Affinage

FSTL3

Follistatin-related protein 3 · UniProt O95633

Length
263 aa
Mass
27.7 kDa
Annotated
2026-06-09
48 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FSTL3 is a secreted follistatin-family glycoprotein that functions as an extracellular antagonist of TGF-β superfamily ligands, principally activin A, restraining activin/Smad signaling across reproductive and metabolic tissues (PMID:9671416, PMID:11451569, PMID:17671190). It binds activin with affinity and selectivity comparable to follistatin but, unlike follistatin, lacks a heparin-binding sequence and therefore does not associate with cell surfaces, conferring distinct tissue-level bioavailability (PMID:11451569, PMID:15471966). The 2.5 Å crystal structure of the FSTL3–activin A complex shows two FSTL3 molecules encircling the ligand to occlude all receptor-binding sites, with the FSTL3 N-terminal domain making intimate contacts that explain its activin specificity (PMID:18768470). FSTL3 transcription is induced by TGF-β and activin A through Smad3/Smad4 binding to a Smad-binding element in its promoter, and by TNF-α through NF-κB elements, with TGF-β potentiating the TNF-α response—establishing a negative feedback loop that limits activin signaling (PMID:11571638, PMID:11948405, PMID:17395406). In vivo, loss of FSTL3 releases activin and myostatin bioactivity, producing pancreatic islet and beta-cell hyperplasia, increased α-to-β cell transdifferentiation, reduced visceral fat, improved glucose tolerance, and enlarged testes with delayed age-related regression (PMID:17229845, PMID:26727106, PMID:23407452). Beyond ligand sequestration, FSTL3 has an intranuclear role enhancing AF10 oligomerization and AF10-mediated transcription (PMID:17868029), and in cancer it acts through activin-independent routes—stabilizing c-Myc to promote immune evasion (PMID:38302412), binding transferrin receptor TfR1 to activate AKT/mTOR and drive vasculogenic mimicry (PMID:41053124), and modulating the SLC25A10/succinate/DLAT axis to govern cuproptosis susceptibility (PMID:41996175).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1998 Medium

    Identification of FSTL3 from a leukemia-associated chromosomal translocation established it as a novel secreted member of the follistatin family, framing later questions about its ligand-binding function.

    Evidence cDNA cloning and molecular characterization of a t(11;19) translocation in B-cell CLL

    PMID:9671416

    Open questions at the time
    • No ligand or binding partner identified at cloning stage
    • Functional role of the translocation unresolved
  2. 2001 High

    Demonstrating that FSTL3 binds activin and is itself induced by TGF-β/activin via direct Smad3/4 promoter binding defined it as a transcriptionally regulated activin antagonist within a feedback loop.

    Evidence Immunoprecipitation/Far-Western binding assays, promoter reporter with deletion/point mutagenesis, dominant-negative Smad, and EMSA

    PMID:11274757 PMID:11451569 PMID:11571638

    Open questions at the time
    • Quantitative ligand selectivity across activin isoforms not yet resolved
    • Structural basis of antagonism unknown
  3. 2002 High

    Showing FSTL3 blocks activin-induced gene transcription and growth inhibition while being activin-inducible closed the negative feedback loop functionally.

    Evidence Transcriptional reporter and HepG2 growth-inhibition assays with phospho-Smad2 readout

    PMID:11948405

    Open questions at the time
    • In vivo relevance of feedback not yet tested
    • Ligand specificity beyond activin A not addressed
  4. 2003 Medium

    Quantifying differential binding and neutralization of activin A versus activin B established FSTL3 as a ligand-selective antagonist rather than a pan-activin sink.

    Evidence Binding assays and 293-cell neutralization reporter assays

    PMID:12697670

    Open questions at the time
    • Structural basis of isoform discrimination not defined
    • Selectivity against other TGF-β ligands untested here
  5. 2004 High

    Mapping the absence of a heparin-binding sequence and the trade-off between heparin and activin binding explained why FSTL3, unlike follistatin, does not bind cell surfaces, distinguishing their bioavailability.

