ArticleThe Journal of biological chemistry2011
Tethering function of the caspase cleavage fragment of Golgi protein p115 promotes apoptosis via a p53-dependent pathway.
Article in The Journal of biological chemistry, 2011. 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, 24 citations in OpenAlex.
- USO1 Coordinates Centriolar Satellites to Regulate Male Germ Cell Proliferation and Cell Cycle Progression.International journal of molecular sciences · 2025Article
- Cdk1 protects against oxygen-glucose deprivation and reperfusion-induced Golgi fragmentation and apoptosis through mediating GM130 phosphorylation.Journal of molecular histology · 2023Article
- Golgi apparatus-targeted aggregation-induced emission luminogens for effective cancer photodynamic therapy.Nature communications · 2022Article
- Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis.Frontiers in cell and developmental biology · 2021Review
- Wiskott-Aldrich syndrome protein senses irradiation-induced DNA damage to coordinate the cell-protective Golgi dispersal response in human T and B lymphocytes.The Journal of allergy and clinical immunology · 2020Article
- The Golgi Apparatus May Be a Potential Therapeutic Target for Apoptosis-Related Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- 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
- Alterations in the nucleocytoplasmic transport in apoptosis: Caspases lead the way.Cell proliferation · 2018Review
- Regulatory non-coding RNA: new instruments in the orchestration of cell death.Cell death & disease · 2016Review
- Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells.Medical oncology (Northwood, London, England) · 2015Article
- Hsp20 Protects against Oxygen-Glucose Deprivation/Reperfusion-Induced Golgi Fragmentation and Apoptosis through Fas/FasL Pathway.Oxidative medicine and cellular longevity · 2015Article
- The Golgi complex in stress and death.Frontiers in neuroscience · 2015Review
- Organelle-specific initiation of cell death.Nature cell biology · 2014Review
- Fragmented inositol 1,4,5-trisphosphate receptors retain tetrameric architecture and form functional Ca2+ release channels.The Journal of biological chemistry · 2013Article
- p53 and Ceramide as Collaborators in the Stress Response.International journal of molecular sciences · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
The Golgi apparatus undergoes extensive fragmentation during apoptosis due in part to caspase-mediated cleavage of its structural proteins. Significantly, the Golgi-vesicle-tethering protein p115 is cleaved at Asp(757) early during apoptosis and the nuclear translocation of its 205 amino acid C-terminal fragment (CTF) precedes observable Golgi fragmentation. Nuclear localization of the p115 CTF induces apoptosis. The regulation of CTF nuclear translocation and the mechanism of its apoptotic activity however, remain unknown. Here, we demonstrate that nuclear translocation of the CTF is regulated by SUMOylation. CTF-induced apoptosis is transcription dependent and mediated by the tumor suppressor, p53. Expression of the CTF led to the phosphorylation and stabilization of p53 and results in the expression of PUMA, a pro-apoptotic target of p53. CTF-induced stabilization of p53 is sensitive to the MEK/ERK inhibitor U0126. Co-immunoprecipitation studies indicate that the p115 CTF can bind to both p53 and ERK1. The CTF is also able to form dimers and its dimerization is dependent on residues 859-884, previously determined to be required for apoptosis. Indeed, CTF expression promotes p53-ERK interaction, which is diminished upon deletion of residues 859-884. Together, our results indicate a conserved tethering function of the Golgi protein p115 CTF which promotes p53-ERK interaction for the amplification of the apoptotic signal.
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.