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Showing FBLIM1 — CAL is a alias.

FBLIM1

Filamin-binding LIM protein 1 · UniProt Q8WUP2

Length
373 aa
Mass
40.7 kDa
Annotated
2026-06-09
38 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FBLIM1 (migfilin) is a focal-adhesion adaptor protein that scaffolds the connection between cell-matrix adhesion sites and the actin cytoskeleton, bridging filamin and the kindlin family to regulate cell shape, adhesion, and migration (PMID:12679033). Its N-terminal region binds all three filamins through a site on IgFLNa21 that overlaps the integrin beta-tail binding site, allowing migfilin to compete with integrin tails, displace filamin, and thereby license talin-mediated integrin activation — a molecular-switch function established by crystallography, NMR, and cell-based activation assays (PMID:18829455, PMID:19074766, PMID:22043318). Its C-terminal LIM domains bind kindlin-1/2 and dictate focal-adhesion localization and dynamics, while the N-terminal filamin interaction drives association with actin-rich stress fibers (PMID:12679033, PMID:24165133). Migfilin additionally recruits VASP via a proline-rich LPPPPP motif to tune actin-dependent migration biphasically (PMID:16531412) and binds Src to relieve its autoinhibition, promoting survival signaling and protecting cells from detachment-induced apoptosis (PMID:19833732). Beyond adhesion, migfilin localizes to cadherin-based cell-cell junctions in association with beta-catenin (PMID:15671069) and drives autophagosome-lysosome fusion by interacting with SNAP29 and Vamp8 to promote assembly of the Stx17-SNAP29-Vamp8 SNARE complex (PMID:39283311). Constitutive knockout mice are developmentally normal but reveal context-specific roles: severe osteopenia with elevated RANKL via ERK1/2 (PMID:22556421), attenuated pressure-overload cardiac hypertrophy with reduced Akt activation (PMID:25852081), and impaired platelet outside-in alphaIIbbeta3 signaling causing bleeding and thrombosis defects (PMID:33131250). A homozygous mutation in the FBLIM1 filamin-binding domain is associated with chronic recurrent multifocal osteomyelitis (CRMO) (PMID:28301468).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2003 High

    Established migfilin as a focal-adhesion adaptor that physically bridges kindlin (Mig-2) and filamin, defining the architecture by which it links adhesions to actin.

    Evidence Co-IP, pulldown, siRNA knockdown and dominant-negative overexpression with fluorescence microscopy in cultured cells

    PMID:12679033

    Open questions at the time
    • Did not resolve the structural basis of either interaction
    • Did not define downstream signaling consequences
  2. 2005 High

    Showed migfilin function extends beyond cell-matrix adhesion to cadherin-based cell-cell junctions, linking it to adherens junction organization.

    Evidence siRNA knockdown, immunoelectron microscopy, detergent fractionation and domain deletion mutants in epithelial/endothelial cells

    PMID:15671069

    Open questions at the time
    • Direct binding partner at junctions (beta-catenin association) not biochemically mapped
    • Functional consequence for tissue integrity in vivo untested
  3. 2006 High

    Identified VASP as a direct migfilin partner and explained migfilin's biphasic control of migration through recruitment of actin-regulatory machinery.

    Evidence Co-IP, site-directed mutagenesis of the LPPPPP motif, siRNA knockdown and migration assays

    PMID:16531412

    Open questions at the time
    • Molecular basis of the biphasic dose-response not resolved
    • In vivo relevance untested
  4. 2008 High

    Resolved the structural basis of migfilin-filamin binding and established the molecular-switch model whereby migfilin competes with integrin tails to enable integrin activation.

    Evidence X-ray crystallography, NMR, competition binding assays and cell-based integrin activation assays

    PMID:18829455 PMID:19074766

    Open questions at the time
    • Cellular conditions triggering the switch not defined
    • Quantitative affinity hierarchy across tissues unknown
  5. 2008 Medium

    Placed migfilin within a kindlin-1/kindlin-2 adhesion module and showed kindlin-1 can act independently of migfilin.

