Affinage

GDF3

Growth/differentiation factor 3 · UniProt Q9NR23

Length
364 aa
Mass
41.4 kDa
Annotated
2026-06-10
43 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GDF3 is a secreted TGF-β superfamily ligand that operates dually as a Nodal-pathway cofactor in embryonic axis formation and as a BMP inhibitor, with distinct pleiotropic roles in adult macrophages (PMID:8429021, PMID:16339188, PMID:16368929). During development, GDF3 antagonizes BMP signaling through both its poorly processed precursor and its mature form (PMID:16339188, PMID:18823971), and—acting cooperatively at the same pathway step as Nodal ligands rather than independently—signals through the EGF-CFC co-receptor Cripto and the type I/II receptors ALK4, ActRIIA and ActRIIB to drive Smad-dependent transcription (PMID:16368929, PMID:17936261, PMID:29140249). The native precursor is largely inactive until processed, an activity unmasked by Furin co-expression or heterologous prodomains (PMID:17936261). Together with GDF1, GDF3 is required for anterior visceral endoderm formation, mesendoderm specification, and left-right patterning, with maternal Gdf3 acting upstream of Nodal-dependent events (PMID:17936261, PMID:29140250, PMID:29140249). In adults, macrophage-derived GDF3 is a paracrine and autocrine cytokine: PPARγ and Brd4 drive its transcription in repair and adipose tissue macrophages (PMID:27836432, PMID:33830083), and secreted GDF3 promotes muscle progenitor fusion and regeneration—an output that becomes limiting with age (PMID:27836432, PMID:30003692). Through SMAD2/3 signaling GDF3 suppresses adipocyte lipase expression and lipolysis, lowering β3-adrenergic receptor and cAMP/PKA signaling, and acts as an agonist of ALK5, ALK7, ACVR2A and ACVR2B while antagonizing BMPR2 (PMID:33830083, PMID:40360531). Autocrine GDF3-SMAD2/3 signaling drives an inflammatory macrophage state by increasing chromatin accessibility, and its loss reduces endotoxemia-induced inflammation (PMID:41398392). Missense variants in GDF3 cause human ocular (coloboma, microphthalmia) and skeletal (Klippel-Feil) anomalies (PMID:19864492).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1993 Medium

    Establishing GDF3 as a TGF-β superfamily member defined the structural framework—signal sequence, proteolytic processing site, and an atypical absence of the conserved intersubunit cysteine—for all later functional studies.

    Evidence cDNA cloning, sequence analysis, and Northern blot

    PMID:8429021

    Open questions at the time
    • No functional activity or receptor assigned
    • Consequences of the missing intersubunit cysteine for dimerization not tested
    • Tissue distribution of activity unknown
  2. 2005 High

    Identifying GDF3 as a physical BMP-interacting inhibitor expressed in the node established its first concrete mechanistic role in developmental patterning and stem cell state.

    Evidence Gain/loss-of-function, reporter assays, and co-IP in Xenopus and mouse ES cells

    PMID:16339188

    Open questions at the time
    • Which BMP ligands are bound was not exhaustively mapped
    • Did not reconcile BMP-inhibitory with Nodal-like activity
    • Species-specific ES cell effects unexplained
  3. 2006 High

    Showing GDF3 signals via Cripto and is blocked by Lefty, like Nodal, and that Gdf3-null mice have AVE defects with reduced Nodal, placed GDF3 within the Nodal signaling pathway.

    Evidence Cell reporter assays, Xenopus misexpression, mouse knockout, in situ hybridization

    PMID:16368929

    Open questions at the time
    • Type I/II receptor identity not resolved here
    • Relationship between Nodal-like and BMP-inhibitory activities unclear
    • Whether GDF3 signals as a ligand or cofactor unresolved
  4. 2007 High

    Defining ALK4/ActRIIA/ActRIIB/Cripto as the receptor module and demonstrating that the poorly-processed precursor requires Furin or prodomain swap to activate explained why native GDF3 has weak activity and unified it with GDF1 as a Vg1 homolog.

    Evidence Luciferase reporters, chimeric/Furin co-expression, Gdf1/Gdf3 compound knockout

    PMID:17936261

    Open questions at the time
    • Physiological processing trigger in vivo not identified
    • Quantitative contribution of GDF1 vs GDF3 not separated
    • Mature dimer structure not determined
  5. 2008 High

    Resolving that BMP inhibition occurs at physiological doses via both precursor and mature forms, while Nodal activation requires non-physiological overexpression, clarified GDF3's predominant in vivo activity.

