ReviewInternational journal of molecular sciences2018
Regulating Apoptosis by Degradation: The N-End Rule-Mediated Regulation of Apoptotic Proteolytic Fragments in Mammalian Cells.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Cognitive and Pyroptotic Outcomes of Neonatal Ketamine and Dexmedetomidine: Potential Neuroprotection via Caspase-1 Modulation.Developmental neurobiology · 2026Article
- N-Degron PROTACs as a Potential Therapeutic Approach for Chronic Myeloid Leukemia.Anti-cancer agents in medicinal chemistry · 2025Review
- Recent Advances in Understanding the Role of PEST Sequence- Containing Proteins in Retinal Neovascularization.Current drug targets · 2025Review
- Cacalol Acetate as Anticancer Agent: Antiproliferative, Pro-Apoptotic, Cytostatic, and Anti-Migratory Effects.Current issues in molecular biology · 2024Article
- UBR1 promotes anaplastic thyroid carcinoma progression via stabilizing YAP through monoubiquitylation.Scientific reports · 2024Article
- Insights into the recognition mechanism in the UBR box of UBR4 for its specific substrates.Communications biology · 2023Article
- Mitochondrial Dysfunction and Apoptosis in Brain Microvascular Endothelial Cells Following Blast Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Article
- Regulation of Neurodegeneration-associated Protein Fragments by the N-degron Pathways.Neurotoxicity research · 2022Review
- Mitochondrial DNA variants modulate N-formylmethionine, proteostasis and risk of late-onset human diseases.Nature medicine · 2021Article
- tRNACell chemical biology · 2020Article
- New cellular imaging of oocytes and preimplantation embryos using Lumitein™: Evaluation of oocyte quality and new information on protein dynamics within the perivitelline space during the one-cell oocyte stage in mice.The Journal of reproduction and development · 2020Article
- Up-regulation of FAT4 enhances the chemosensitivity of colorectal cancer cells treated by 5-FU.Translational cancer research · 2020Article
- Article
- Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix.Bioscience reports · 2019Article
- Degradation of proteins with N-terminal glycine.Nature structural & molecular biology · 2019Article
- Protective autophagy or autophagic death: effects of BEZ235 on chronic myelogenous leukemia.Cancer management and research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A pivotal hallmark of some cancer cells is the evasion of apoptotic cell death. Importantly, the initiation of apoptosis often results in the activation of caspases, which, in turn, culminates in the generation of proteolytically-activated protein fragments with potentially new or altered roles. Recent investigations have revealed that the activity of a significant number of the protease-generated, activated, pro-apoptotic protein fragments can be curbed via their selective degradation by the N-end rule degradation pathways. Of note, previous work revealed that several proteolytically-generated, pro-apoptotic fragments are unstable in cells, as their destabilizing N-termini target them for proteasomal degradation via the N-end rule degradation pathways. Remarkably, previous studies also showed that the proteolytically-generated anti-apoptotic Lyn kinase protein fragment is targeted for degradation by the UBR1/UBR2 E3 ubiquitin ligases of the N-end rule pathway in chronic myeloid leukemia cells. Crucially, the degradation of cleaved fragment of Lyn by the N-end rule counters imatinib resistance in these cells, implicating a possible linkage between the N-end rule degradation pathway and imatinib resistance. Herein, we highlight recent studies on the role of the N-end rule proteolytic pathways in regulating apoptosis in mammalian cells, and also discuss some possible future directions with respect to apoptotic proteolysis signaling.
Indexed as
Identifiers
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.