ArticleCell research2013
Caspase-mediated cleavage of C53/LZAP protein causes abnormal microtubule bundling and rupture of the nuclear envelope.
Article in Cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 36 citations in OpenAlex.
- CDK5RAP3 Deficiency Is Associated with Hepatic Inflammation and Increased Expression of NLRP3 Inflammasome Components.Biomedicines · 2025Article
- Insights about circadian clock in glioma: From molecular pathways to therapeutic drugs.CNS neuroscience & therapeutics · 2022Review
- NUP62 localizes to ALS/FTLD pathological assemblies and contributes to TDP-43 insolubility.Nature communications · 2022Article
- CDK5RAP3, an essential regulator of checkpoint, interacts with RPL26 and maintains the stability of cell growth.Cell proliferation · 2022Article
- C53 Interacting with UFM1-Protein Ligase 1 Regulates Microtubule Nucleation in Response to ER Stress.Cells · 2022Article
- Role of Apoptotic Cell Clearance in Pneumonia and Inflammatory Lung Disease.Pathogens (Basel, Switzerland) · 2021Review
- Identification of Prognostic Biomarkers Among FAM83 Family Genes in Human Ovarian Cancer Through Bioinformatic Analysis and Experimental Verification.Cancer management and research · 2021Article
- Cyclin-Dependent Kinase 5 Regulatory Subunit Associated Protein 3: Potential Functions and Implications for Development and Disease.Frontiers in oncology · 2021Review
- The nuclear envelope: target and mediator of the apoptotic process.Cell death discovery · 2020Review
- LZAP promotes the proliferation and invasiveness of cervical carcinoma cells by targeting AKT and EMT.Journal of Cancer · 2020Article
- Mutant Proteomics of Lung Adenocarcinomas Harboring DifferentFrontiers in oncology · 2020Article
- Overexpression of IC53d promotes the proliferation of gastric cancer cells by activating the AKT/GSK3β/cyclin D1 signaling pathway.Oncology reports · 2019Article
- CDK5RAP3 Participates in Autophagy Regulation and Is Downregulated in Renal Cancer.Disease markers · 2019Article
- Ufm1-Specific Ligase Ufl1 Regulates Endoplasmic Reticulum Homeostasis and Protects Against Heart Failure.Circulation. Heart failure · 2018Article
- Alterations in the nucleocytoplasmic transport in apoptosis: Caspases lead the way.Cell proliferation · 2018Review
- Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons.Neural regeneration research · 2018Article
- Article
- DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways.Molecular neurobiology · 2016Article
- RCAD/Ufl1, a Ufm1 E3 ligase, is essential for hematopoietic stem cell function and murine hematopoiesis.Cell death and differentiation · 2015Article
- Structural and functional analysis of cell adhesion and nuclear envelope nano-topography in cell death.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 4 countries.
Funding
Abstract
Apoptotic nucleus undergoes distinct morphological and biochemical changes including nuclear shrinkage, chromatin condensation and DNA fragmentation, which are attributed to caspase-mediated cleavage of several nuclear substrates such as lamins. As most of active caspases reside in the cytoplasm, disruption of the nuclear-cytoplasmic barrier is essential for caspases to reach their nuclear targets. The prevailing proposed mechanism is that the increase in the permeability of nuclear pores induced by caspases allows the caspases and other apoptotic factors to diffuse into the nucleus, thereby resulting in the nuclear destruction. Here, we report a novel observation that physical rupture of the nuclear envelope (NE) occurs in the early stage of apoptosis. We found that the NE rupture was caused by caspase-mediated cleavage of C53/LZAP, a protein that has been implicated in various signaling pathways, including NF-κB signaling and DNA damage response, as well as tumorigenesis and metastasis. We also demonstrated that C53/LZAP bound indirectly to the microtubule (MT), and expression of the C53/LZAP cleavage product caused abnormal MT bundling and NE rupture. Taken together, our findings suggest a novel role of C53/LZAP in the regulation of MT dynamics and NE structure during apoptotic cell death. Our study may provide an additional mechanism for disruption of the nuclear-cytoplasmic barrier during apoptosis.
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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.