    Evidence Domain-insertion mutagenesis with heparin affinity, cell-surface binding, activin binding, and pituitary FSH bioassay

    PMID:15471966

    Open questions at the time
    • Physiological consequence of non-surface localization not directly tested
    • Whether soluble distribution alters tissue targeting unmeasured
  6. 2005 Medium

    Discovery of direct interactions with fibronectin and ADAM12, with functional effects on hematopoietic adhesion and osteoclast differentiation, extended FSTL3's roles beyond soluble ligand antagonism into matrix and cellular contexts.

    Evidence Yeast two-hybrid, co-IP/pulldown, cell adhesion assays, and osteoclast differentiation assays

    PMID:15574124 PMID:16336961

    Open questions at the time
    • Mechanistic link between these interactions and activin biology unclear
    • Single-lab interactions without reciprocal in vivo validation
  7. 2007 Medium

    Showing TNF-α drives FSTL3 transcription via NF-κB, with TGF-β/Smad potentiation, integrated inflammatory signaling into the control of FSTL3 expression.

    Evidence Promoter deletion/reporter analysis, phylogenetic footprinting, and NF-κB binding assays

    PMID:17395406

    Open questions at the time
    • Physiological context of TNF-α induction not established
    • Cross-talk between NF-κB and Smad inputs in vivo untested
  8. 2007 High

    Knockout mice and breast cancer knockdown placed FSTL3 antagonism of activin/myostatin causally upstream of beta-cell mass, glucose homeostasis, visceral fat, and tumor proliferation.

    Evidence Homozygous FSTL3 knockout metabolic phenotyping and siRNA silencing with activin-receptor rescue in breast cancer cells

    PMID:17229845 PMID:17671190

    Open questions at the time
    • Tissue-specific contributions not dissected
    • Distinguishing activin- versus myostatin-driven phenotypes incomplete
  9. 2007 Medium

    Identifying nuclear FSTL3 interaction with AF10 and enhancement of its transcriptional activity revealed an intranuclear function distinct from secreted ligand antagonism.

    Evidence Yeast two-hybrid, Far-Western, co-IP in COS-7, oligomerization, and Gal4 transactivation assays

    PMID:17868029

    Open questions at the time
    • Mechanism of nuclear entry for a secreted protein unexplained
    • Endogenous chromatin targets of FSTL3/AF10 unknown
  10. 2008 High

    The crystal structure of the FSTL3–activin A complex defined the molecular mechanism of antagonism—two FSTL3 molecules encircling the ligand to block all receptor sites—and the N-terminal domain basis of specificity.

    Evidence 2.5 Å X-ray crystallography with domain-swap binding studies

    PMID:18768470

    Open questions at the time
    • Structures with other ligands (activin B, myostatin) not solved
    • Conformational dynamics in solution not addressed
  11. 2016 High

    Lineage tracing showing increased α-to-β cell transdifferentiation in knockouts, reproduced by activin treatment, identified a cell-fate mechanism underlying FSTL3's control of beta-cell mass.

    Evidence Gluc-Cre/YFP lineage tracing, flow cytometry, and activin treatment of isolated islets

    PMID:26727106

    Open questions at the time
    • Human relevance of transdifferentiation not established
    • Downstream beta-cell maturation program undefined
  12. 2013 Medium

    Testicular enlargement and delayed aging in knockouts, with elevated AKT/SIRT1 signaling, linked FSTL3 ligand antagonism to AKT pathway cross-talk in reproductive tissue.

    Evidence FSTL3 knockout histomorphometry and western blot for AKT/SIRT1

    PMID:23407452

    Open questions at the time
    • Direct mechanistic connection between activin release and AKT activation unproven
    • Single-model finding
  13. 2021 Medium

    Discovery that FSTL3 stabilizes c-Myc by suppressing its ubiquitination to upregulate PDL1/IDO1, plus a selective neutralizing antibody enhancing islet insulin secretion, revealed activin-independent oncogenic activity and therapeutic targetability.

