ArticleHuman molecular genetics2008
The lamin B receptor under transcriptional control of C/EBPepsilon is required for morphological but not functional maturation of neutrophils.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Shaping neutrophil morphology and function: the importance of a segmented nucleus.Nature reviews. Immunology · 2026Review
- Nucleoskeletal Proteins in Early Embryogenesis.Advances in experimental medicine and biology · 2026Review
- A Family ofMolecular syndromology · 2025Article
- SHMT2 is essential for mammalian preimplantation embryonic development throughMolecular therapy. Nucleic acids · 2025Article
- Chromatin phase separation and nuclear shape fluctuations are correlated in a polymer model of the nucleus.Nucleus (Austin, Tex.) · 2024Article
- Autosomal recessive hyposegmentation of granulocytes in Australian Shepherd Dogs indicates a role for LMBR1L in myeloid leukocytes.PLoS genetics · 2023Article
- The circadian neutrophil, inside-out.Journal of leukocyte biology · 2023Review
- Molecular Pathology of Laminopathies.Annual review of pathology · 2022Review
- Deletion of LBR N-terminal domains recapitulates Pelger-Huet anomaly phenotypes in mouse without disrupting X chromosome inactivation.Communications biology · 2021Article
- Article
- Progress toward understanding chromosome silencing by Xist RNA.Genes & development · 2020Review
- Twin enzymes, divergent control: The cholesterogenic enzymes DHCR14 and LBR are differentially regulated transcriptionally and post-translationally.The Journal of biological chemistry · 2020Article
- The B-side ofF1000Research · 2020Review
- Xist RNA in action: Past, present, and future.PLoS genetics · 2019Review
- Systematic allelic analysis defines the interplay of key pathways in X chromosome inactivation.Nature communications · 2019Article
- A novel case of Greenberg dysplasia and genotype-phenotype correlation analysis for LBR pathogenic variants: An instructive example of one gene-multiple phenotypes.American journal of medical genetics. Part A · 2019Article
- Article
- Development of an efficient screening system to identify novel bone metabolism-related genes using the exchangeable gene trap mutagenesis mouse models.Scientific reports · 2017Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
The lamin B receptor (LBR) is an integral nuclear envelope protein that interacts with chromatin and has homology to sterol reductases. Mutations in LBR result in Pelger-Huët anomaly and HEM-Greenberg skeletal dysplasia, whereas in mice Lbr mutations result in ichthyosis. To further understand the function of the LBR and its role in disease, we derived a novel mouse model with a gene-trap insertion into the Lbr locus (Lbr(GT/GT)). Phenotypically, the Lbr(GT/GT) mice are similar to ichthyosis mice. The Lbr(GT/GT) granulocytes lack a mature segmented nucleus and have a block in late maturation. Despite these changes in nuclear morphology, the innate granulocyte immune function in the killing of Staphylococcus aureus bacteria appears to be intact. Granulocyte differentiation requires the transcription factor C/EBPepsilon. We identified C/EBPepsilon binding sites within the Lbr promoter and used EMSAs and luciferase assays to show that Lbr is transcriptionally regulated by C/EBPepsilon. Our findings indicate that the Lbr(GT/GT) mice are a model for Pelger-Huët anomaly and that Lbr, under transcriptional regulation of C/EBPepsilon, is necessary for morphological but not necessarily functional granulocyte maturation.
Indexed as
Identifiers
What OpenQuestion holds
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.