ArticleThe Journal of biological chemistry2015
A new role for annexin A11 in the early secretory pathway via stabilizing Sec31A protein at the endoplasmic reticulum exit sites (ERES).
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Annexin A11 and TDP-43: core players in neurodegeneration.Acta neuropathologica · 2026Review
- Physiological and pathological roles of ANXA11: a multifunctional regulator in neurodegeneration and other disorders.Cell communication and signaling : CCS · 2026Review
- Beyond Vesicular Traffic: The ERES as the Gateway for Biosynthetic Secretion.Sub-cellular biochemistry · 2026Review
- Nuclear Fraction Proteome Analyses During rAAV Production of AAV2-Plasmid-Transfected HEK-293 Cells.International journal of molecular sciences · 2025Article
- Potential biomarkers in early detection of gastric cancer.Frontiers in pharmacology · 2025Review
- TFG regulates inner COPII coat recruitment to facilitate anterograde secretory protein transport.Molecular biology of the cell · 2024Article
- Disease-specific protein corona formed in pathological intestine enhances the oral absorption of nanoparticles.Acta pharmaceutica Sinica. B · 2023Article
- Development of intensiometric indicators for visualizing N-cadherin interaction across cells.Communications biology · 2022Article
- Role of the IgG4-related cholangitis autoantigen annexin A11 in cholangiocyte protection.Journal of hepatology · 2022Article
- Article
- CaFaculty reviews · 2022Review
- Development of FRET-based indicators for visualizing homophilic trans interaction of a clustered protocadherin.Scientific reports · 2021Article
- Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021Review
- The Novel ALG-2 Target Protein CDIP1 Promotes Cell Death by Interacting with ESCRT-I and VAPA/B.International journal of molecular sciences · 2021Article
- Article
- COPII-mediated trafficking at the ER/ERGIC interface.Traffic (Copenhagen, Denmark) · 2019Review
- Specific Proteomes of Hippocampal Regions CA2 and CA1 Reveal Proteins Linked to the Unique Physiology of Area CA2.Journal of proteome research · 2019Article
- Association of PDCD6 polymorphisms with the risk of cancer: Evidence from a meta-analysis.Oncotarget · 2018Review
- Stat3-mediated alterations in lysosomal membrane protein composition.The Journal of biological chemistry · 2018Article
- Nanoluciferase Reporter Gene System Directed by Tandemly Repeated Pseudo-Palindromic NFAT-Response Elements Facilitates Analysis of Biological Endpoint Effects of Cellular CaInternational journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exit of cargo molecules from the endoplasmic reticulum (ER) for transport to the Golgi is the initial step in intracellular vesicular trafficking. The coat protein complex II (COPII) machinery is recruited to specialized regions of the ER, called ER exit sites (ERES), where it plays a central role in the early secretory pathway. It has been known for more than two decades that calcium is an essential factor in vesicle trafficking from the ER to Golgi apparatus. However, the role of calcium in the early secretory pathway is complicated and poorly understood. We and others previously identified Sec31A, an outer cage component of COPII, as an interacting protein for the penta-EF-hand calcium-binding protein ALG-2. In this study, we show that another calcium-binding protein, annexin A11 (AnxA11), physically associates with Sec31A by the adaptor function of ALG-2. Depletion of AnxA11 or ALG-2 decreases the population of Sec31A that is stably associated with the ERES and causes scattering of juxtanuclear ERES to the cell periphery. The synchronous ER-to-Golgi transport of transmembrane cargoes is accelerated in AnxA11- or ALG-2-knockdown cells. These findings suggest that AnxA11 maintains architectural and functional features of the ERES by coordinating with ALG-2 to stabilize Sec31A at the ERES.
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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.