    Evidence mRNA vs recombinant protein dose-response reporter assays, Western blot of protein forms

    PMID:18823971

    Open questions at the time
    • Context determining BMP-inhibition vs Nodal-cofactor role unclear
    • Mechanism by which the precursor inhibits BMP not defined
    • In vivo dose dependence not directly measured
  6. 2009 High

    Linking GDF3 missense variants to human ocular and skeletal malformations, with zebrafish knockdown phenocopy, established GDF3 as necessary for human eye and axial skeletal development.

    Evidence Patient variant Western blot/reporter assays and zebrafish morpholino knockdown

    PMID:19864492

    Open questions at the time
    • Mechanism linking signaling defect to specific malformations not detailed
    • Penetrance and genotype-phenotype correlation limited
    • Morpholino specificity caveats
  7. 2011 Medium

    Demonstrating ALK7 association in a Cripto-dependent manner and GDF3-driven neuronal differentiation extended its receptor repertoire and suggested non-developmental cellular effects.

    Evidence Co-IP receptor association, conditioned medium on PC12/neurons, immunofluorescence

    PMID:21805089

    Open questions at the time
    • Cripto-dependence not fully characterized
    • Conditioned medium lacked protein quantification
    • Physiological relevance of neuronal effect untested in vivo
  8. 2012 Medium

    Identifying miR-483-3p as a translational repressor of GDF3 revealed post-transcriptional control of GDF3 in adipocyte differentiation and lipid storage.

    Evidence miRNA overexpression/knockdown, luciferase target validation, adipocyte assays

    PMID:22223106

    Open questions at the time
    • Fraction of phenotype attributable to GDF3 vs other targets unclear
    • In vivo regulation not demonstrated
    • Downstream signaling not mapped
  9. 2016 High

    Showing PPARγ transcriptionally drives macrophage GDF3, which acts on myoblasts to promote fusion and regeneration, established GDF3 as a macrophage-derived effector of tissue repair.

    Evidence Macrophage-specific PPARγ knockout, muscle injury model, recombinant GDF3 fusion assay

    PMID:27836432

    Open questions at the time
    • Receptor on myoblasts not identified here
    • Direct vs indirect fusion mechanism unresolved
    • Whether developmental and repair pathways share components unknown
  10. 2018 Medium

    Demonstrating that macrophage GDF3 declines with age and that recombinant supplementation restores regeneration established GDF3 as a functionally limiting factor in aged muscle repair.

    Evidence Aged vs young muscle injury, macrophage flow cytometry, recombinant GDF3 rescue

    PMID:30003692

    Open questions at the time
    • Cause of age-related downregulation not identified
    • Single-lab extension of prior work
    • Receptor/signaling in aged myoblasts not dissected
  11. 2020 Medium

    Linking GDF3 to Smad2/3-dependent NLRP3 suppression and M2 polarization defined a signaling axis for its anti-inflammatory macrophage effects.

    Evidence Recombinant GDF3, pSmad2/3 Western, NLRP3 assays, SB431542 inhibition, endotoxemia model

    PMID:31947892

    Open questions at the time
    • Anti-inflammatory effect here conflicts with later pro-inflammatory role
    • Specific receptor mediating Smad2/3 in macrophages not defined
    • Single lab
  12. 2021 High

    Identifying Brd4 binding at the Gdf3 locus to enable PPARγ-dependent expression, and the resulting paracrine suppression of adipocyte lipases, mapped both upstream control and a metabolic output of macrophage GDF3.

    Evidence ChIP-seq, myeloid Brd4 knockout, RNA-seq, conditioned medium, lipase Westerns

    PMID:33830083

    Open questions at the time
    • Adipocyte receptor mediating lipase suppression not pinpointed here
    • Relationship between PPARγ and Brd4 cooperativity not fully defined
    • Systemic metabolic consequences not yet tested
  13. 2021 Medium

    Placing LXRα/CD5L downstream of GDF3 in promoting macrophage phagocytosis and bacterial killing identified a distinct antimicrobial effector arm.

    Evidence Recombinant GDF3, RNA-seq, LXRα translocation, LXRα knockout, phagocytosis assays

    PMID:33679812

    Open questions at the time
    • Receptor coupling GDF3 to LXRα not defined
    • In vivo infection relevance limited
    • Single lab
  14. 2022 Medium

    Showing cardiac PW1+ cell-derived GDF3 drives fibroblast proliferation via activin-like kinases after infarction extended its paracrine role to adverse cardiac fibrotic remodeling.