    Evidence Co-IP with domain mapping, ubiquitination assays, FSTL3-knockout immunocompetent tumor models, and FP-101 neutralizing antibody islet assays

    PMID:33539535 PMID:38302412

    Open questions at the time
    • How secreted FSTL3 accesses cytoplasmic/nuclear c-Myc unresolved
    • Antibody efficacy in vivo for diabetes not yet established
  14. 2024 Medium

    Mapping KDM1B-driven H3K9me2 loss at the FSTL3 promoter under prenatal dexamethasone defined an epigenetic route to FSTL3 upregulation that impairs blood-testis barrier function via reduced TGF-β signaling.

    Evidence ChIP for H3K9me2, dexamethasone treatment of Sertoli cells, and in vivo rat model

    PMID:38472317

    Open questions at the time
    • Generalizability beyond dexamethasone exposure unknown
    • Human translation untested
  15. 2025 Medium

    Multiple cancer studies established new activin-independent FSTL3 axes—TfR1/AKT/mTOR-driven vasculogenic mimicry, SLC25A10/succinate/DLAT-controlled cuproptosis, and ZNF454-repressed HIF-1α glycolysis—broadening its role in tumor metabolism and metastasis.

    Evidence Co-IP/binding assays, scRNA-seq, CRISPR screens, metabolomics/succinylation assays, ChIP/luciferase, and in vivo metastasis/xenograft models with antibody neutralization

    PMID:41053124 PMID:41522747 PMID:41996175

    Open questions at the time
    • Whether these axes operate through the same secreted FSTL3 pool is unclear
    • Interplay between activin-dependent and activin-independent functions undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a secreted activin antagonist accesses intracellular and nuclear targets (c-Myc, AF10) and whether its diverse cancer-associated metabolic and signaling functions share a unifying mechanism.
  • No mechanism for cellular re-entry or nuclear localization of secreted FSTL3
  • Integration of activin-dependent and activin-independent roles not established
  • Structural basis of TfR1 and c-Myc binding undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0140313 molecular sequestering activity 2 GO:0140110 transcription regulator activity 1
Localization
GO:0005576 extracellular region 3 GO:0005634 nucleus 1 GO:0031012 extracellular matrix 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-1430728 Metabolism 2
Partners
ADAM12AF10FN1INHBAMYCSLC25A10TFRC

