ArticleNature communications2021
WFS1 functions in ER export of vesicular cargo proteins in pancreatic β-cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 41 citations in OpenAlex.
- Deletion ofBiology · 2026Article
- Functional characterization of porcine septin12 and its role in male reproduction.Animal bioscience · 2026Article
- Targeting WFS1 overcomes KRASNPJ precision oncology · 2026Article
- WFS1-related isolated diabetes induced by a WFS1 missense mutation: focus on the isolated diabetes phenotype.Orphanet journal of rare diseases · 2026Article
- Synaptic Alterations Are Preceding the Axonal Loss in Optic Atrophy of Wolfram Syndrome Mouse Model.bioRxiv : the preprint server for biology · 2026Article
- The integrated stress response in pancreatic β-cell failure in diabetes: from molecular mechanisms to precision therapeutics.Frontiers in endocrinology · 2026Review
- Synaptic alterations are preceding the axonal loss in optic atrophy of Wolfram syndrome mouse model.Frontiers in neuroscience · 2026Article
- Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells.Nature reviews. Endocrinology · 2025Review
- Article
- Characterization of Novel WFS1 Variants in Three Diabetes Pedigrees.Journal of diabetes · 2025Article
- MyoD1 localization at the nuclear periphery is mediated by association of WFS1 with active enhancers.Nature communications · 2025Article
- Diabetes mellitus and pregnancy in Wolfram syndrome type 1: a case report with review of clinical and pathophysiological aspects.Frontiers in medicine · 2025Article
- Integration of multi-omics transcriptome-wide analysis for the identification of novel therapeutic drug targets in diabetic retinopathy.Journal of translational medicine · 2024Article
- Wolfram Syndrome Type I Case Report and Review-Focus on Early Diagnosis and Genetic Variants.Medicina (Kaunas, Lithuania) · 2024Review
- COPII cage assembly factor Sec13 integrates information flow regulating endomembrane function in response to human variation.Scientific reports · 2024Article
- Comprehensive overview of disease models for Wolfram syndrome: toward effective treatments.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Review
- ISR inhibition reverses pancreatic β-cell failure in Wolfram syndrome models.Cell death and differentiation · 2024Article
- Nlp-dependent ER-to-Golgi transport.International journal of biological sciences · 2024Article
- Wolfram syndrome type 1: a case series.Orphanet journal of rare diseases · 2023Article
- A proximity labeling strategy enables proteomic analysis of inter-organelle membrane contacts.iScience · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sorting of soluble secretory proteins from the endoplasmic reticulum (ER) to the Golgi complex is mediated by coat protein complex II (COPII) vesicles and thought to required specific ER membrane cargo-receptor proteins. However, these receptors remain largely unknown. Herein, we show that ER to Golgi transfer of vesicular cargo proteins requires WFS1, an ER-associated membrane protein whose loss of function leads to Wolfram syndrome. Mechanistically, WFS1 directly binds to vesicular cargo proteins including proinsulin via its ER luminal C-terminal segment, whereas pathogenic mutations within this region disrupt the interaction. The specific ER export signal encoded in the cytosolic N-terminal segment of WFS1 is recognized by the COPII subunit SEC24, generating mature COPII vesicles that traffic to the Golgi complex. WFS1 deficiency leads to abnormal accumulation of proinsulin in the ER, impeding the proinsulin processing as well as insulin secretion. This work identifies a vesicular cargo receptor for ER export and suggests that impaired peptide hormone transport underlies diabetes resulting from pathogenic WFS1 mutations.
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