    Evidence Secretome analysis, conditioned medium proliferation, receptor pharmacology, plasma GDF3

    PMID:36484260

    Open questions at the time
    • Receptor identity inferred pharmacologically, not by genetic knockdown
    • Causal in vivo role of cardiac GDF3 not established by loss-of-function
    • Single lab
  15. 2025 High

    Defining GDF3 as an ALK5/ALK7/ACVR2A/ACVR2B agonist and BMPR2 antagonist, and showing inducible loss reduces lipolysis via β3-AR/cAMP/PKA while improving glucose tolerance, provided the adult receptor logic and metabolic consequences of GDF3 signaling.

    Evidence Inducible conditional knockout in obese mice, receptor signaling assays, metabolic phenotyping

    PMID:40360531

    Open questions at the time
    • How agonist/antagonist activities are balanced on individual cells unclear
    • Tissue source of the active GDF3 in this context not fully resolved
    • Human translatability untested
  16. 2025 High

    Demonstrating that autocrine GDF3-SMAD2/3 signaling drives an inflammatory macrophage state through increased chromatin accessibility, and that Gdf3 deletion or SMAD3 inhibition reduces endotoxemia, reframed GDF3 as a pro-inflammatory chromatin regulator in aging.

    Evidence Systemic/myeloid Gdf3 knockout, scRNA-seq, ATAC-seq, SIS3 and JQ1 treatment, endotoxemia mortality

    PMID:41398392

    Open questions at the time
    • Reconciliation with the earlier anti-inflammatory/NLRP3-suppressive report needed
    • Molecular link between SMAD2/3 and chromatin compaction machinery not fully defined
    • Receptor mediating autocrine signaling not specified