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 FSTL3 (FLRG) encodes a secreted glycoprotein belonging to the follistatin-module-protein family, identified from a chromosomal translocation t(11;19)(q13;p13) in B-cell chronic lymphocytic leukemia, establishing it as a novel secreted protein of the follistatin family. cDNA cloning and molecular characterization of chromosomal translocation Oncogene Medium 9671416
2001 FSTL3 (FLRG) binds activin A, as demonstrated by immunoprecipitation and Far-Western blot analysis, and its expression in bone marrow stromal cells is dramatically upregulated by TGF-β at both mRNA and protein levels. Immunoprecipitation, Far-Western blot, RT-PCR, Northern blot Experimental hematology Medium 11274757
2001 FSTL3 (FSRP) binds activin with similar affinity and selectivity as follistatin but does not bind heparin. FSTL3 inhibits activin-mediated gene transcription in heterologous assays but is much less active than follistatin in the rat pituitary bioassay. Overexpression in transgenic mice disrupts follicular development and fertility in females. Binding assays, transcriptional reporter assay, pituitary bioassay, transgenic mouse overexpression Molecular and cellular endocrinology Medium 11451569
2001 TGF-β induces FSTL3 (FLRG) transcription through Smad proteins binding to a Smad-binding element in the FLRG promoter. Dominant-negative Smad3 and Smad4 mutants block TGF-β-induced transactivation. Smad3 and Smad4 proteins directly bind the SBE motif in the FLRG promoter as shown by EMSA. Promoter reporter assay, deletion/point-mutation analysis, dominant-negative Smad transfection, EMSA (gel shift) Oncogene High 11571638
2002 FSTL3 (FLRG) protein inhibits activin A signaling in transcriptional reporter assays and blocks activin A-induced growth inhibition of HepG2 cells. Activin A induces FSTL3 and follistatin expression via Smad proteins, and FSTL3 protein in turn regulates its own activin-induced expression, constituting a negative feedback loop. Transcriptional reporter assay, cell growth assay, phospho-Smad2 analysis, Smad transfection Oncogene High 11948405
2003 FSTL3 binds activin B approximately 10-fold less potently than activin A, and is approximately 3-fold more effective in neutralizing activin A relative to activin B in reporter assays, demonstrating differential binding and neutralization specificity. Binding assays, 293 cell reporter assays for neutralization Endocrinology Medium 12697670
2004 FSTL3 lacks a heparin-binding sequence and cannot associate with cell surfaces or heparin, unlike follistatin. Insertion of the full follistatin domain 1 (containing the HBS) into FSTL3 conferred heparin binding but abolished activin binding, implying an evolutionary safeguard against surface binding by FSTL3. Mutational analysis, cell surface binding assay, heparin affinity binding, competitive activin binding, pituitary cell FSH secretion bioassay Endocrinology High 15471966
2005 FSTL3 (FLRG) physically interacts with human fibronectin; the interaction is mediated by type I motifs of fibronectin and follistatin domains of FSTL3/follistatin. This interaction increases adhesion of hematopoietic cells to fibronectin in a dose-dependent manner, including immature hematopoietic precursors (CFC, LTC-IC). Yeast two-hybrid screen, co-immunoprecipitation/pulldown, cell adhesion assay with primary hematopoietic cells and cell lines Experimental cell research Medium 16336961
2005 FSTL3 (FLRG) directly interacts with ADAM12 via its cysteine-rich domain, as identified by yeast two-hybrid and confirmed by direct interaction assay. FSTL3 protein inhibits osteoclast differentiation from murine primary spleen cells and RAW264.7 macrophages stimulated with RANK-L and M-CSF, reducing osteoclast number and nuclei per osteoclast. Yeast two-hybrid screen, direct protein interaction assay, osteoclast differentiation assay (primary spleen cells and RAW264.7 cells) Biology of the cell Medium 15574124
2007 TNF-α activates FSTL3 (FLRG) transcription through NF-κB binding to four tandem 107-108 bp DNA repeats in the FLRG promoter, each containing an NF-κB responsive element (5'-GGGAGAG/TTCC-3'). TGF-β through Smad proteins potentiates TNF-α-induced FSTL3 expression. Promoter reporter assay, deletion analysis, phylogenetic footprinting, NF-κB binding assay Gene Medium 17395406
2007 FSTL3 knockout adult mice develop increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, attributable to increased activin and myostatin bioactivity in specific tissues in the absence of the FSTL3 antagonist. Homozygous FSTL3 knockout mouse model with metabolic phenotyping (glucose tolerance, insulin sensitivity, histomorphometry) Proceedings of the National Academy of Sciences of the United States of America High 17229845
2007 FSTL3 (FLRG) silencing in breast cancer cell lines restores endogenous activin signaling (increased phospho-Smad2 and activin target gene transcripts), causes growth inhibition reversible by exogenous FSTL3 or soluble type II activin receptor, demonstrating FSTL3 promotes tumor cell proliferation by antagonizing endogenous activin. siRNA silencing, phospho-Smad2 western blot, gene expression analysis, cell growth assay, receptor rescue experiment Cancer research High 17671190