    Evidence Reciprocal Co-IP, confocal microscopy and siRNA knockdown in keratinocytes

    PMID:18528435

    Open questions at the time
    • Single lab, limited mechanistic follow-up
    • Functional consequence of the tripartite complex not defined
  6. 2009 Medium

    Connected migfilin to survival signaling by showing it directly activates Src and protects against detachment-induced apoptosis.

    Evidence Co-IP, pulldown, knockdown/overexpression and apoptosis assays

    PMID:19833732

    Open questions at the time
    • Src activation mechanism mapped biochemically but not structurally
    • In vivo survival role untested
  7. 2011 Medium

    Refined the filamin mechanism by showing migfilin relieves filamin autoinhibition and engages multiple repeats simultaneously, implying mechanical regulation of filamin.

    Evidence NMR spectroscopy and binding assays on filamin repeats 19/21

    PMID:21524097

    Open questions at the time
    • No cellular functional validation of the mechanical-stretch model
    • Single lab
  8. 2011 Medium

    Demonstrated migfilin overcomes filamin-mediated suppression of multiple integrin classes and is required for endothelial spreading and migration.

    Evidence Flow cytometry integrin activation, siRNA knockdown and migration assays in endothelial cells and neutrophils

    PMID:22043318

    Open questions at the time
    • In vivo vascular relevance untested
    • Single lab
  9. 2011 High

    Tested the in vivo necessity of migfilin, revealing functional redundancy during development and homeostasis despite the strong in vitro adhesion phenotypes.

    Evidence Constitutive knockout mouse with adhesion, spreading, integrin activation and wound migration readouts

    PMID:21224394

    Open questions at the time
    • Compensating factors not identified
    • Tissue-stress contexts not probed in this study
  10. 2012 Medium

    Revealed a non-adhesion role in transcriptional/signaling control by showing migfilin promotes GSK-3beta-dependent beta-catenin degradation in cancer cells.

    Evidence Overexpression/knockdown, GSK-3beta and proteasome inhibitors, Co-IP and Western blot in esophageal cancer cells

    PMID:22246236

    Open questions at the time
    • Direct vs scaffold-mediated effect on the destruction complex unresolved
    • In vivo tumor relevance untested
  11. 2012 High

    Uncovered a stress-context bone phenotype, defining migfilin as a regulator of osteoblast/osteoclast balance via ERK1/2-dependent RANKL control.

    Evidence Knockout mouse, primary BMSC assays, RANKL ELISA, ERK inhibitor rescue and histology

    PMID:22556421

    Open questions at the time
    • Link between adhesion function and ERK/RANKL signaling not mechanistically bridged
    • Direct transcriptional control of RANKL not shown
  12. 2013 High

    Mapped kindlin-1/2 binding to migfilin's LIM domains and showed kindlin governs migfilin focal-adhesion recruitment and mobility.

    Evidence Pulldown, FRET, FRAP, kindlin siRNA knockdown and domain deletion mutants

    PMID:24165133

    Open questions at the time
    • Structural basis of LIM-kindlin binding not resolved
    • Regulation of the switch between FA and stress-fiber localization unclear
  13. 2015 Medium

    Identified a Src-kindlin-2-migfilin positive feedback loop regulating migfilin recruitment to focal adhesions.

    Evidence Co-IP, mutagenesis of kindlin-2 Y193, kinase assays and microscopy

    PMID:26037143

    Open questions at the time
    • Physiological trigger of the feedback loop unknown
    • In vivo significance untested
  14. 2015 Medium

    Implicated migfilin in cardiac hypertrophic remodeling, including nuclear translocation and Akt activation under pressure overload.

    Evidence Knockout mouse with transverse aortic constriction, echocardiography, immunofluorescence and Akt phosphorylation Western blot

    PMID:25852081

    Open questions at the time
    • Nuclear function of migfilin not defined
    • Mechanism linking migfilin to Akt unresolved
  15. 2017 Medium

    Provided human genetic and regulatory evidence linking FBLIM1 to chronic recurrent multifocal osteomyelitis.

