ArticleCell death and differentiation2014
Caspase-cleaved arrestin-2 and BID cooperatively facilitate cytochrome C release and cell death.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 53 citations in OpenAlex.
- TAX1BP1 protects against doxorubicin-induced cardiotoxicity via maintaining mitochondrial function in a mTORC2-SGK1-VDAC1 manner.Molecular medicine (Cambridge, Mass.) · 2026Article
- Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025Review
- A pH-sensitive peptide amphiphilic-based drug delivery system inhibits hepatocellular carcinoma growth by suppressing hepatic stellate cell activation.Materials today. Bio · 2025Article
- Unveiling BID: a key biomarker in apoptosis post-intracerebral hemorrhage.Frontiers in neurology · 2025Article
- Antagonism of β-arrestins in IL-4-driven microglia reactivity via the Samd4/mTOR/OXPHOS axis in Parkinson's disease.Science advances · 2024Article
- GPCR-dependent and -independent arrestin signaling.Trends in pharmacological sciences · 2024Review
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Review
- Expression of Untagged Arrestins in E. coli and Their Purification.Current protocols · 2023Article
- Double life: How GRK2 and β-arrestin signaling participate in diseases.Cellular signalling · 2022Review
- How Do Hexokinases Inhibit Receptor-Mediated Apoptosis?Biology · 2022Review
- Mdm2 enhances ligase activity of parkin and facilitates mitophagy.Scientific reports · 2020Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Cleavage of arrestin-3 by caspases attenuates cell death by precluding arrestin-dependent JNK activation.Cellular signalling · 2019Article
- Arrestin-3 scaffolding of the JNK3 cascade suggests a mechanism for signal amplification.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- GRKs and β-Arrestins: "Gatekeepers" of Mitochondrial Function in the Failing Heart.Frontiers in pharmacology · 2019Review
- GPCR Signaling Regulation: The Role of GRKs and Arrestins.Frontiers in pharmacology · 2019Review
- Regulation of response to radiotherapy by β-arrestin1 in Non-small cell lung cancer.Journal of Cancer · 2019Article
- BEZ235 enhances chemosensitivity of paclitaxel in hepatocellular carcinoma through inhibiting the PI3K/Akt/mTOR pathway.American journal of translational research · 2019Article
- Arrestin-mediated signaling: Is there a controversy?World journal of biological chemistry · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptosis is programmed cell death triggered by activation of death receptors or cellular stress. Activation of caspases is the hallmark of apoptosis. Arrestins are best known for their role in homologous desensitization of G protein-coupled receptors (GPCRs). Arrestins quench G protein activation by binding to activated phosphorylated GPCRs. Recently, arrestins have been shown to regulate multiple signalling pathways in G protein-independent manner via scaffolding signalling proteins. Here we demonstrate that arrestin-2 isoform is cleaved by caspases during apoptosis induced via death receptor activation or by DNA damage at evolutionarily conserved sites in the C-terminus. Caspase-generated arrestin-2-(1-380) fragment translocates to mitochondria increasing cytochrome C release, which is the key checkpoint in cell death. Cells lacking arrestin-2 are significantly more resistant to apoptosis. The expression of wild-type arrestin-2 or its cleavage product arrestin-2-(1-380), but not of its caspase-resistant mutant, restores cell sensitivity to apoptotic stimuli. Arrestin-2-(1-380) action depends on tBID: at physiological concentrations, arrestin-2-(1-380) directly binds tBID and doubles tBID-induced cytochrome C release from isolated mitochondria. Arrestin-2-(1-380) does not facilitate apoptosis in BID knockout cells, whereas its ability to increase caspase-3 activity and facilitate cytochrome C release is rescued when BID expression is restored. Thus, arrestin-2-(1-380) cooperates with another product of caspase activity, tBID, and their concerted action significantly contributes to cell death.
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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.