2007 Nuclear FSTL3 (FLRG) interacts with AF10 (MLL fusion partner) via AF10's N-terminal PHD domain. FSTL3 enhances AF10 homo-oligomerization and increases AF10-mediated transcriptional activation in transient transfection assays, revealing an intranuclear transcriptional co-regulatory function. Yeast two-hybrid, Far-Western blot, co-immunoprecipitation in COS-7 cells, oligomerization assay, Gal4-fusion transactivation assay Biology of the cell Medium 17868029
2008 X-ray crystal structure of FSTL3 in complex with activin A (2.5 Å resolution) shows two FSTL3 molecules encircling the ligand and blocking all receptor-binding sites. The FSTL3 N-terminal domain makes more intimate contact with activin A than the corresponding follistatin domain, and replacing the FSTL3 N-terminal domain with the follistatin N-terminal domain considerably lowers activin A affinity, explaining FSTL3's specificity. X-ray crystallography, domain-swap binding studies The Journal of biological chemistry High 18768470
2013 FSTL3 knockout mice develop markedly enlarged testes with increased Sertoli cell numbers and enhanced spermatogenesis, and show delayed age-related testicular regression. FSTL3 deletion leads to increased AKT signaling and SIRT1 expression in the testis, demonstrating cross-talk between TGF-β ligand and AKT signaling pathways. FSTL3 knockout mouse model, histomorphometry, western blot for AKT/SIRT1 signaling Endocrinology Medium 23407452
2016 In FSTL3 knockout mice, α-to-β cell transdifferentiation is increased, as demonstrated by Gluc-Cre/YFP lineage tracing showing significantly more Ins+/YFP+ cells versus wild-type. Activin treatment of isolated islets significantly increased YFP+/Ins+ cells, demonstrating that activin signaling (released from FSTL3 antagonism) drives this transdifferentiation. Gluc-Cre/YFP α-cell lineage tracing, flow cytometry, fluorescent cell counting in pancreatic sections, activin treatment of isolated islets Endocrinology High 26727106
2019 FSTL3 promotes lipid accumulation in macrophages and upregulates scavenger receptors CD36 and LOX-1 in a dose-dependent manner. FSTL3 also induces secretion of inflammatory cytokines (IL-1β, MCP-1, TNF-α, MMP-9) in macrophages. Oxidized LDL induces FSTL3 expression and secretion. Cell treatment assays, western blot for CD36/LOX-1, ELISA for cytokines, lipid accumulation assay, FSTL3 knockdown Journal of cardiovascular pharmacology Medium 31815869
2021 FSTL3 binds to transcription factor c-Myc (at amino acids 354–406), suppresses c-Myc ubiquitination and increases its stability, thereby upregulating PDL1 and IDO1 expression to promote tumor immune evasion in colorectal cancer. FSTL3 expression in CRC cells is induced by hypoxia via HIF1α. Co-immunoprecipitation, ubiquitination assay, western blot, FSTL3 knockout immunocompetent tumor models, flow cytometry for immune cell populations Cell death & disease Medium 38302412
2021 An FSTL3-neutralizing antibody (FP-101) that selectively disrupts FSTL3-activin complexes (without affecting follistatin) enhances glucose-responsive insulin secretion from dysfunctional mouse and human islets in vitro under conditions modeling diabetes. Neutralizing antibody development, in vitro activin-complex disruption assay, insulin secretion assay from mouse and human islets Endocrinology Medium 33539535
2024 Prenatal dexamethasone exposure increases KDM1B expression in fetal testicular Sertoli cells, which decreases H3K9me2 levels at the FSTL3 promoter, thereby epigenetically upregulating FSTL3 expression. Increased FSTL3 inhibits TGF-β signaling and reduces CX43/E-cadherin expression, impairing blood-testis barrier function and sperm quality. ChIP for H3K9me2 at FSTL3 promoter, western blot, dexamethasone treatment of TM4 Sertoli cells, in vivo rat model Acta pharmacologica Sinica Medium 38472317
2025 FSTL3 expressed by cancer-associated fibroblasts binds to transferrin receptor (TfR1) on cancer cells, activating the TfR1/AKT/mTOR pathway and elevating VE-Cadherin to support endothelial-like transformation, vasculogenic mimicry, and metastatic progression in colon cancer. FSTL3-targeting antibodies inhibited vasculogenic mimicry and synergized with bevacizumab. Co-immunoprecipitation/binding assay, single-cell RNA sequencing, in vitro and in vivo functional assays, antibody neutralization Cell death & disease Medium 41053124
2025 FSTL3 loss in OSCC cells induces cuproptosis susceptibility by suppressing SLC25A10, leading to mitochondrial succinate accumulation, succinate-driven succinylation and upregulation of DLAT (essential for cuproptosis execution), thereby suppressing lymph node metastasis. CRISPR-Cas9 screening, knockdown studies, metabolomics for succinate, succinylation assay, in vivo metastasis models Journal of dental research Medium 41996175
2025 ZNF454 binds directly to the FSTL3 promoter (confirmed by ChIP and dual-luciferase assay) and transcriptionally represses FSTL3, which in turn suppresses HIF-1α-mediated glycolysis in colorectal cancer cells under hypoxic conditions. FSTL3 overexpression reverses ZNF454-mediated suppression of proliferation, migration, invasion, and glycolysis. ChIP assay, dual-luciferase reporter assay, RT-qPCR, western blot, metabolic flux assays (ECAR/OCR), in vivo xenograft Journal of gastrointestinal oncology Medium 41522747