    Evidence Whole-exome sequencing, microarray in cmo model, enhancer reporter assay in SaOS2 cells

    PMID:28301468

    Open questions at the time
    • Causality of the coding mutation not functionally proven
    • Single study
  16. 2017 Medium

    Extended migfilin function to nervous system development, showing it is required for neocortical neuronal migration and neurite elongation.

    Evidence In utero electroporation gain/loss of function and primary hippocampal neuron culture with siRNA

    PMID:29114925

    Open questions at the time
    • Molecular partners mediating neuronal migration not identified
    • Bidirectional disruption mechanism unexplained
  17. 2020 High

    Defined a specific role in platelet outside-in alphaIIbbeta3 signaling, where migfilin prevents filamin A re-association with beta3.

    Evidence Knockout mouse, tail-bleeding and FeCl3 thrombosis models, aggregation/secretion assays and filamin-binding peptide rescue

    PMID:33131250

    Open questions at the time
    • Spatiotemporal regulation of filamin displacement during signaling not resolved
    • Upstream signal controlling migfilin engagement unknown
  18. 2024 High

    Established a membrane-trafficking role by showing migfilin drives autophagosome-lysosome fusion through SNARE assembly, with consequences for cancer cell growth.

    Evidence Co-IP, siRNA knockdown, autophagy flux assays and SNARE reassembly experiments

    PMID:39283311

    Open questions at the time
    • How an adhesion adaptor is recruited to the autophagic SNARE machinery unclear
    • Relationship to migfilin's adhesion functions undefined
  19. 2025 Medium

    Linked FBLIM1 to liver fibrosis via TGF-beta signaling and revealed WTAP/m6A-dependent stabilization of its mRNA as an upstream regulatory layer.

    Evidence Rat bile-duct-ligation model, in vivo/in vitro knockdown, m6A analysis and histopathology

    PMID:40334627

    Open questions at the time
    • Direct molecular link between FBLIM1 and TGF-beta/Smad components not mapped
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single focal-adhesion adaptor is partitioned between its distinct roles — integrin switch, junctional, transcriptional, autophagic, and tissue-specific signaling functions — and what determines context-specific deployment remains unresolved.
  • No unifying model reconciling adhesion vs autophagy vs nuclear roles
  • Regulatory inputs selecting among partners unknown
  • Structural basis of LIM-kindlin and migfilin-SNARE interactions not solved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005856 cytoskeleton 2 GO:0005634 nucleus 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-109582 Hemostasis 1 R-HSA-9612973 Autophagy 1
Partners
CTNNB1FERMT1FERMT2FLNASNAP29SRCVAMP8VASP
Complex memberships
Stx17-SNAP29-Vamp8 SNARE complexkindlin-migfilin-filamin adhesion module

