ArticleThe Journal of cell biology2002
A caspase cleavage fragment of p115 induces fragmentation of the Golgi apparatus and apoptosis.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 152 citations in OpenAlex.
- USO1 Coordinates Centriolar Satellites to Regulate Male Germ Cell Proliferation and Cell Cycle Progression.International journal of molecular sciences · 2025Article
- A novel golgi related genes based correlation prognostic index can better predict the prognosis of glioma and responses to immunotherapy.Discover oncology · 2025Article
- The PDE4DIP-AKAP9 axis promotes lung cancer growth through modulation of PKA signalling.Communications biology · 2025Article
- Golgi-derived extracellular vesicle production induced by SARS-CoV-2 envelope protein.Apoptosis : an international journal on programmed cell death · 2025Article
- Golgi dispersal in cancer stem cells promotes chemoresistance of colorectal cancer via the Golgi stress response.Cell death & disease · 2024Article
- Reevaluating Golgi fragmentation and its implications in wound repair.Cell regeneration (London, England) · 2024Review
- Split but merge: Golgi fragmentation in physiological and pathological conditions.Molecular biology reports · 2024Review
- Cdk1 protects against oxygen-glucose deprivation and reperfusion-induced Golgi fragmentation and apoptosis through mediating GM130 phosphorylation.Journal of molecular histology · 2023Article
- AtypicalScience advances · 2022Article
- The Capillary Morphogenesis Gene 2 Triggers the Intracellular Hallmarks of Collagen VI-Related Muscular Dystrophy.International journal of molecular sciences · 2022Article
- Golgi apparatus-targeted aggregation-induced emission luminogens for effective cancer photodynamic therapy.Nature communications · 2022Article
- Non-Apoptotic Role of Apoptotic Caspases in theFrontiers in cell and developmental biology · 2022Review
- Biogenesis of Extracellular Vesicles.Sub-cellular biochemistry · 2021Article
- Golgi organization is regulated by proteasomal degradation.Nature communications · 2020Article
- The Golgi Apparatus May Be a Potential Therapeutic Target for Apoptosis-Related Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- ACBD3 is required for FAPP2 transferring glucosylceramide through maintaining the Golgi integrity.Journal of molecular cell biology · 2019Article
- HDAC6 Inhibition Protects against OGDR-Induced Golgi Fragmentation and Apoptosis.Oxidative medicine and cellular longevity · 2019Article
- Golgi Structure and Function in Health, Stress, and Diseases.Results and problems in cell differentiation · 2019Review
- GOLPH3 promotes glioma progression via facilitating JAK2-STAT3 pathway activation.Journal of neuro-oncology · 2018Article
- N-Terminomics TAILS Identifies Host Cell Substrates of Poliovirus and Coxsackievirus B3 3C Proteinases That Modulate Virus Infection.Journal of virology · 2018Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In mammalian cells, the Golgi apparatus undergoes extensive fragmentation during apoptosis. p115 is a key vesicle tethering protein required for maintaining the structural organization of the Golgi apparatus. Here, we demonstrate that p115 was cleaved during apoptosis by caspases 3 and 8. Compared with control cells expressing native p115, those expressing a cleavage-resistant form of p115 delayed Golgi fragmentation during apoptosis. Expression of cDNAs encoding full-length or an NH2-terminal caspase cleavage fragment of p115 had no effect on Golgi morphology. In contrast, expression of the COOH-terminal caspase cleavage product of p115 itself caused Golgi fragmentation. Furthermore, this fragment translocated to the nucleus and its expression was sufficient to induce apoptosis. Most significantly, in vivo expression of the COOH-terminal fragment in the presence of caspase inhibitors, or upon coexpression with a cleavage-resistant mutant of p115, showed that p115 degradation plays a key role in amplifying the apoptotic response independently of Golgi fragmentation.
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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.