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown what determines the context-dependent switch between GDF3's BMP-inhibitory, Nodal-cofactor, and SMAD2/3-agonist activities, and how the same ligand produces opposing pro- and anti-inflammatory outcomes in macrophages.
  • No unifying model reconciles agonist vs inhibitor behavior across tissues
  • Structural basis of GDF3 dimerization and receptor selectivity undefined
  • In vivo processing/activation triggers not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005576 extracellular region 5 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 6 R-HSA-162582 Signal Transduction 4 R-HSA-1430728 Metabolism 3 R-HSA-168256 Immune System 3
Partners
ACVR1BACVR1CACVR2AACVR2BBMPBMPR2TDGF1TGFBR1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 GDF3 and GDF9 are novel members of the TGF-β superfamily, predicted to contain a signal sequence for secretion, a tetrabasic proteolytic processing site, and a C-terminal region homologous to known TGF-β superfamily members. Unlike all other superfamily members, GDF3 and GDF9 lack the conserved cysteine residue believed to form the intersubunit disulfide bond, suggesting different subunit interaction mechanisms. cDNA cloning, sequence analysis, Northern blot The Journal of biological chemistry Medium 8429021
2005 GDF3 inhibits BMP signaling in multiple developmental contexts and interacts physically with BMP proteins. GDF3 is expressed in the node during gastrulation consistent with a BMP-inhibitory role. Gain- and loss-of-function experiments show GDF3 regulates both maintenance of the undifferentiated state and differentiation capacity of embryonic stem cells in a species-specific manner. mRNA gain-of-function, reduction-of-function (antisense/RNAi), reporter assays, co-immunoprecipitation/interaction assay, in vivo Xenopus and mouse ES cell experiments Development (Cambridge, England) High 16339188
2006 GDF3 signals via the EGF-CFC co-receptor Cripto and can be inhibited by Lefty antagonists in cell culture, similar to Nodal. In Xenopus, GDF3 misexpression induces secondary axis formation and mesendoderm formation. In mice, Gdf3 null mutants show defects in anterior visceral endoderm formation and reduced Nodal expression, placing GDF3 in a Nodal-like signaling pathway. Cell-based reporter assays, Xenopus misexpression, mouse knockout analysis, in situ hybridization Development (Cambridge, England) High 16368929
2007 GDF3 signaling is mediated by type I receptor ALK4, type II receptors ActRIIA and ActRIIB, and co-receptor Cripto to activate Smad-dependent reporter genes. Native GDF3 precursor is poorly processed and inactive; activity can be unmasked by heterologous prodomains, co-expression with Furin pro-protein convertase, or co-expression with Nodal. GDF1 and GDF3 together represent functional mammalian homologs of Xenopus Vg1, as compound Gdf1/Gdf3 double-knockout mice show more severe AVE and mesoderm defects than either single mutant. Luciferase reporter assays, chimeric construct expression, Furin co-expression, genetic compound knockout analysis Developmental biology High 17936261
2008 GDF3 acts as a specific BMP inhibitor at physiological expression levels. BMP-inhibitory activity resides redundantly in both the unprocessed precursor form and the mature processed form of GDF3 protein. GDF3 can activate Nodal signaling only at very high (non-physiological) doses of mRNA overexpression, not as recombinant protein at normal doses. mRNA overexpression, recombinant protein treatment, dose-response reporter assays, Western blot for protein forms Developmental biology High 18823971
2009 Missense variants in GDF3 cause ocular (coloboma, microphthalmia) and skeletal (Klippel-Feil) anomalies in humans. Functional assessment using Western blot and luciferase reporter assays demonstrated appreciable effects of the variants. Antisense morpholino inhibition of zebrafish GDF3 co-ortholog recapitulates patient phenotypes, establishing GDF3 as necessary for ocular and skeletal development. Western blot, luciferase reporter assay, zebrafish antisense morpholino knockdown, patient variant characterization Human molecular genetics High 19864492
2011 GDF3 activates downstream signaling through associating with ALK7 (Activin receptor-like kinase 7) in a Cripto-dependent fashion. Secreted GDF3 protein from stable CHO-GDF3 cells reduces PC12 cell growth and induces neuronal differentiation. GDF3 protein is distributed mainly in the cytoplasm of expressing cells and in primary hippocampal neurons. Co-immunoprecipitation/receptor association assay, stable cell line conditioned medium treatment, immunofluorescence, Western blot Molecular and cellular biochemistry Medium 21805089
2012 miR-483-3p targets GDF3 mRNA for translational repression in adipocytes. Manipulation of miR-483-3p levels substantially modulates adipocyte differentiation and lipid storage, with some effects mediated through GDF3 suppression. miRNA overexpression/knockdown in vitro, luciferase reporter assay for target validation, adipocyte differentiation assay Cell death and differentiation Medium 22223106
2016 Macrophage PPARγ transcriptionally controls GDF3 expression in repair macrophages. GDF3 secreted by macrophages acts as an extrinsic effector on myoblasts to promote muscle progenitor cell fusion and skeletal muscle regeneration. PPARγ-null macrophages fail to upregulate GDF3, and this deficiency impairs muscle regeneration. Conditional macrophage-specific PPARγ knockout mice, muscle injury model, ChIP/transcriptional analysis, recombinant GDF3 treatment of myoblasts, fusion assay Immunity High 27836432
