ArticleMolecular biology of the cell2010
Induction of a massive endoplasmic reticulum and perinuclear space expansion by expression of lamin B receptor mutants and the related sterol reductases TM7SF2 and DHCR7.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
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- Transient receptor potential vanilloid channel 2 contributes to multi-modal endoplasmic reticulum and perinuclear space dilations that can also be observed in prion-infected mice.Acta neuropathologica · 2025Article
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- Discovery of key genes as novel biomarkers specifically associated with HPV-negative cervical cancer.Molecular therapy. Methods & clinical development · 2021Article
- Extracts Prepared from a Canadian Toxic Plant Induce Light-Dependent Perinuclear Vacuoles in Human Cells.Toxins · 2021Article
- Interplay of the nuclear envelope with chromatin in physiology and pathology.Nucleus (Austin, Tex.) · 2020Review
- Autosis: A New Target to Prevent Cell Death.JACC. Basic to translational science · 2020Review
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- Interaction between the autophagy protein Beclin 1 and Na+,K+-ATPase during starvation, exercise, and ischemia.JCI insight · 2020Article
- A common pathomechanism in GMAP-210- and LBR-related diseases.JCI insight · 2018Article
- Effects of host cell sterol composition upon internalization ofThe Journal of biological chemistry · 2018Article
- Lamina-associated polypeptide 1 is dispensable for embryonic myogenesis but required for postnatal skeletal muscle growth.Human molecular genetics · 2017Article
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- Hexavalent chromium induces expression of mesenchymal and stem cell markers in renal epithelial cells.Molecular carcinogenesis · 2016Article
- Altering lamina assembly reveals lamina-dependent and -independent functions for A-type lamins.Journal of cell science · 2015Article
- Autosis and autophagic cell death: the dark side of autophagy.Cell death and differentiation · 2015Review
- Cellular stress induces Bax-regulated nuclear bubble budding and rupture followed by nuclear protein release.Nucleus (Austin, Tex.) · 2014Article
- Autosis is a Na+,K+-ATPase-regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia-ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamin B receptor (LBR) is an inner nuclear membrane protein involved in tethering the nuclear lamina and the underlying chromatin to the nuclear envelope. In addition, LBR exhibits sterol reductase activity. Mutations in the LBR gene cause two different human diseases: Pelger-Huët anomaly and Greenberg skeletal dysplasia, a severe chrondrodystrophy causing embryonic death. Our study aimed at investigating the effect of five LBR disease mutants on human cultured cells. Three of the tested LBR mutants caused a massive compaction of chromatin coincidental with the formation of a large nucleus-associated vacuole (NAV) in several human cultured cell lines. Live cell imaging and electron microscopy revealed that this structure was generated by the separation of the inner and outer nuclear membrane. During NAV formation, nuclear pore complexes and components of the linker of nucleoskeleton and cytoskeleton complex were lost in areas of membrane separation. Concomitantly, a large number of smaller vacuoles formed throughout the cytoplasm. Notably, forced expression of the two structurally related sterol reductases transmembrane 7 superfamily member 2 and 7-dehydrocholesterol reductase caused, even in their wild-type form, a comparable phenotype in susceptible cell lines. Hence, LBR mutant variants and sterol reductases can severely interfere with the regular organization of the nuclear envelope and the endoplasmic reticulum.
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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.