ArticleMolecular biology of the cell2006
The Ca2+-binding protein ALG-2 is recruited to endoplasmic reticulum exit sites by Sec31A and stabilizes the localization of Sec31A.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 93 citations in OpenAlex.
- Review
- TFG regulates inner COPII coat recruitment to facilitate anterograde secretory protein transport.Molecular biology of the cell · 2024Article
- Mechanism and cellular function of direct membrane binding by the ESCRT and ERES-associated CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Steady-state regulation of COPII-dependent secretory cargo sorting by inositol trisphosphate receptors, calcium, and penta EF hand proteins.The Journal of biological chemistry · 2023Article
- Mechanism and cellular function of direct membrane binding by the ESCRT and ERES-associated CabioRxiv : the preprint server for biology · 2023Article
- Sorting and Export of Proteins at the Endoplasmic Reticulum.Cold Spring Harbor perspectives in biology · 2023Review
- Oxidative stress-induced phosphorylation of JIP4 regulates lysosomal positioning in coordination with TRPML1 and ALG2.The EMBO journal · 2022Article
- CaFaculty reviews · 2022Review
- Article
- Article
- The Novel ALG-2 Target Protein CDIP1 Promotes Cell Death by Interacting with ESCRT-I and VAPA/B.International journal of molecular sciences · 2021Article
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- PDCD6 cooperates with C-Raf to facilitate colorectal cancer progression via Raf/MEK/ERK activation.Journal of experimental & clinical cancer research : CR · 2020Article
- Alix and Syntenin-1 direct amyloid precursor protein trafficking into extracellular vesicles.BMC molecular and cell biology · 2020Article
- ALG-2 couples T cell activation and apoptosis by regulating proteasome activity and influencing MCL1 stability.Cell death & disease · 2020Article
- Export Control: Post-transcriptional Regulation of the COPII Trafficking Pathway.Frontiers in cell and developmental biology · 2020Review
- COPII-mediated trafficking at the ER/ERGIC interface.Traffic (Copenhagen, Denmark) · 2019Review
- PAQR3 Regulates Endoplasmic Reticulum-to-Golgi Trafficking of COPII Vesicle via Interaction with Sec13/Sec31 Coat Proteins.iScience · 2018Article
- COPII-dependent ER export in animal cells: adaptation and control for diverse cargo.Histochemistry and cell biology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of transport vesicles that bud from endoplasmic reticulum (ER) exit sites is dependent on the COPII coat made up of three components: the small GTPase Sar1, the Sec23/24 complex, and the Sec13/31 complex. Here, we provide evidence that apoptosis-linked gene 2 (ALG-2), a Ca(2+)-binding protein of unknown function, regulates the COPII function at ER exit sites in mammalian cells. ALG-2 bound to the Pro-rich region of Sec31A, a ubiquitously expressed mammalian orthologue of yeast Sec31, in a Ca(2+)-dependent manner and colocalized with Sec31A at ER exit sites. A Ca(2+) binding-deficient ALG-2 mutant, which did not bind Sec31A, lost the ability to localize to ER exit sites. Overexpression of the Pro-rich region of Sec31A or RNA interference-mediated Sec31A depletion also abolished the ALG-2 localization at these sites. In contrast, depletion of ALG-2 substantially reduced the level of Sec31A associated with the membrane at ER exit sites. Finally, treatment with a cell-permeable Ca(2+) chelator caused the mislocalization of ALG-2, which was accompanied by a reduced level of Sec31A at ER exit sites. We conclude that ALG-2 is recruited to ER exit sites via Ca(2+)-dependent interaction with Sec31A and in turn stabilizes the localization of Sec31A at these sites.
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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.