2017 Maternal (not zygotic) Gdf3 is required for mesendoderm formation and dorsal-ventral patterning in zebrafish. Gdf3 affects left-right patterning by regulating cell morphology in Kupffer's vesicle and southpaw expression in lateral plate mesoderm. Gdf3 maternal-zygotic mutants are refractory to Nodal ligands and Lefty1 repressor, but Activin signaling and constitutively active Alk4/Alk2 remain intact, placing Gdf3 at the same pathway step as Nodal. Maternal-zygotic mutant zebrafish, RNA rescue experiments, epistasis analysis with Nodal pathway components, morphological analysis of Kupffer's vesicle eLife High 29140250
2017 Gdf3 is an essential cofactor of Nodal signaling during embryonic axis establishment in zebrafish. Maternal-zygotic gdf3 mutants are fully rescued by gdf3 RNA only when co-expressed with endogenous Nodal, indicating Gdf3 acts cooperatively at the same step as Nodal ligands rather than independently. Signaling through constitutively active Alk4 and Alk2 is intact in gdf3 mutants, indicating that Gdf3 functions specifically at the Nodal pathway level. Maternal-zygotic mutant zebrafish, lineage-specific RNA targeting rescue experiments, constitutively active receptor epistasis eLife High 29140249
2018 In aged mice, repair macrophage-derived GDF3 is markedly downregulated in injured muscle compared to young mice. Supplementation of recombinant GDF3 in aged mice ameliorates the deficient regenerative response, establishing that macrophage-secreted GDF3 is functionally limiting for muscle regeneration during aging. Aged vs. young mouse muscle injury model, flow cytometry for macrophage subsets, recombinant GDF3 administration, histological analysis of regeneration Aging cell Medium 30003692
2020 GDF3 activates Smad2/Smad3 phosphorylation in macrophages and consequently inhibits NLRP3 expression, mediating anti-inflammatory effects. Recombinant GDF3 suppresses macrophage pro-inflammatory (M1) phenotype and promotes anti-inflammatory (M2) polarization. Blockade of Smad2/Smad3 phosphorylation with SB431542 offsets rGDF3-mediated anti-inflammatory effects. Recombinant GDF3 protein treatment of macrophages, Western blot for pSmad2/3, NLRP3 expression assay, pharmacological inhibition of Smad2/3 with SB431542, in vivo endotoxemia mouse model Cells Medium 31947892
2021 Brd4 binds to the promoter and enhancers of Gdf3 to facilitate PPARγ-dependent Gdf3 expression in macrophages. Macrophage-derived GDF3 acts as a paracrine signal on adipocytes to suppress lipase expression (ATGL, HSL) and inhibit lipolysis. Myeloid-specific Brd4 knockout reduces GDF3 in adipose tissue macrophages and increases lipolysis. ChIP-seq (Brd4 at Gdf3 locus), myeloid-specific Brd4 knockout mice, RNA-seq of adipose tissue macrophages, co-culture/conditioned medium experiments, Western blot for lipases JCI insight High 33830083
2021 Recombinant GDF3 promotes macrophage phagocytosis and intracellular bacterial killing by promoting LXRα nuclear translocation. RNA-seq identified CD5L (regulated by LXRα) as the most significantly upregulated gene in rGDF3-treated macrophages. GDF3 failed to enhance bacterial uptake or killing in LXRα-knockout macrophages, placing LXRα downstream of GDF3 in this pathway. Recombinant GDF3 treatment of macrophages, RNA-seq, LXRα nuclear translocation assay, LXRα knockout macrophages, bacterial phagocytosis/killing assay, pharmacological LXRα antagonism Frontiers in immunology Medium 33679812
2022 GDF3 secreted by cardiac stromal PW1+ cells induces fibroblast proliferation via stimulation of activin-receptor-like kinases. GDF3 is markedly upregulated in ischemic hearts post-MI and detectable in plasma, implicating it as a paracrine cardiokine promoting adverse fibrotic remodeling. Secretome bioinformatic analysis, conditioned medium fibroblast proliferation assay, GDF3-enriched conditioned medium functional assay, activin receptor kinase pharmacological inhibition, mouse and human plasma GDF3 measurement Circulation Medium 36484260
2025 GDF3 is an agonist of ALK5, ALK7, ACVR2A, and ACVR2B, and an antagonist of BMPR2. Inducible GDF3 loss-of-function in obese mice reduces lipolysis by lowering β3-adrenergic receptor levels and decreasing cAMP/PKA signaling. GDF3 loss improves glucose tolerance and reduces glycemic variability without affecting body weight or energy balance. Inducible conditional knockout in adult obese mice, receptor signaling assays (ALK5/ALK7/ACVR2A/ACVR2B/BMPR2 activity), metabolic phenotyping (glucose tolerance, lipolysis, β3-AR/cAMP/PKA measurements) Nature communications High 40360531
2025 GDF3 promotes the inflammatory phenotype in adipose tissue macrophages through autocrine GDF3-SMAD2/3 signaling, driving chromatin accessibility toward an inflammatory state by limiting methylation-dependent chromatin compaction. Lifelong systemic or myeloid-specific Gdf3 deletion reduces endotoxemia-induced inflammation. Pharmacological inhibition of SMAD3 with SIS3 mimics Gdf3 deletion and reduces mortality from endotoxemia in old mice. Systemic and myeloid-specific Gdf3 knockout mice, scRNA-seq, ATAC-seq of ATMs, SMAD3 pharmacological inhibition (SIS3), BRD4 inhibitor (JQ1) treatment, endotoxemia mortality assay Nature aging High 41398392

