ArticleCell cycle (Georgetown, Tex.)2014
Loss of Extended Synaptotagmins ESyt2 and ESyt3 does not affect mouse development or viability, but in vitro cell migration and survival under stress are affected.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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.
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Genome-wide association for sarcoidosis identifies novel risk loci and genetic heritability in African and European ancestries: a meta-analysis from the Finngen, Million Veteran Program, UK Biobank, and Biobank Japan datasets.Orphanet journal of rare diseases · 2025Pooled it
- The Transcriptomic and Proteomic Molecular Signatures of Equine Multiple-System Neuropathy (Grass Sickness).Cells · 2026Article
- Article
- Extended synaptotagmin regulates membrane contact site structure and lipid transfer function in vivo.EMBO reports · 2020Article
- Hypothalamic extended synaptotagmin-3 contributes to the development of dietary obesity and related metabolic disorders.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Sticking With It: ER-PM Membrane Contact Sites as a Coordinating Nexus for Regulating Lipids and Proteins at the Cell Cortex.Frontiers in cell and developmental biology · 2020Review
- Lipid transporter TMEM24/C2CD2L is a CaProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Homozygous PCDH12 variants result in phenotype of cerebellar ataxia, dystonia, retinopathy, and dysmorphism.Journal of human genetics · 2019Article
- NeurodegenERation: The Central Role for ER Contacts in Neuronal Function and Axonopathy, Lessons From Hereditary Spastic Paraplegias and Related Diseases.Frontiers in neuroscience · 2019Review
- Loss of all 3 Extended Synaptotagmins does not affect normal mouse development, viability or fertility.Cell cycle (Georgetown, Tex.) · 2016Article
- Homeostatic regulation of the PI(4,5)P2-Ca(2+) signaling system at ER-PM junctions.Biochimica et biophysica acta · 2016Review
- Extended Synaptotagmin (ESyt) Triple Knock-Out Mice Are Viable and Fertile without Obvious Endoplasmic Reticulum Dysfunction.PloS one · 2016Article
- The ER/PM microdomain, PI(4,5)P₂ and the regulation of STIM1-Orai1 channel function.Cell calcium · 2015Review
- Extended Synaptotagmin Interaction with the Fibroblast Growth Factor Receptor Depends on Receptor Conformation, Not Catalytic Activity.The Journal of biological chemistry · 2015Article
- The Arabidopsis synaptotagmin1 is enriched in endoplasmic reticulum-plasma membrane contact sites and confers cellular resistance to mechanical stresses.Plant physiology · 2015Article
- Unveiling physiological functions of extended synaptotagmins.Cell cycle (Georgetown, Tex.) · 2015Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Extended Synaptotagmins (Esyts) are a family of multi-C2 domain membrane proteins with orthologs in organisms from yeast to human. Three Esyt genes exist in mouse and human and these have most recently been implicated in the formation of junctions between endoplasmic reticulum and plasma membrane, as well as the Ca(2+) dependent replenishment of membrane phospholipids. The data are consistent with a function in extracellular signal transduction and cell adhesion, and indeed Esyt2 was previously implicated in both these functions in Xenopus. Despite this, little is known of the function of the Esyts in vivo. We have generated mouse lines carrying homozygous deletions in one or both of the genes encoding the highly homologous Esyt2 and Esyt3 proteins. Surprisingly, esyt2(-/-)/esyt3(-/-) mice develop normally and are both viable and fertile. In contrast, esyt2(-/-)/esyt3(-/-) mouse embryonic fibroblasts display a reduced ability to migrate in standard in vitro assays, and are less resistant to stringent culture conditions and to oxidative stress than equivalent wild type fibroblasts.
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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.