Source papers

Stage 0 corpus · 48 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults. Proceedings of the National Academy of Sciences of the United States of America 135 17229845
1998 FLRG (follistatin-related gene), a new target of chromosomal rearrangement in malignant blood disorders. Oncogene 104 9671416
2002 Transcription activation of FLRG and follistatin by activin A, through Smad proteins, participates in a negative feedback loop to modulate activin A function. Oncogene 79 11948405
2003 Differential binding and neutralization of activins A and B by follistatin and follistatin like-3 (FSTL-3/FSRP/FLRG). Endocrinology 63 12697670
2007 Silencing of FLRG, an antagonist of activin, inhibits human breast tumor cell growth. Cancer research 61 17671190
2008 The structure of FSTL3.activin A complex. Differential binding of N-terminal domains influences follistatin-type antagonist specificity. The Journal of biological chemistry 60 18768470
2001 Follistatin-related protein (FSRP): a new member of the follistatin gene family. Molecular and cellular endocrinology 56 11451569
2001 Expression of FLRG, a novel activin A ligand, is regulated by TGF-beta and during hematopoiesis [corrected]. Experimental hematology 41 11274757
2004 Heparin and activin-binding determinants in follistatin and FSTL3. Endocrinology 40 15471966
2009 Differential expression of follistatin and FLRG in human breast proliferative disorders. BMC cancer 39 19740438
2001 FLRG, an activin-binding protein, is a new target of TGFbeta transcription activation through Smad proteins. Oncogene 37 11571638
2020 Up-Regulation of FSTL3, Regulated by lncRNA DSCAM-AS1/miR-122-5p Axis, Promotes Proliferation and Migration of Non-Small Cell Lung Cancer Cells. OncoTargets and therapy 35 32280246
2004 FLRG, member of the follistatin family, a new player in hematopoiesis. Molecular and cellular endocrinology 33 15451575
2013 Follistatin-like 3 (FSTL3) mediated silencing of transforming growth factor β (TGFβ) signaling is essential for testicular aging and regulating testis size. Endocrinology 32 23407452
2017 FSTL3 is increased in renal dysfunction. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 24 28339962
2007 Identification of NF-kappaB responsive elements in follistatin related gene (FLRG) promoter. Gene 24 17395406
2005 FLRG, a new ADAM12-associated protein, modulates osteoclast differentiation. Biology of the cell 22 15574124
2005 A novel role for fibronectin type I domain in the regulation of human hematopoietic cell adhesiveness through binding to follistatin domains of FLRG and follistatin. Experimental cell research 22 16336961
2004 Human endometrium and decidua express follistatin-related gene (FLRG) mRNA and peptide. Molecular and cellular endocrinology 21 15130517
2003 Follistatin-related gene (FLRG) expression in human endometrium: sex steroid hormones regulate the expression of FLRG in cultured human endometrial stromal cells. The Journal of clinical endocrinology and metabolism 19 12970321
2024 FSTL3 promotes tumor immune evasion and attenuates response to anti-PD1 therapy by stabilizing c-Myc in colorectal cancer. Cell death & disease 18 38302412
2019 FSTL3 Induces Lipid Accumulation and Inflammatory Response in Macrophages and Associates With Atherosclerosis. Journal of cardiovascular pharmacology 16 31815869
2016 Activin Enhances α- to β-Cell Transdifferentiation as a Source For β-Cells In Male FSTL3 Knockout Mice. Endocrinology 16 26727106
2002 Regulation of follistatin-related gene (FLRG) expression by protein kinase C and prostaglandin E(2) in cultured granulosa-luteal cells. Molecular human reproduction 15 12397211
