Affinage

FSTL3

Follistatin-related protein 3 · UniProt O95633

Length
263 aa
Mass
27.7 kDa
Annotated
2026-04-28
48 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FSTL3 is a secreted glycoprotein antagonist of TGF-β superfamily ligands that functions as a freely circulating inhibitor of activin A/B and myostatin signaling, forming negative feedback loops that regulate pancreatic β-cell mass, glucose homeostasis, gonadal development, and adiposity. Two FSTL3 molecules encircle one activin A dimer to block all receptor-binding sites, and unlike follistatin, FSTL3 lacks a heparin-binding sequence and therefore cannot associate with cell surfaces, restricting its activity to the extracellular space (PMID:18768470, PMID:15471966). FSTL3 transcription is induced by activin/TGF-β via Smad3/4 and by TNF-α via NF-κB, establishing it as an inducible feedback antagonist; accordingly, FSTL3 knockout mice exhibit β-cell hyperplasia with enhanced α-to-β transdifferentiation, reduced visceral fat, improved insulin sensitivity, and enlarged testes (PMID:11571638, PMID:17395406, PMID:17229845, PMID:26727106, PMID:23407452). In cancer contexts, FSTL3 stabilizes c-Myc by suppressing its ubiquitination under hypoxia-induced HIF1α-driven expression and can activate TfR1/AKT/mTOR signaling on tumor cells when secreted by cancer-associated fibroblasts (PMID:38302412, PMID:41053124).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1998 High

    Identification of FSTL3 as a new member of the follistatin-module family established a candidate TGF-β superfamily modulator, addressing whether additional secreted antagonists existed beyond follistatin.

    Evidence cDNA cloning from t(11;19) translocation in B-CLL

    PMID:9671416

    Open questions at the time
    • No ligand-binding activity demonstrated at this stage
    • Disease relevance of translocation unclear
  2. 2001 High

    Demonstration that FSTL3 directly binds activin A with similar affinity to follistatin but lacks heparin binding established its identity as a soluble-only activin antagonist, resolving its functional relationship to follistatin.

    Evidence Immunoprecipitation, Far-Western blot, binding assays, reporter assays, and rat pituitary bioassay

    PMID:11274757 PMID:11451569

    Open questions at the time
    • Structural basis for activin binding unknown
    • In vivo significance undemonstrated
  3. 2001 High

    Identification of Smad3/4-dependent transcriptional induction of FSTL3 by TGF-β and activin A revealed a negative feedback loop in which the ligand induces its own antagonist.

    Evidence Promoter deletion/mutation analysis, luciferase reporters, dominant-negative Smads in HepG2 cells

    PMID:11571638 PMID:11948405

    Open questions at the time
    • Whether feedback operates in vivo in specific tissues not shown
    • Other transcriptional inputs not yet explored
  4. 2003 High

    Quantification of differential binding showed FSTL3 neutralizes activin A ~3-fold more potently than activin B, defining its ligand selectivity hierarchy.

    Evidence Quantitative binding and functional neutralization assays in 293 cells

    PMID:12697670

    Open questions at the time
    • Binding to myostatin and GDF11 not yet measured
    • Mechanism of selectivity difference unresolved
  5. 2004 High

    Systematic mutagenesis demonstrated that the absence of a heparin-binding sequence in FSTL3 prevents cell-surface association, and that inserting one abolishes activin binding — establishing a structural trade-off that confines FSTL3 to the extracellular milieu.

    Evidence Domain-swap mutagenesis, heparin affinity, cell-surface binding, and pituitary FSH bioassay

    PMID:15471966

    Open questions at the time
    • No crystal structure yet to explain the trade-off at atomic level
  6. 2005 Medium

    Discovery of FSTL3 interactions with fibronectin (promoting hematopoietic adhesion) and ADAM12 (inhibiting osteoclastogenesis) expanded its functional repertoire beyond ligand sequestration to extracellular matrix and cell differentiation contexts.

    Evidence Yeast two-hybrid screens, biochemical confirmation, hematopoietic adhesion and osteoclast differentiation assays

    PMID:15574124 PMID:16336961

    Open questions at the time
    • Yeast two-hybrid interactions not confirmed by endogenous co-IP
    • In vivo relevance of fibronectin and ADAM12 interactions not tested
    • Whether these interactions depend on or compete with activin binding unknown
  7. 2007 High

    FSTL3 knockout mice revealed that endogenous FSTL3 restrains activin/myostatin bioactivity in specific tissues: its absence causes pancreatic β-cell hyperplasia, reduced visceral fat, improved insulin sensitivity, and enlarged testes, defining FSTL3 as a physiological regulator of metabolic and gonadal homeostasis.

