ArticleProceedings of the National Academy of Sciences of the United States of America2007
Filamin B deficiency in mice results in skeletal malformations and impaired microvascular development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- GWAS for systemic sclerosis identifies multiple risk loci and highlights fibrotic and vasculopathy pathways.Nature communications · 2019Pooled it
- Drak is a potential binding partner of Drosophila Filamin.Biology open · 2026Article
- Patient-informed CRISPR screen identifies FLNB as a congenital heart disease and ciliopathy gene.HGG advances · 2026Article
- Complement Anaphylatoxin C5a-Induced Mouse Lymphatic Functions Modulate Interactions Between Endothelial Cells and T Lymphocytes.Immune network · 2026Article
- Deciphering the Genetic Basis of Congenital Vertebral Malformations Through a Stepwise Diagnostic Approach.International journal of molecular sciences · 2026Article
- Signature of Selection Analysis Reveals Candidate Genes Related to Climate Adaptation and Production Traits in Lao Native Goats.Journal of animal breeding and genetics = Zeitschrift fur Tierzuchtung und Zuchtungsbiologie · 2026Article
- Exploration of candidate genes associated with rare SNVs in pulmonary stenosis using whole-exome sequencing and machine learning.Frontiers in genetics · 2026Article
- Patient-informed CRISPR Screen Identifies FLNB as a Novel Congenital Heart Disease and Ciliopathy Gene.bioRxiv : the preprint server for biology · 2025Article
- Severe Osteoporosis in Larsen Syndrome-A Case Report of Bone Morphology and A Novel Filamin B (FLNB) Variant.Calcified tissue international · 2025Article
- Unveiling the multifaceted role of the FLNC gene: implications for cancer diagnosis and prognosis.European journal of medical research · 2025Article
- Association of placental weight and placental-fetal weight ratio with DNA methylation in placenta.Epigenomics · 2025Article
- NovelJournal of pediatric genetics · 2024Article
- Article
- Cancer EV stimulate endothelial glycolysis to fuel protein synthesis via mTOR and AMPKα activation.Journal of extracellular vesicles · 2024Article
- Filamin protects myofibrils from contractile damage through changes in its mechanosensory region.PLoS genetics · 2024Article
- Filamin B restricts vaccinia virus spread and is targeted by vaccinia virus protein C4.Journal of virology · 2024Article
- Disruption ofBone reports · 2024Article
- Extracellular vesicles produced by irradiated endothelial or Glioblastoma stem cells promote tumor growth and vascularization modulating tumor microenvironment.Cancer cell international · 2024Article
- Transcriptional reprogramming during human osteoclast differentiation identifies regulators of osteoclast activity.Bone research · 2024Article
- An Integrative ATAC-Seq and RNA-Seq Analysis of the Endometrial Tissues of Meishan and Duroc Pigs.International journal of molecular sciences · 2023Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in filamin B (FLNB), a gene encoding a cytoplasmic actin-binding protein, have been found in human skeletal disorders, including boomerang dysplasia, spondylocarpotarsal syndrome, Larsen syndrome, and atelosteogenesis phenotypes I and III. To examine the role of FLNB in vivo, we generated mice with a targeted disruption of Flnb. Fewer than 3% of homozygous embryos reached term, indicating that Flnb is important in embryonic development. Heterozygous mutant mice were indistinguishable from their wild-type siblings. Flnb was ubiquitously expressed; strong expression was found in endothelial cells and chondrocytes. Flnb-deficient fibroblasts exhibited more disorganized formation of actin filaments and reduced ability to migrate compared with wild-type controls. Flnb-deficient embryos exhibited impaired development of the microvasculature and skeletal system. The few Flnb-deficient mice that were born were very small and had severe skeletal malformations, including scoliotic and kyphotic spines, lack of intervertebral discs, fusion of vertebral bodies, and reduced hyaline matrix in extremities, thorax, and vertebrae. These mice died or had to be euthanized before 4 weeks of age. Thus, the phenotypes of Flnb-deficient mice closely resemble those of human skeletal disorders with mutations in FLNB.
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