ArticleHuman molecular genetics2018
Non-canonical role of cancer-associated mutant SEC23B in the ribosome biogenesis pathway.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- Burden of rare genetic variants in genes associated with cancer among Malawian cervical cancer patients.African journal of laboratory medicine · 2026Article
- The proximity interactome of PML isoforms I and II under fatty acid stress.FEBS letters · 2025Article
- Non-canonical role of wild-type SEC23B in the cellular stress response pathway.Cell death & disease · 2021Article
- PTEN hamartoma tumour syndrome: what happens when there is no PTEN germline mutation?Human molecular genetics · 2020Review
- Transcriptome, Spliceosome and Editome Expression Patterns of the Porcine Endometrium in Response to a Single Subclinical Dose ofInternational journal of molecular sciences · 2020Article
- Membrane trafficking in health and disease.Disease models & mechanisms · 2020Review
- The Functional Role of SEC23 in Vesicle Transportation, Autophagy and Cancer.International journal of biological sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
SEC23B is a component of coat protein complex II (COPII) vesicles that transport secretory proteins from the endoplasmic reticulum (ER) to the Golgi apparatus. Loss-of-function SEC23B mutations cause a rare form of anemia, resulting from decreased SEC23B levels. We recently identified germline heterozygous SEC23B variants as potentially cancer-predisposing. Mutant SEC23B associated with ER stress-mediated tumorigenesis, without decreased SEC23B expression. However, our understanding of the processes behind these observations remain limited. Here, we show mutant SEC23B exists within nucleoli, in addition to classical distribution at the ER/Golgi. This occurs independent of other COPII proteins and does not compromise secretory function. Mutant cells have increased ribosomal protein and translation-related gene expression, and enhanced translational capacity, in the presence of ER stress. We show that mutant SEC23B binds to UBF transcription factor, with increased UBF transcription factor binding at the ribosomal DNA promoter. Our data indicate SEC23B has potential non-canonical COPII-independent function, particularly within the ribosome biogenesis pathway, and that may contribute to the pathogenesis of cancer-predisposition.
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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.