    Evidence Constitutive FSTL3 KO mice with metabolic phenotyping, histomorphometry, glucose tolerance, and insulin sensitivity testing

    PMID:17229845 PMID:23407452

    Open questions at the time
    • Tissue-specific contributions of FSTL3 not dissected (global KO)
    • Which ligand (activin vs. myostatin vs. GDF11) mediates each phenotype not resolved
  8. 2007 Medium

    TNF-α was shown to activate FSTL3 transcription via NF-κB elements, and nuclear FSTL3 was found to enhance AF10-mediated transcription, revealing both a new upstream inducer and an unexpected intranuclear function.

    Evidence Promoter mutagenesis/reporter assays for NF-κB; yeast two-hybrid, co-IP, and transactivation assays for AF10 interaction

    PMID:17395406 PMID:17868029

    Open questions at the time
    • Nuclear localization mechanism and signal undefined
    • Transcriptional targets of AF10 enhanced by FSTL3 unknown
    • AF10 interaction not confirmed in endogenous setting
  9. 2008 High

    The 2.5 Å crystal structure of the FSTL3·activin A complex revealed the atomic mechanism of antagonism: two FSTL3 molecules wrap around the activin dimer, blocking all type I and type II receptor-binding epitopes, and showed the N-terminal domain makes uniquely intimate contacts.

    Evidence X-ray crystallography with domain-swap mutagenesis and affinity measurements

    PMID:18768470

    Open questions at the time
    • No structure with myostatin or GDF11
    • Dynamics of complex assembly in solution unknown
  10. 2016 High

    Genetic lineage tracing in FSTL3 KO mice proved that increased activin signaling drives α-to-β cell transdifferentiation, establishing FSTL3 as a gatekeeper of islet cell identity.

    Evidence Gluc-Cre/YFP lineage tracing in FSTL3 KO, flow cytometry, ex vivo activin treatment of islets

    PMID:26727106

    Open questions at the time
    • Whether therapeutic FSTL3 neutralization can replicate this in diabetic models not shown at this time point
  11. 2021 Medium

    An FSTL3-neutralizing antibody (FP-101) enhanced insulin secretion in dysfunctional mouse and human islets, providing proof-of-concept that targeting FSTL3 can restore β-cell function under diabetic conditions.

    Evidence Antibody neutralization assay, glucose-stimulated insulin secretion in isolated islets

    PMID:33539535

    Open questions at the time
    • No in vivo efficacy data in diabetic animal models
    • Long-term safety and specificity not assessed
  12. 2024 Medium

    FSTL3 was found to stabilize c-Myc by directly binding and suppressing its ubiquitination under hypoxic HIF1α-driven induction, linking FSTL3 to immune evasion (PDL1/IDO1 upregulation) in colorectal cancer — a ligand-sequestration-independent oncogenic mechanism.

    Evidence Co-IP, domain mapping (aa 354–406), ubiquitination assay, immunocompetent tumor models

    PMID:38302412

    Open questions at the time
    • Whether c-Myc stabilization occurs in non-hypoxic or non-cancer contexts unknown
    • Ubiquitin ligase displaced by FSTL3 not identified
    • Single-lab finding not yet replicated
  13. 2025 Medium

    Two studies expanded FSTL3's cancer biology: one identified TfR1 as a cell-surface receptor through which fibroblast-derived FSTL3 activates AKT/mTOR signaling and vasculogenic mimicry; the other showed FSTL3 loss triggers cuproptosis via SLC25A10/succinate/DLAT — both mechanisms independent of classical activin antagonism.

    Evidence Binding assays, scRNA-seq, in vivo tumor models (colon cancer); CRISPR screen, metabolic profiling, succinylation assay (OSCC)

    PMID:41053124 PMID:41996175

    Open questions at the time
    • TfR1 interaction not confirmed by structural or biophysical methods
    • Cuproptosis link requires independent replication
    • Relationship between FSTL3's activin-binding and TfR1-binding surfaces uncharacterized

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions include tissue-specific versus circulating contributions of FSTL3 (no conditional KO studies), structures of FSTL3 complexes with myostatin/GDF11, the mechanism and physiological relevance of nuclear FSTL3, and whether the newly identified cancer-related functions (c-Myc stabilization, TfR1 binding, cuproptosis modulation) operate through activin-dependent or fully independent pathways.
  • No tissue-specific knockout models reported
  • No structural data for FSTL3–myostatin or FSTL3–GDF11 complexes
  • Nuclear localization signal and trafficking mechanism undefined
  • Activin-dependent vs. independent functions in tumors not delineated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0048018 receptor ligand activity 4 GO:0140110 transcription regulator activity 1
Localization
GO:0005576 extracellular region 4 GO:0005634 nucleus 1 GO:0031012 extracellular matrix 1
Pathway
R-HSA-162582 Signal Transduction 8 R-HSA-1266738 Developmental Biology 3 R-HSA-1430728 Metabolism 2 R-HSA-168256 Immune System 2
Partners
ADAM12FN1INHBAINHBBMLLT10MYCTFRC