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 Migfilin localizes to cell-matrix adhesions, associates with actin filaments, and is essential for cell shape modulation. Migfilin interacts with Mig-2 (kindlin/UNC-112 homolog) through its C-terminal domain and with filamin through its N-terminal domain. Mig-2 recruits migfilin to cell-matrix adhesions, while the interaction with filamin mediates migfilin's association with actin filaments. Co-immunoprecipitation, pulldown assays, siRNA knockdown, dominant-negative overexpression, fluorescence microscopy Cell High 12679033
2005 Migfilin localizes to cell-cell junctions in epithelial and endothelial cells in response to cadherin-mediated adhesion, forming detergent-resistant clusters associated with actin bundles. The C-terminal LIM domains mediate localization to cell-cell junctions. siRNA depletion of migfilin compromised adherens junction organization and weakened cell-cell association. Immunoelectron microscopy showed migfilin associates with beta-catenin (not desmosomes) at cell-cell junctions. siRNA knockdown, immunoelectron microscopy, confocal microscopy, detergent fractionation, domain deletion mutants Journal of cell science High 15671069
2006 Migfilin interacts with VASP through the VASP EVH1 domain and a single LPPPPP site (L104) in migfilin's proline-rich domain. Migfilin facilitates VASP localization to cell-matrix adhesions. Both loss and overexpression of migfilin reduce cell migration (biphasic regulation). VASP-binding defective migfilin mutants abolish migfilin-mediated regulation of cell migration. Co-immunoprecipitation, site-directed mutagenesis, siRNA knockdown, migration assay, fluorescence colocalization The Journal of biological chemistry High 16531412
2008 X-ray crystallography and NMR revealed the structural basis of migfilin binding to filamin. The filamin-binding site in migfilin is localized between Pro5 and Pro19, binding to the CD face of IgFLNa21 beta-sandwich. Migfilin binds all three human filamins (FLNa, -b, -c) with preference for IgFLNa21, and also more weakly to IgFLNa19 and IgFLNa22. Migfilin and integrin beta tails compete for the same binding site on IgFLNa21, suggesting migfilin can displace integrin from filamin. X-ray crystallography, NMR spectroscopy, protein-protein interaction assays, competition binding assays The Journal of biological chemistry High 18829455
2008 Migfilin structurally interacts with the same region in filamin where integrin beta cytoplasmic tails bind, and this interaction dissociates filamin from integrin beta tails, thereby promoting talin-integrin interaction and integrin activation. Migfilin thus acts as a molecular switch to disconnect filamin from integrin for regulating integrin activation. Structural studies (NMR/biochemical), competition binding assays, cell-based integrin activation assays The Journal of biological chemistry High 19074766
2008 Kindlin-1 interacts with both kindlin-2 and migfilin; the three proteins co-immunoprecipitate and colocalize at focal adhesions in keratinocytes. Loss of kindlin-1 expression does not affect KIND2 or FBLIM1 gene expression or kindlin-2/migfilin protein localization, indicating kindlin-1 can function independently of kindlin-2 and migfilin. Co-immunoprecipitation, confocal microscopy, siRNA knockdown, immunohistochemistry The Journal of investigative dermatology Medium 18528435
2009 Migfilin directly interacts with Src kinase; the migfilin binding surface overlaps with the inhibitory intramolecular interaction sites in Src, resulting in Src activation upon migfilin binding. Loss of cell-ECM adhesion reduces migfilin levels and induces apoptosis. Migfilin overexpression desensitizes cells to detachment-induced apoptosis; migfilin depletion promotes apoptosis despite cell-ECM adhesion. Co-immunoprecipitation, pulldown assays, siRNA knockdown, overexpression, apoptosis assays The Journal of biological chemistry Medium 19833732
