ArticleHuman molecular genetics2014
Formin 1 and filamin B physically interact to coordinate chondrocyte proliferation and differentiation in the growth plate.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Genetic Analysis in Fetal Skeletal Dysplasias by Trio Whole-Exome Sequencing.BioMed research international · 2019Trial
- Global transcriptional changes across multiple isogeniciScience · 2026Article
- FLNB and TTC26 regulate ciliary Hedgehog signaling to maintain intervertebral disc matrix homeostasis in adolescent idiopathic scoliosis.Genome biology · 2026Article
- LncRNA CISTR-ACT regulates cell size in human and mouse by guiding FOSL2.Nature communications · 2025Article
- MTMR7 regulates human spermatogonial stem cells proliferation and migration via targeting FLNB.PloS one · 2025Article
- Article
- Disruption ofBone reports · 2024Article
- Transcriptional profiling of human cartilage endplate cells identifies novel genes and cell clusters underlying degenerated and non-degenerated phenotypes.Arthritis research & therapy · 2024Article
- Characterization of Expression and Function of the Formins FHOD1, INF2, and DAAM1 in HER2-Positive Breast Cancer.Journal of breast cancer · 2023Article
- A Stop-gain Variant c.220C>T (p.(Gln74*)) inThe Yale journal of biology and medicine · 2023Review
- Ultra-Rare Variants Identify Biological Pathways and Candidate Genes in the Pathobiology of Non-Syndromic Cleft Palate Only.Biomolecules · 2023Article
- Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.PLoS biology · 2022Article
- Cell-Dependent Pathogenic Roles of Filamin B in Different Skeletal Malformations.Oxidative medicine and cellular longevity · 2022Article
- Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function.International journal of molecular sciences · 2021Review
- Placental Epigenome-Wide Association Study Identified Loci Associated with Childhood Adiposity at 3 Years of Age.International journal of molecular sciences · 2020Article
- Exome sequencing analysis identifies frequent oligogenic involvement andJournal of medical genetics · 2020Article
- Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells.Oncology reports · 2020Article
- Non-syndromic Cleft Palate: An Overview on Human Genetic and Environmental Risk Factors.Frontiers in cell and developmental biology · 2020Review
- Comparative analysis of the two extremes ofAmerican journal of translational research · 2018Article
- Opposing FlnA and FlnB interactions regulate RhoA activation in guiding dynamic actin stress fiber formation and cell spreading.Human molecular genetics · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Filamin B (FlnB) is an actin-binding protein thought to transduce signals from various membrane receptors and intracellular proteins onto the actin cytoskeleton. Formin1 (Fmn1) is an actin-nucleating protein, implicated in actin assembly and intracellular signaling. Human mutations in FLNB cause several skeletal disorders associated with dwarfism and early bone fusion. Mouse mutations in Fmn1 cause aberrant fusion of carpal digits. We report here that FlnB and Fmn1 physically interact, are co-expressed in chondrocytes in the growth plate and share overlapping expression in the cell cytoplasm and nucleus. Loss of FlnB leads to a dramatic decrease in Fmn1 expression at the hypertrophic-to-ossification border. Loss of Fmn1-FlnB in mice leads to a more severe reduction in body size, weight and growth plate length, than observed in mice following knockout of either gene alone. Shortening of the long bone is associated with a decrease in chondrocyte proliferation and an overall delay in ossification in the double-knockout mice. In contrast to FlnB null, Fmn1 loss results in a decrease in the width of the prehypertrophic zone. Loss of both proteins, however, causes an overall decrease in the width of the proliferation zone and an increase in the differentiated hypertrophic zone. The current findings suggest that Fmn1 and FlnB have shared and independent functions. FlnB loss promotes prehypertrophic differentiation whereas Fmn1 leads to a delay. Both proteins, however, regulate chondrocyte proliferation, and FlnB may regulate Fmn1 function at the hypertrophic-to-ossification border, thereby explaining the overall delay in ossification.
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