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 FSTL3 (FLRG) was identified as a secreted glycoprotein of the follistatin-module-protein family, cloned from a t(11;19)(q13;p13) translocation in B-cell chronic lymphocytic leukemia, establishing it as an evolutionarily conserved, secreted glycoprotein. cDNA cloning, molecular characterization of chromosomal translocation Oncogene High 9671416
2001 FSTL3 (FLRG) binds activin A directly, as demonstrated by immunoprecipitation and Far-Western blot analysis, establishing its role as an activin-binding antagonist. Immunoprecipitation, Far-Western blot Experimental hematology High 11274757
2001 FSTL3 (FSRP) binds activin with similar affinity and selectivity as follistatin but does not bind heparin; it inhibits activin-mediated gene transcription in heterologous assays but is much less active than follistatin in the rat pituitary bioassay. Binding assays, transcriptional reporter assay, rat pituitary bioassay, transgenic mouse overexpression Molecular and cellular endocrinology High 11451569
2001 FSTL3 (FLRG) gene transcription is activated by TGF-β via Smad proteins; a Smad-binding element in the FLRG promoter mediates TGF-β-inducible expression, and dominant-negative Smad3/Smad4 abolish this activation. Promoter deletion/point-mutation analysis, luciferase reporter assay, EMSA, dominant-negative Smad constructs, transfection in HepG2 cells Oncogene High 11571638
2002 Activin A induces FSTL3 (FLRG) and follistatin expression at both mRNA and protein levels via Smad proteins, and FSTL3 protein in turn inhibits activin A signaling and blocks activin A-induced growth inhibition of HepG2 cells, constituting a negative feedback loop. Transcriptional reporter assay, RT-PCR, protein expression analysis, growth inhibition assay, Smad pathway analysis Oncogene High 11948405
2003 FSTL3 binds activin B at approximately 10-fold lower potency than activin A, and is approximately 3-fold more effective at neutralizing activin A than activin B, demonstrating differential binding and neutralization specificity. Binding assays, 293 cell reporter assays for biological activity neutralization Endocrinology High 12697670
2004 FSTL3 lacks a heparin-binding sequence (HBS) and cannot associate with cell surfaces; mutational analysis showed that inserting the full FS domain 1 (including HBS) into FSTL3 confers heparin binding but abolishes activin binding, implying an evolutionary safeguard against surface binding by FSTL3. Mutational analysis, cell surface binding assays, heparin affinity binding, competitive activin binding assays, pituitary cell FSH secretion bioassay Endocrinology High 15471966
2005 FSTL3 (FLRG) physically interacts with fibronectin via type I motifs of fibronectin and follistatin domains of FSTL3 (identified by yeast two-hybrid screen and confirmed biochemically); this interaction promotes hematopoietic cell adhesion to fibronectin. Yeast two-hybrid screen, biochemical interaction assays, cell adhesion assays with hematopoietic cell line and primary cells Experimental cell research Medium 16336961
2005 FSTL3 (FLRG) directly interacts with ADAM12 via its cysteine-rich domain (identified by yeast two-hybrid); FSTL3 protein inhibits osteoclast differentiation from murine primary spleen cells and RAW264.7 macrophages stimulated with RANK-L and M-CSF. Yeast two-hybrid, direct interaction confirmation, osteoclast differentiation assay with primary murine cells and macrophage cell line Biology of the cell Medium 15574124
2007 Homozygous FSTL3 knockout 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 FSTL3 antagonism. FSTL3 knockout mouse model, histomorphometry, metabolic phenotyping, glucose tolerance testing, insulin sensitivity testing Proceedings of the National Academy of Sciences of the United States of America High 17229845
2007 TNF-α activates FSTL3 (FLRG) expression at the transcriptional level through NF-κB binding elements (5'-GGGAGAG/TTCC-3') located in four conserved 107-108 bp DNA repeats in the promoter; TGF-β via Smad proteins potentiates TNF-α-induced FSTL3 expression. Promoter deletion analysis, luciferase reporter assay, biochemical binding assays, phylogenetic analysis Gene Medium 17395406
2007 Silencing FSTL3 (FLRG) in breast cancer cell lines induces growth inhibition via restoration of endogenous activin signaling (increased pSmad2, upregulation of activin target genes); growth inhibition is reversible by exogenous FSTL3 or soluble type II activin receptor. siRNA knockdown, transcriptional reporter assay, phospho-Smad2 measurement, RT-PCR for target genes, rescue experiments Cancer research High 17671190
2007 Nuclear FSTL3 (FLRG) interacts with AF10 transcription factor (identified by yeast two-hybrid, confirmed by Far-Western blot and co-immunoprecipitation in COS-7 cells); the N-terminal PHD domain of AF10 mediates this interaction, and FSTL3 enhances AF10 homo-oligomerization and AF10-mediated transcriptional activation. Yeast two-hybrid, Far-Western blot, co-immunoprecipitation, transient transfection transactivation assay Biology of the cell Medium 17868029
