ArticleNature cell biology2012
A 14-3-3γ dimer-based scaffold bridges CtBP1-S/BARS to PI(4)KIIIβ to regulate post-Golgi carrier formation.
Article in Nature cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 127 citations in OpenAlex.
- Reversible control of post-Golgi transport by brefeldin A reveals recycling endosome maturation during glycosylphosphatidylinositol-anchored protein transport.Nature communications · 2026Article
- Molecular mechanism of CtBP1-S/BARS-driven membrane fission and its cellular control by metabolic ligands.Science advances · 2026Article
- 14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.Journal of cell science · 2025Article
- Phosphoinositide kinases in cancer: from molecular mechanisms to therapeutic opportunities.Nature reviews. Cancer · 2025Review
- Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy.Frontiers in neuroscience · 2025Review
- Identification and characterization of a new potent inhibitor targeting CtBP1/BARS in melanoma cells.Journal of experimental & clinical cancer research : CR · 2024Article
- Unraveling the Multifaceted Role of the Golgi Apparatus: Insights into Neuronal Plasticity, Development, Neurogenesis, Alzheimer's Disease, and SARS-CoV-2 Interactions.Brain sciences · 2023Review
- Phosphoinositides as membrane organizers.Nature reviews. Molecular cell biology · 2022Review
- Actin-driven Golgi apparatus dispersal during collective migration of epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- PKD-dependent PARP12-catalyzed mono-ADP-ribosylation of Golgin-97 is required for E-cadherin transport from Golgi to plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Endogenous and Exogenous Regulatory Signaling in the Secretory Pathway: Role of Golgi Signaling Molecules in Cancer.Frontiers in cell and developmental biology · 2022Review
- V-ATPase V0a1 promotes Weibel-Palade body biogenesis through the regulation of membrane fission.eLife · 2021Article
- Review
- Mitotic HOOK3 phosphorylation by ERK1c drives microtubule-dependent Golgi destabilization and fragmentation.iScience · 2021Article
- Picornaviruses: A View from 3A.Viruses · 2021Review
- Article
- Article
- The 14-3-3 Proteins as Important Allosteric Regulators of Protein Kinases.International journal of molecular sciences · 2020Review
- Direct trafficking pathways from the Golgi apparatus to the plasma membrane.Seminars in cell & developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Large pleiomorphic carriers leave the Golgi complex for the plasma membrane by en bloc extrusion of specialized tubular domains, which then undergo fission. Several components of the underlying molecular machinery have been identified, including those involved in the budding/initiation of tubular carrier precursors (for example, the phosphoinositide kinase PI(4)KIIIβ, the GTPase ARF, and FAPP2), and in the fission of these precursors (for example, PKD, CtBP1-S/BARS). However, how these proteins interact to bring about carrier formation is poorly understood. Here, we describe a protein complex that mediates carrier formation and contains budding and fission molecules, as well as other molecules, such as the adaptor protein 14-3-3γ. Specifically, we show that 14-3-3γ dimers bridge CtBP1-S/BARS with PI(4)KIIIβ, and that the resulting complex is stabilized by phosphorylation by PKD and PAK. Disrupting the association of these proteins inhibits the fission of elongating carrier precursors, indicating that this complex couples the carrier budding and fission processes.
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.