2011 NMR spectroscopy showed that filamin autoinhibition of repeats 19 and 21 can be relieved by migfilin (or integrin), and repeats 19 and 21 can simultaneously engage ligands, suggesting migfilin mechanically stretches filamin via multisite binding to regulate cytoskeleton and integrin-mediated cell adhesion. NMR spectroscopy, binding assays Biochemistry Medium 21524097
2011 Flow cytometry demonstrated that filamin inhibits β1 and αIIbβ3 integrin activation, and migfilin can overcome this inhibitory effect. Migfilin can activate β1, β2, and β3 integrins in endothelial cells and neutrophils. Migfilin depletion impairs spreading and migration of endothelial cells. Flow cytometry, siRNA knockdown, cell spreading and migration assays PloS one Medium 22043318
2011 In migfilin-null mice generated by genetic inactivation, development and postnatal aging were normal. Fibroblasts and keratinocytes from migfilin-null mice displayed normal spreading, adhesion, integrin expression, and integrin activation. Migration velocity of null embryonic fibroblasts was normal, but migfilin-null keratinocyte migration was slightly reduced in wound scratch assays. This indicates migfilin roles are functionally redundant during mouse development and tissue homeostasis. Genetic knockout mouse, cell spreading/adhesion assays, flow cytometry for integrin activation, wound scratch migration assay Journal of cell science High 21224394
2012 Genetic inactivation of FBLIM1 in mice caused severe osteopenic phenotype. FBLP-1 null bone marrow stromal cells (BMSCs) showed reduced ECM adhesion and migration. Loss of FBLP-1 impaired BMSC growth and survival, decreased osteoblast progenitor numbers and differentiation, and dramatically increased osteoclast differentiation in vivo. RANKL levels were markedly elevated in FBLP-1 null BMSCs. Loss of FBLP-1 promoted activating phosphorylation of ERK1/2, and ERK1/2 inhibition suppressed the increase of RANKL. FBLP-1 null bone marrow monocytes differentiated normally into osteoclasts when provided exogenous RANKL. Genetic knockout mouse, primary cell culture, cell adhesion/migration assays, RANKL ELISA, ERK inhibitor treatment, histology The Journal of biological chemistry High 22556421
2012 Migfilin promotes GSK-3β-mediated degradation of β-catenin in esophageal cancer cells. Overexpression of migfilin reduced free β-catenin levels and transcriptional activity; this was reversed by siRNA knockdown of migfilin, a Ser37 phosphorylation-deficient β-catenin mutant, GSK-3β inhibitor (LiCl), or proteasome inhibitor (MG132). Migfilin reinforced the association between β-catenin and GSK-3β. Overexpression, siRNA knockdown, GSK-3β inhibitor, proteasome inhibitor, co-immunoprecipitation, Western blot Molecular cancer research : MCR Medium 22246236
2013 Kindlin-1 and kindlin-2 interact with the C-terminal LIM domains of migfilin in vitro and in cells. The C-terminal LIM domains of migfilin dictate FA localization; deletion of this region reveals the N-terminal filamin-binding region drives localization to actin-rich stress fibers. Kindlin knockdown disrupts normal migfilin dynamics (FA recruitment and mobility) as shown by FRAP and FRET assays. Pulldown assays, fluorescence microscopy, FRET, FRAP, kindlin siRNA knockdown, domain deletion mutants The Journal of biological chemistry High 24165133
2015 Kindlin-2 phosphorylation by Src at Y193 is involved in Migfilin binding to kindlin-2 and recruitment of Migfilin to focal adhesions. Src phosphorylates kindlin-2 at Y193; reciprocally, this phosphorylation activates and maintains Src kinase activity, forming a positive feedback loop involving Src, kindlin-2, and migfilin. Co-immunoprecipitation, site-directed mutagenesis, kinase assays, Western blot for phosphorylation, fluorescence microscopy FEBS letters Medium 26037143
