ArticleOncogene2010
Tid1 is a new regulator of p53 mitochondrial translocation and apoptosis in cancer.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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.
The trial behind it
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
61 citing papers in PubMed, 85 citations in OpenAlex.
- DNAJA: emerging targets for anti-tumor therapy.Future oncology (London, England) · 2025Review
- Non-Coding RNAs of Mitochondrial Origin: Roles in Cell Division and Implications in Cancer.International journal of molecular sciences · 2024Review
- DNAJC10 maintains survival and self-renewal of leukemia stem cells through PERK branch of the unfolded protein response.Haematologica · 2024Article
- ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor.Biology · 2024Review
- Human mtDNA-Encoded Long ncRNAs: Knotty Molecules and Complex Functions.International journal of molecular sciences · 2024Review
- Proximity-labeling chemoproteomics defines the subcellular cysteinome and inflammation-responsive mitochondrial redoxome.Cell chemical biology · 2023Article
- Elephant TP53-RETROGENE 9 induces transcription-independent apoptosis at the mitochondria.Cell death discovery · 2023Article
- Proximity-labeling chemoproteomics defines the subcellular cysteinome and inflammation-responsive mitochondrial redoxome.bioRxiv : the preprint server for biology · 2023Article
- DNAJC8: a prognostic marker and potential therapeutic target for hepatocellular carcinoma.Frontiers in immunology · 2023Article
- Quantitative omics analyses of NCOA4 deficiency reveal an integral role of ferritinophagy in iron homeostasis of hippocampal neuronal HT22 cells.Frontiers in nutrition · 2023Article
- Structural resemblance of the DNAJA-family protein, Tid1, to the DNAJB-family Hsp40.BMB reports · 2022Article
- Leveraging the Structure of DNAJA1 to Discover Novel Potential Pancreatic Cancer Therapies.Biomolecules · 2022Article
- Putting human Tid-1 in context: an insight into its role in the cell and in different disease states.Cell communication and signaling : CCS · 2022Review
- Nuclear-Mitochondrial Interactions.Biomolecules · 2022Review
- DRAM1 increases the secretion of PKM2-enriched EVs from hepatocytes to promote macrophage activation and disease progression in ALD.Molecular therapy. Nucleic acids · 2022Article
- Abrogating the Interaction Between p53 and Mortalin (Grp75/HSPA9/mtHsp70) for Cancer Therapy: The Story so far.Frontiers in cell and developmental biology · 2022Review
- Regulation of p53 and Cancer Signaling by Heat Shock Protein 40/J-Domain Protein Family Members.International journal of molecular sciences · 2021Review
- DNAJA1 Dysregulates Metabolism Promoting an Antiapoptotic Phenotype in Pancreatic Ductal Adenocarcinoma.Journal of proteome research · 2021Article
- Article
- Mitochondrial HSP70 Chaperone System-The Influence of Post-Translational Modifications and Involvement in Human Diseases.International journal of molecular sciences · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor protein induces apoptosis in response to genotoxic and environmental stresses. Recent studies have revealed the existence of a transcription-independent mitochondrial p53 apoptotic pathway; however, the mechanism that regulates its translocation to the mitochondria has been unknown. In this study, we show that the tumor suppressor Tid1 forms a complex with p53 under hypoxic conditions that directs p53 translocation to the mitochondria and the subsequent initiation of the mitochondrial apoptosis pathway. Loss of Tid1 expression abrogated p53 translocation to the mitochondria and inhibited apoptosis, whereas the over-expression of Tid1 promoted p53 mitochondrial localization and apoptosis. Tid1's mitochondrial signal sequence and DnaJ domain were both required for the movement of the p53-Tid1 complex from the cytosol to the mitochondria. When Tid is over-expressed in cancer cell lines expressing mutant p53 isoforms defective in transcriptional activity, mitochondrial localization and pro-apoptotic activities of the mutant p53 proteins was restored. Our results establish Tid1 as a novel regulator of p53-mediated apoptosis, and suggest that therapies designed to enhance Tid1's function in promoting mitochondrial localization of p53 and apoptosis could be an effective therapy in many cancers.
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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.