2008 The crystal structure of the FSTL3·activin A complex at 2.5 Å resolution shows that two FSTL3 molecules encircle one activin A dimer, blocking all receptor-binding sites; the N-terminal domain of FSTL3 forms a more intimate contact with activin A than the corresponding FS domain, and replacing the FSTL3 N-terminal domain with the FS N-terminal domain considerably lowers activin A affinity. X-ray crystallography (2.5 Å), domain-swap mutagenesis, binding affinity measurements The Journal of biological chemistry High 18768470
2013 FSTL3 knockout mice develop markedly enlarged testes with increased Sertoli cell numbers and delayed age-related testicular regression; FSTL3 deletion leads to increased AKT signaling and SIRT1 expression in the testis, revealing cross-talk between TGF-β ligand signaling and AKT pathway in testicular homeostasis. FSTL3 knockout mouse model, histomorphometry, phosphoproteomics, Western blot for AKT/SIRT1 Endocrinology Medium 23407452
2016 In FSTL3 knockout mice, α-to-β cell transdifferentiation is increased, as shown by α-cell lineage tracing (Gluc-Cre/YFP); activin treatment of isolated islets significantly increases YFP+/Ins+ cells, demonstrating that increased activin signaling (due to absence of FSTL3 antagonism) drives α-to-β cell transdifferentiation. Genetic lineage tracing (Gluc-Cre/YFP), flow cytometry, FSTL3 KO mice, ex vivo islet activin treatment Endocrinology High 26727106
2019 FSTL3 promotes lipid accumulation in macrophages by upregulating scavenger receptors CD36 and LOX-1 in a dose-dependent manner, and induces inflammatory cytokine secretion (IL-1β, MCP-1, TNF-α, MMP-9); FSTL3 expression is induced by oxidized LDL in macrophages. Cell-based assays, dose-response experiments, cytokine measurement, knockdown experiments Journal of cardiovascular pharmacology Medium 31815869
2021 FSTL3-neutralizing antibody FP-101 prevents FSTL3 from complexing with activin or related ligands; FP-101 treatment enhances insulin secretion and glucose responsiveness in dysfunctional mouse and human islets under diabetic conditions. Antibody development, in vitro neutralization assay, islet glucose-stimulated insulin secretion assay Endocrinology Medium 33539535
2024 FSTL3 binds to transcription factor c-Myc (at amino acids 354-406) to suppress its ubiquitination and increase its stability, thereby upregulating PDL1 and IDO1 expression; hypoxic tumor microenvironment induces FSTL3 expression via HIF1α in colorectal cancer cells. Co-immunoprecipitation, domain mapping, ubiquitination assay, Western blot, flow cytometry, immunocompetent tumor models Cell death & disease Medium 38302412
2024 Prenatal dexamethasone exposure increases KDM1B expression in fetal testicular Sertoli cells, decreasing H3K9me2 at the FSTL3 promoter and thereby increasing FSTL3 expression, which inhibits TGF-β signaling and CX43/E-cadherin expression, impairing blood-testis barrier function. Animal model (prenatal dexamethasone), ChIP for H3K9me2 at FSTL3 promoter, Western blot, TM4 Sertoli cell validation, human sample correlation Acta pharmacologica Sinica Medium 38472317
2025 FSTL3 loss in OSCC induces cuproptosis susceptibility by suppressing SLC25A10, triggering mitochondrial succinate accumulation, which promotes succinylation and upregulation of DLAT, a key cuproptosis executor; FSTL3 also recruits erythroid progenitor cells (EPCs) via CCR5 upregulation to establish an immunosuppressive niche. CRISPR-Cas9 screening, metabolic profiling, succinylation assay, EPC recruitment assays, in vivo tumor models Journal of dental research Medium 41996175
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 vasculogenic mimicry and metastatic progression in colon cancer. Binding assays, pathway activation analysis, in vitro and in vivo tumor models, FSTL3-targeting antibody inhibition studies, single-cell RNA sequencing Cell death & disease Medium 41053124

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 134 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 62 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 16 38302412
2016 Activin Enhances α- to β-Cell Transdifferentiation as a Source For β-Cells In Male FSTL3 Knockout Mice. Endocrinology 16 26727106
2019 FSTL3 Induces Lipid Accumulation and Inflammatory Response in Macrophages and Associates With Atherosclerosis. Journal of cardiovascular pharmacology 15 31815869
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.) 12 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 8 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
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 Cancer-associated fibroblasts expressing FSTL3 promote vasculogenic mimicry formation and drive colon cancer malignancy. Cell death & disease 0 41053124
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