2015 In a migfilin knockout mouse subjected to transverse aortic constriction (TAC), migfilin-null hearts showed reduced extent of hypertrophic remodeling and maintained cardiac function longer than WT mice. Migfilin translocated into the nucleus of TAC-treated cardiomyocytes. Migfilin KO hearts showed reduced Akt activation during early response to pressure overload. Knockout mouse model, transverse aortic constriction, echocardiography, immunofluorescence for nuclear translocation, Western blot for Akt phosphorylation Cardiovascular research Medium 25852081
2017 A homozygous mutation in the filamin-binding domain of FBLIM1 was identified in a CRMO patient. Microarray analysis showed the Fblim1 ortholog is the most differentially expressed gene (downregulated >20-fold) in bone marrow macrophages from the cmo murine CRMO model. An enhancer element flanking FBLIM1 was identified; a regulatory variant in a second proband ablates this enhancer activity in SaOS2 cells. Whole-exome sequencing, microarray gene expression, enhancer reporter assay in SaOS2 cells, Sanger sequencing PloS one Medium 28301468
2017 Either silencing or overexpression of migfilin in mouse embryos (in utero electroporation) disrupted neocortical neuronal migration. Migfilin silencing in cultured hippocampal neurons impaired neurite elongation. Migfilin was detected specifically in embryonic and perinatal stages of mouse brain. In utero electroporation (gain/loss of function), primary hippocampal neuron culture with siRNA, immunohistochemistry Journal of neuroscience research Medium 29114925
2020 Migfilin-knockout mice showed approximately doubled tail-bleeding time and prolonged FeCl3-induced thrombosis occlusion time. Migfilin deficiency impaired platelet thrombus formation on collagen, platelet aggregation, and dense-granule secretion. Functional defects were associated with compromised outside-in αIIbβ3 signaling (not inside-out signaling). A cell-permeable migfilin peptide harboring the filamin A binding sequence rescued defective function. In resting platelets migfilin does not influence filamin A–β3 binding, but migfilin hampers re-association of filamin A with β3 during outside-in signaling. Migfilin-knockout mouse, tail-bleeding assay, FeCl3 thrombosis model, platelet aggregation assay, phosphorylation analysis of signaling molecules, cell-permeable peptide rescue Haematologica High 33131250
2024 Migfilin promotes autophagosome-lysosome fusion by directly interacting with SNAP29 and Vamp8, facilitating assembly of the Stx17-SNAP29-Vamp8 SNARE complex. Depletion of migfilin disrupts SNAP29-mediated SNARE complex formation, blocking autophagosome-lysosome fusion and suppressing autophagic flux, ultimately inhibiting cancer cell growth. Restoration of SNARE complex formation rescued migfilin-deficiency-induced autophagic flux defects. Co-immunoprecipitation, siRNA knockdown, autophagy flux assays, SNARE complex reconstitution/reassembly experiments, cell proliferation assays The Journal of cell biology High 39283311
2025 FBLIM1 promotes liver fibrosis in bile duct ligation rats via the TGF-β signaling pathway. FBLIM1 knockdown attenuated liver fibrosis and blocked TGF-β signaling. FBLIM1 mRNA is stabilized by WTAP in an m6A-dependent manner, regulating FBLIM1 expression. In TGF-β1-stimulated hepatic stellate cells, FBLIM1 promoted cell activation and fibrosis through TGF-β signaling. Rat BDL model, siRNA knockdown in vivo and in vitro, Western blot, histopathology, m6A modification analysis International immunopharmacology Medium 40334627

