ArticleMolecular biology of the cell2005
Caspase-resistant Golgin-160 disrupts apoptosis induced by secretory pathway stress and ligation of death receptors.
Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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.
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Who cites it
32 citing papers in PubMed, 65 citations in OpenAlex.
- B cell receptor-induced protein dynamics and the emerging role of SUMOylation revealed by proximity proteomics.Journal of cell science · 2023Article
- Review
- The crescent-like Golgi ribbon is shaped by the Ajuba/PRMT5/Aurora-A complex-modified HURP.Cell communication and signaling : CCS · 2023Article
- The Capillary Morphogenesis Gene 2 Triggers the Intracellular Hallmarks of Collagen VI-Related Muscular Dystrophy.International journal of molecular sciences · 2022Article
- Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis.Frontiers in cell and developmental biology · 2021Review
- The diversity of ACBD proteins - From lipid binding to protein modulators and organelle tethers.Biochimica et biophysica acta. Molecular cell research · 2020Review
- The Golgi Apparatus May Be a Potential Therapeutic Target for Apoptosis-Related Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- The mechanism on phosphorylation of Hsp20Ser16 inhibit GA stress and ER stress during OGD/R.PloS one · 2019Article
- Golgi Structure and Function in Health, Stress, and Diseases.Results and problems in cell differentiation · 2019Review
- GOLPH3 Mediated Golgi Stress Response in Modulating N2A Cell Death upon Oxygen-Glucose Deprivation and Reoxygenation Injury.Molecular neurobiology · 2016Article
- GRASPs in Golgi Structure and Function.Frontiers in cell and developmental biology · 2015Review
- The Golgi complex in stress and death.Frontiers in neuroscience · 2015Review
- An unbiased proteomic screen reveals caspase cleavage is positively and negatively regulated by substrate phosphorylation.Molecular & cellular proteomics : MCP · 2014Article
- Glycobiology of cell death: when glycans and lectins govern cell fate.Cell death and differentiation · 2013Review
- Article
- Golgin160 recruits the dynein motor to position the Golgi apparatus.Developmental cell · 2012Article
- Inactivation of ceramide transfer protein during pro-apoptotic stress by Golgi disassembly and caspase cleavage.The Biochemical journal · 2012Article
- New components of the Golgi matrix.Cell and tissue research · 2011Review
- Golgi positioning.Cold Spring Harbor perspectives in biology · 2011Review
- Tethering function of the caspase cleavage fragment of Golgi protein p115 promotes apoptosis via a p53-dependent pathway.The Journal of biological chemistry · 2011Article
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 1 institution in 1 country.
Funding
Abstract
Golgin-160 is a coiled-coil protein on the cytoplasmic face of the Golgi complex that is cleaved by caspases during apoptosis. We assessed the sensitivity of cell lines stably expressing wild-type or caspase-resistant golgin-160 to several proapoptotic stimuli. Cells expressing a caspase-resistant mutant of golgin-160 were strikingly resistant to apoptosis induced by ligation of death receptors and by drugs that induce endoplasmic reticulum (ER) stress, including brefeldin-A, dithiothreitol, and thapsigargin. However, both cell lines responded similarly to other proapoptotic stimuli, including staurosporine, anisomycin, and etoposide. The caspase-resistant golgin-160 dominantly prevented cleavage of endogenous golgin-160 after ligation of death receptors or induction of ER stress, which could be explained by a failure of initiator caspase activation. The block in apoptosis in cells expressing caspase-resistant golgin-160 could not be bypassed by expression of potential caspase cleavage fragments of golgin-160, or by drug-induced disassembly of the Golgi complex. Our results suggest that some apoptotic signals (including those initiated by death receptors and ER stress) are sensed and integrated at Golgi membranes and that golgin-160 plays an important role in transduction of these signals.
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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.