin lacking p53 binding, fail to induce Bax gene and apoptosis, leading to the formation of large tumor in athymic mice. Our results suggest that fortilin is a novel p53-interacting molecule and p53 inhibitor and that it is a logical molecular target in cancer therapy.
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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.