ArticleProceedings of the National Academy of Sciences of the United States of America2014
Calpain-generated natural protein fragments as short-lived substrates of the N-end rule pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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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
63 citing papers in PubMed, 93 citations in OpenAlex.
- Trypsin exhibits exopeptidase-like activity toward N-terminal arginine that biases proteomic analyses.bioRxiv : the preprint server for biology · 2026Article
- Detection of Calpain-Mediated Beclin-1 Cleavage for Drug Discovery in Inflammatory Bowel Diseases.Cells · 2026Article
- A C-degron regulates Chk1 kinase by allowing stability of inactive Chk1 and by making it short- lived upon activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Global profiling of N-terminal cysteine-dependent degradation mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Identification of Proteolytic Substrates of Calpain-5 with N-Terminomics.International journal of molecular sciences · 2025Article
- Oxygen sensing and plant adaptation to flooding in a changing climate.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Regulation of N-degron recognin-mediated autophagy by the SARS-CoV-2 PLpro ubiquitin deconjugase.Autophagy · 2025Article
- N-degron pathways.Proceedings of the National Academy of Sciences of the United States of America · 2024Review
- Dipeptidyl peptidases and E3 ligases of N-degron pathways cooperate to regulate protein stability.The Journal of cell biology · 2024Article
- Regulation of developmental gatekeeping and cell fate transition by the calpain protease DEK1 in Physcomitrium patens.Communications biology · 2024Article
- A Systematic Investigation of Proteoforms with N-Terminal Glycine and Their Dynamics Reveals Its Impacts on Protein Stability.Angewandte Chemie (International ed. in English) · 2024Article
- Stability dynamics of neurofilament and GFAP networks and protein fragments.Current opinion in cell biology · 2023Review
- Proteostasis in T cell aging.Seminars in immunology · 2023Review
- ERFVII action and modulation through oxygen-sensing in Arabidopsis thaliana.Nature communications · 2023Article
- Membrane-anchored calpains - hidden regulators of growth and development beyond plants?Frontiers in plant science · 2023Article
- Degradation of p0071 and p120-catenin during adherens junction disassembly byFrontiers in cellular and infection microbiology · 2023Article
- Dipeptidyl peptidase 9 triggers BRCA2 degradation and promotes DNA damage repair.EMBO reports · 2022Article
- Classifying Integrated Signature Molecules in Macrophages of Rheumatoid Arthritis, Osteoarthritis, and Periodontal Disease: An Omics-Based Study.Current issues in molecular biology · 2022Article
- Crystal structure of the Ate1 arginyl-tRNA-protein transferase and arginylation of N-degron substrates.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Calpains are Ca(2+)-dependent intracellular proteases. We show here that calpain-generated natural C-terminal fragments of proteins that include G protein-coupled receptors, transmembrane ion channels, transcriptional regulators, apoptosis controllers, kinases, and phosphatases (Phe-GluN2a, Lys-Ica512, Arg-Ankrd2, Tyr-Grm1, Arg-Atp2b2, Glu-Bak, Arg-Igfbp2, Glu-IκBα, and Arg-c-Fos), are short-lived substrates of the Arg/N-end rule pathway, which targets destabilizing N-terminal residues. We also found that the identity of a fragment's N-terminal residue can change during evolution, but the residue's destabilizing activity is virtually always retained, suggesting selection pressures that favor a short half-life of the calpain-generated fragment. It is also shown that a self-cleavage of a calpain can result in an N-end rule substrate. Thus, the autoprocessing of calpains can control them by making active calpains short-lived. These and related results indicate that the Arg/N-end rule pathway mediates the remodeling of oligomeric complexes by eliminating protein fragments that are produced in these complexes through cleavages by calpains or other nonprocessive proteases. We suggest that this capability of the Arg/N-end rule pathway underlies a multitude of its previously known but mechanistically unclear functions.
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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.