2003 Regulation of FLRG expression in rat primary astroglial cells and injured brain tissue by transforming growth factor-beta 1 (TGF-beta 1). Journal of neuroscience research 14 12645077
2022 FSTL3 is highly expressed in adipose tissue of individuals with overweight or obesity and is associated with inflammation. Obesity (Silver Spring, Md.) 13 36502285
2021 Bioinformatic Analyses and Experimental Verification Reveal that High FSTL3 Expression Promotes EMT via Fibronectin-1/α5β1 Interaction in Colorectal Cancer. Frontiers in molecular biosciences 12 34901156
2012 Synexpression group analyses identify new functions of FSTL3, a TGFβ ligand inhibitor. Biochemical and biophysical research communications 12 23022195
2007 AF10-dependent transcription is enhanced by its interaction with FLRG. Biology of the cell 11 17868029
2023 FSTL3 partially mediates the association of increased nonalcoholic fatty liver disease fibrosis risk with acute myocardial infarction in patients with type 2 diabetes mellitus. Cardiovascular diabetology 9 37904173
2021 The Activin/FLRG Pathway Associates with Poor COVID-19 Outcomes in Hospitalized Patients. Molecular and cellular biology 8 34723652
2021 LBX2-AS1 Activates FSTL3 by Binding to Transcription Factor RARα to Foster Proliferation, Migration, and Invasion of Thyroid Cancer. Frontiers in genetics 8 34858481
2021 Inhibition of FSTL3 abates the proliferation and metastasis of renal cell carcinoma via the GSK-3β/β-catenin signaling pathway. Aging 7 34555811
2002 Genomic organization and promoter analysis of mouse follistatin-related gene (FLRG). Molecular and cellular endocrinology 7 12039070
2006 Purification of recombinant activin A using the second follistatin domain of follistatin-related gene (FLRG). Protein expression and purification 6 16737827
2025 Multiomic traits reveal that critical irinotecan-related core regulator FSTL3 promotes CRC progression and affects ferroptosis. Cancer cell international 4 40140870
2021 FSTL3-Neutralizing Antibodies Enhance Glucose-Responsive Insulin Secretion in Dysfunctional Male Mouse and Human Islets. Endocrinology 4 33539535
2018 Uteroglobin and FLRG concentrations in aqueous humor are associated with age in primary open angle glaucoma patients. BMC ophthalmology 4 29482497
2020 Expression and functional analysis of the Follistatin-like 3 (FSTL3) gene in the sheep ovary during the oestrous cycle. Reproduction in domestic animals = Zuchthygiene 3 33314336
2025 FSTL3 promotes colorectal cancer by activating the HIF1 pathway. Gene 2 40154584
2024 Prenatal dexamethasone exposure impairs rat blood-testis barrier function and sperm quality in adult offspring via GR/KDM1B/FSTL3/TGFβ signaling. Acta pharmacologica Sinica 2 38472317
2003 Purification, cDNA cloning, and secretory properties of FLRG protein from PC12 cells and the distribution of FLRG mRNA and protein in rat tissues. Archives of histology and cytology 2 14692692
2025 Cancer-associated fibroblasts expressing FSTL3 promote vasculogenic mimicry formation and drive colon cancer malignancy. Cell death & disease 1 41053124
2023 Stroma-associated FSTL3 is a factor of calcium channel-derived tumor fibrosis. Scientific reports 1 38044354
2026 Cinnamaldehyde Regulates the EMT Process and Drug Resistance of Gastric Cancer Through FSTL3-Mediated Cytoskeletal Remodeling. Phytotherapy research : PTR 0 41871850
2026 FSTL3-Driven Cuproptosis Resistance and EPCs Promote OSCC Metastasis. Journal of dental research 0 41996175
2025 ZNF454-FSTL3 axis inhibits colorectal cancer progression by inhibiting HIF-1α-mediated glycolysis in hypoxia. Journal of gastrointestinal oncology 0 41522747
2019 Gene structure, recombinant expression and function characterization of Siniperca chuatsi Fsrp-3. Journal of fish biology 0 30756375

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