ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Lamin B receptor regulates the growth and maturation of myeloid progenitors via its sterol reductase domain: implications for cholesterol biosynthesis in regulating myelopoiesis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Lamin B receptor upregulation in metastatic melanoma causes nuclear envelope fragility in confined migration during cancer invasion.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Lamin A upregulation reorganizes the genome during rod photoreceptor degeneration.Cell death & disease · 2023Article
- Hepatic transcript profiling in beef cattle: Effects of rumen-protected niacin supplementation.PloS one · 2023Article
- Evolution and diversification of the nuclear envelope.Nucleus (Austin, Tex.) · 2021Article
- Aged neutrophils form mitochondria-dependent vital NETs to promote breast cancer lung metastasis.Journal for immunotherapy of cancer · 2021Article
- Beyond the Extra Respiration of Phagocytosis: NADPH Oxidase 2 in Adaptive Immunity and Inflammation.Frontiers in immunology · 2021Review
- Article
- Characterization of lamin B receptor of Sf9 cells and its fate during Autographa californica nucleopolyhedrovirus infection.Cytotechnology · 2020Article
- Metabolism and Biological Activities of 4-Methyl-Sterols.Molecules (Basel, Switzerland) · 2019Review
- Coordinated increase of nuclear tension and lamin-A with matrix stiffness outcompetes lamin-B receptor that favors soft tissue phenotypes.Molecular biology of the cell · 2017Article
- Review
- Cooperative Activity of GABP with PU.1 or C/EBPε Regulates Lamin B Receptor Gene Expression, Implicating Their Roles in Granulocyte Nuclear Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- The Lamin B receptor is essential for cholesterol synthesis and perturbed by disease-causing mutations.eLife · 2016Article
- Pelger-Huët anomaly and Greenberg skeletal dysplasia: LBR-associated diseases of cholesterol metabolism.Rare diseases (Austin, Tex.) · 2016Article
- Nuclear hormone receptors put immunity on sterols.European journal of immunology · 2015Review
- ELCS in ice: cryo-electron microscopy of nuclear envelope-limited chromatin sheets.Chromosoma · 2014Article
- Statin use and peripheral blood progenitor cells mobilization in patients with multiple myeloma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Article
- Outfits for different occasions: tissue-specific roles of Nuclear Envelope proteins.Current opinion in cell biology · 2012Review
- Lymphohematopoietic licence: sterol C-14 reductase activity of lamin B receptor (Lbr) is essential for neutrophil differentiation.Journal of biosciences · 2012Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Lamin B receptor (LBR) is a bifunctional nuclear membrane protein with N-terminal lamin B and chromatin-binding domains plus a C-terminal sterol Δ(14) reductase domain. LBR expression increases during neutrophil differentiation, and deficient expression disrupts neutrophil nuclear lobulation characteristic of Pelger-Huët anomaly. Thus, LBR plays a critical role in regulating myeloid differentiation, but how the two functional domains of LBR support this role is currently unclear. We previously identified abnormal proliferation and deficient functional maturation of promyelocytes (erythroid, myeloid, and lymphoid [EML]-derived promyelocytes) derived from EML-ic/ic cells, a myeloid model of ichthyosis (ic) bone marrow that lacks Lbr expression. In this study, we provide new evidence that cholesterol biosynthesis is important to myeloid cell growth and is supported by the sterol reductase domain of Lbr. Cholesterol biosynthesis inhibitors caused growth inhibition of EML cells that increased in EML-derived promyelocytes, whereas cells lacking Lbr exhibited complete growth arrest at both stages. Lipid production increased during wild-type neutrophil maturation, but ic/ic cells exhibited deficient levels of lipid and cholesterol production. Ectopic expression of a full-length Lbr in EML-ic/ic cells rescued both nuclear lobulation and growth arrest in cholesterol starvation conditions. Lipid production also was rescued, and a deficient respiratory burst was corrected. Expression of just the C-terminal sterol reductase domain of Lbr in ic/ic cells also improved each of these phenotypes. Our data support the conclusion that the sterol Δ(14) reductase domain of LBR plays a critical role in cholesterol biosynthesis and that this process is essential to both myeloid cell growth and functional maturation.
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Registered trials
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