ArticleThe Journal of biological chemistry2012
Critical role of filamin-binding LIM protein 1 (FBLP-1)/migfilin in regulation of bone remodeling.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Critical role of AKT protein in myeloma-induced osteoclast formation and osteolysis.The Journal of biological chemistry · 2013Trial
- An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease.iScience · 2026Article
- The vinculin-β-catenin axis promotes bone formation and repair: an essential prerequisite for the anti-osteoporotic efficacy of sclerostin-neutralizing antibody.Science China. Life sciences · 2026Article
- Longitudinal transcriptomic and epigenetic analysis of the blood in two astronauts.Scientific reports · 2025Article
- Spatiotemporal proteomic and transcriptomic landscape of DAT+ dopaminergic neurons development and function.iScience · 2025Article
- Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8.The Journal of cell biology · 2024Article
- The bone-liver interaction modulates immune and hematopoietic function through Pinch-Cxcl12-Mbl2 pathway.Cell death and differentiation · 2024Article
- Current and future advances in practice: SAPHO syndrome and chronic non-bacterial osteitis (CNO).Rheumatology advances in practice · 2024Review
- Chronic Nonbacterial Osteomyelitis and Inflammatory Bowel Disease: A Literature Review-Based Cohort.Children (Basel, Switzerland) · 2023Review
- Pediatric autoinflammatory bone disorders-a mini review with special focus on pathogenesis and inborn errors of immunity.Frontiers in pediatrics · 2023Review
- Migfilin: Cell Adhesion Effect and Comorbidities.OncoTargets and therapy · 2022Review
- Identification of adhesion-associated DNA methylation patterns in the peripheral nervous system.Experimental and therapeutic medicine · 2021Article
- Chronic nonbacterial osteomyelitis (CNO) and chronic recurrent multifocal osteomyelitis (CRMO).Journal of translational autoimmunity · 2021Review
- Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice.Signal transduction and targeted therapy · 2020Article
- High prevalence of rare FBLIM1 gene variants in an Italian cohort of patients with Chronic Non-bacterial Osteomyelitis (CNO).Pediatric rheumatology online journal · 2020Article
- Chronic non-bacterial osteomyelitis and autoinflammatory bone diseases.Clinical immunology (Orlando, Fla.) · 2020Review
- Genetic variants in FBLIM1 gene do not contribute to SAPHO syndrome and chronic recurrent multifocal osteomyelitis in typical patient groups.BMC medical genetics · 2020Article
- Knee loading repairs osteoporotic osteoarthritis by relieving abnormal remodeling of subchondral bone via Wnt/β-catenin signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Conditional ablation of MAPK7 expression in chondrocytes impairs endochondral bone formation in limbs and adaptation of chondrocytes to hypoxia.Cell & bioscience · 2020Article
- LIM domain proteins Pinch1/2 regulate chondrogenesis and bone mass in mice.Bone research · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Bone remodeling is a complex process that must be precisely controlled to maintain a healthy life. We show here that filamin-binding LIM protein 1 (FBLP-1, also known as migfilin), a kindlin- and filamin-binding focal adhesion protein, is essential for proper control of bone remodeling. Genetic inactivation of FBLIM1 (the gene encoding FBLP-1) in mice resulted in a severe osteopenic phenotype. Primary FBLP-1 null bone marrow stromal cells (BMSCs) exhibited significantly reduced extracellular matrix adhesion and migration compared with wild type BMSCs. Loss of FBLP-1 significantly impaired the growth and survival of BMSCs in vitro and decreased the number of osteoblast (OB) progenitors in bone marrow and OB differentiation in vivo. Furthermore, the loss of FBLP-1 caused a dramatic increase of osteoclast (OCL) differentiation in vivo. The level of receptor activator of nuclear factor κB ligand (RANKL), a key regulator of OCL differentiation, was markedly increased in FBLP-1 null BMSCs. The capacity of FBLP-1 null bone marrow monocytes (BMMs) to differentiate into multinucleated OCLs in response to exogenously supplied RANKL, however, was not different from that of WT BMMs. Finally, we show that a loss of FBLP-1 promotes activating phosphorylation of ERK1/2. Inhibition of ERK1/2 activation substantially suppressed the increase of RANKL induced by the loss of FBLP-1. Our results identify FBLP-1 as a key regulator of bone homeostasis and suggest that FBLP-1 functions in this process through modulating both the intrinsic properties of OB/BMSCs (i.e., BMSC-extracellular matrix adhesion and migration, cell growth, survival, and differentiation) and the communication between OB/BMSCs and BMMs (i.e., RANKL expression) that controls osteoclastogenesis.
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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.