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Migfilin and Mig-2 link focal adhesions to filamin and the actin cytoskeleton and function in cell shape modulation. Cell 312 12679033
2008 Structural basis of the migfilin-filamin interaction and competition with integrin beta tails. The Journal of biological chemistry 97 18829455
2008 Migfilin, a molecular switch in regulation of integrin activation. The Journal of biological chemistry 94 19074766
2008 Colocalization of kindlin-1, kindlin-2, and migfilin at keratinocyte focal adhesion and relevance to the pathophysiology of Kindler syndrome. The Journal of investigative dermatology 67 18528435
2017 Recessive coding and regulatory mutations in FBLIM1 underlie the pathogenesis of chronic recurrent multifocal osteomyelitis (CRMO). PloS one 63 28301468
2005 Migfilin and its binding partners: from cell biology to human diseases. Journal of cell science 63 15701922
2011 Migfilin and filamin as regulators of integrin activation in endothelial cells and neutrophils. PloS one 59 22043318
2006 Migfilin interacts with vasodilator-stimulated phosphoprotein (VASP) and regulates VASP localization to cell-matrix adhesions and migration. The Journal of biological chemistry 54 16531412
2012 Critical role of filamin-binding LIM protein 1 (FBLP-1)/migfilin in regulation of bone remodeling. The Journal of biological chemistry 50 22556421
2005 Physical and functional association of migfilin with cell-cell adhesions. Journal of cell science 40 15671069
2011 Loss of migfilin expression has no overt consequences on murine development and homeostasis. Journal of cell science 32 21224394
2009 Migfilin interacts with Src and contributes to cell-matrix adhesion-mediated survival signaling. The Journal of biological chemistry 32 19833732
2012 Migfilin protein promotes migration and invasion in human glioma through epidermal growth factor receptor-mediated phospholipase C-γ and STAT3 protein signaling pathways. The Journal of biological chemistry 31 22843679
2017 Vasodilator-Stimulated Phosphoprotein (VASP) depletion from breast cancer MDA-MB-231 cells inhibits tumor spheroid invasion through downregulation of Migfilin, β-catenin and urokinase-plasminogen activator (uPA). Experimental cell research 28 28209486
2012 Migfilin regulates esophageal cancer cell motility through promoting GSK-3β-mediated degradation of β-catenin. Molecular cancer research : MCR 26 22246236
2011 Evidence for multisite ligand binding and stretching of filamin by integrin and migfilin. Biochemistry 24 21524097
2015 Kindlin-2 phosphorylation by Src at Y193 enhances Src activity and is involved in Migfilin recruitment to the focal adhesions. FEBS letters 22 26037143
2007 Increased cytoplasmic level of migfilin is associated with higher grades of human leiomyosarcoma. Histopathology 22 17711449
2013 Kindlin binds migfilin tandem LIM domains and regulates migfilin focal adhesion localization and recruitment dynamics. The Journal of biological chemistry 19 24165133
2020 Genetic variants in FBLIM1 gene do not contribute to SAPHO syndrome and chronic recurrent multifocal osteomyelitis in typical patient groups. BMC medical genetics 16 32397996
2015 Experimental evidence of Migfilin as a new therapeutic target of hepatocellular carcinoma metastasis. Experimental cell research 16 25773778
2018 FBLIM1 enhances oral cancer malignancy via modulation of the epidermal growth factor receptor pathway. Molecular carcinogenesis 15 30129678
2020 High prevalence of rare FBLIM1 gene variants in an Italian cohort of patients with Chronic Non-bacterial Osteomyelitis (CNO). Pediatric rheumatology online journal 11 32650789
2013 Mitogen-inducible Gene-2 (MIG2) and migfilin expression is reduced in samples of human breast cancer. Anticancer research 11 23645746
2020 Migfilin supports hemostasis and thrombosis through regulating platelet αIIbβ3 outside-in signaling. Haematologica 10 33131250
2017 Migfilin promotes migration and invasion in glioma by driving EGFR and MMP-2 signalings: A positive feedback loop regulation. Journal of genetics and genomics = Yi chuan xue bao 10 29203120
2014 Expression of migfilin is increased in esophageal cancer and represses the Akt-β-catenin activation. American journal of cancer research 9 24959381
2012 Migfilin's elimination from osteoarthritic chondrocytes further promotes the osteoarthritic phenotype via β-catenin upregulation. Biochemical and biophysical research communications 9 23237804
2012 Migfilin sensitizes cisplatin-induced apoptosis in human glioma cells in vitro. Acta pharmacologica Sinica 8 22983390
2017 Possible involvement of a cell adhesion molecule, Migfilin, in brain development and pathogenesis of autism spectrum disorders. Journal of neuroscience research 7 29114925
2015 In vivo cardiac role of migfilin during experimental pressure overload. Cardiovascular research 7 25852081
2012 Migfilin, α-parvin and β-parvin are differentially expressed in ovarian serous carcinoma effusions, primary tumors and solid metastases. Gynecologic oncology 7 23099104
2024 Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8. The Journal of cell biology 4 39283311
2025 FBLIM1 drives bile duct ligation-induced liver fibrosis by regulating the TGF-β signaling pathway through WTAP-mediated m6A modification. International immunopharmacology 2 40334627
2026 Ligustilide Alleviates Renal Fibrosis Through Fblim1-Dependent Inhibition of the TGF-β1/Smad3 Signaling Pathway. Phytotherapy research : PTR 1 41839487
2022 Migfilin: Cell Adhesion Effect and Comorbidities. OncoTargets and therapy 1 35469339
2026 Curdione alleviates renal fibrosis through Fblim1-dependent inhibition of the TGF-β1/Smad3 signaling pathway. The Journal of nutritional biochemistry 0 41771455
2008 [Cloning of human migfilin N-terminal domain and preparation of anti-migfilin polyclonal antibody]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 18583227

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