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Human embryonic stem cell genes OCT4, NANOG, STELLAR, and GDF3 are expressed in both seminoma and breast carcinoma. Cancer 348 16228988
1993 GDF-3 and GDF-9: two new members of the transforming growth factor-beta superfamily containing a novel pattern of cysteines. The Journal of biological chemistry 232 8429021
2004 Human STELLAR, NANOG, and GDF3 genes are expressed in pluripotent cells and map to chromosome 12p13, a hotspot for teratocarcinoma. Stem cells (Dayton, Ohio) 180 14990856
2016 Macrophage PPARγ, a Lipid Activated Transcription Factor Controls the Growth Factor GDF3 and Skeletal Muscle Regeneration. Immunity 162 27836432
2005 GDF3, a BMP inhibitor, regulates cell fate in stem cells and early embryos. Development (Cambridge, England) 131 16339188
2006 The Vg1-related protein Gdf3 acts in a Nodal signaling pathway in the pre-gastrulation mouse embryo. Development (Cambridge, England) 127 16368929
2009 Mutation of the bone morphogenetic protein GDF3 causes ocular and skeletal anomalies. Human molecular genetics 121 19864492
2012 Programming of adipose tissue miR-483-3p and GDF-3 expression by maternal diet in type 2 diabetes. Cell death and differentiation 116 22223106
2012 Enhanced red emission from GdF3:Yb3+,Er3+ upconversion nanocrystals by Li+ doping and their application for bioimaging. Chemistry (Weinheim an der Bergstrasse, Germany) 81 22729946
2007 Distinct and cooperative roles of mammalian Vg1 homologs GDF1 and GDF3 during early embryonic development. Developmental biology 77 17936261
2020 GDF3 Protects Mice against Sepsis-Induced Cardiac Dysfunction and Mortality by Suppression of Macrophage Pro-Inflammatory Phenotype. Cells 58 31947892
2009 Testicular mixed germ cell tumors: a morphological and immunohistochemical study using stem cell markers, OCT3/4, SOX2 and GDF3, with emphasis on morphologically difficult-to-classify areas. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 58 19396148
2017 Gdf3 is required for robust Nodal signaling during germ layer formation and left-right patterning. eLife 53 29140250
2006 GDF3 at the crossroads of TGF-beta signaling. Cell cycle (Georgetown, Tex.) 43 16721050
2012 PEG-capped, lanthanide doped GdF3 nanoparticles: luminescent and T2 contrast agents for optical and MRI multimodal imaging. Nanoscale 41 23117700
2017 Maternal Gdf3 is an obligatory cofactor in Nodal signaling for embryonic axis formation in zebrafish. eLife 40 29140249
2008 GDF3 is a BMP inhibitor that can activate Nodal signaling only at very high doses. Developmental biology 36 18823971
2004 GDF-3 is an adipogenic cytokine under high fat dietary condition. Biochemical and biophysical research communications 33 15358131
2021 Brd4 modulates diet-induced obesity via PPARγ-dependent Gdf3 expression in adipose tissue macrophages. JCI insight 29 33830083
2018 In vivo GDF3 administration abrogates aging related muscle regeneration delay following acute sterile injury. Aging cell 27 30003692
2022 Novel Cardiokine GDF3 Predicts Adverse Fibrotic Remodeling After Myocardial Infarction. Circulation 23 36484260
2010 An embryo-specific expressing TGF-β family protein, growth-differentiation factor 3 (GDF3), augments progression of B16 melanoma. Journal of experimental & clinical cancer research : CR 17 20950440
2020 Multifunctional Transferrin Encapsulated GdF3 Nanoparticles for Sentinel Lymph Node and Tumor Imaging. Bioconjugate chemistry 15 33155818
2012 GDF3 inhibits the growth of breast cancer cells and promotes the apoptosis induced by Taxol. Journal of cancer research and clinical oncology 14 22488170
2021 Administration of GDF3 Into Septic Mice Improves Survival via Enhancing LXRα-Mediated Macrophage Phagocytosis. Frontiers in immunology 13 33679812
2014 GdF3 as a promising phosphopeptide affinity probe and dephospho-labelling medium: experiments and theoretical explanation. Chemical communications (Cambridge, England) 11 25140354
2012 Klippel-Feil syndrome associated with situs inversus: description of a new case and exclusion of GDF1, GDF3 and GDF6 as causal genes. European journal of medical genetics 11 22522086
2011 The conditioned medium from a stable human GDF3-expressing CHO cell line, induces the differentiation of PC12 cells. Molecular and cellular biochemistry 11 21805089
2021 Multimodal fluorescently labeled polymer-coated GdF3 nanoparticles inhibit degranulation in mast cells. Nanoscale 5 34755752
2018 Phylogenetic evidence for independent origins of GDF1 and GDF3 genes in anurans and mammals. Scientific reports 5 30206386
2014 A novel variation of GDF3 in Chinese Han children with a broad phenotypic spectrum of non-syndromic CHDs. Cardiology in the young 5 25372014
2025 GDF3 promotes adipose tissue macrophage-mediated inflammation via altered chromatin accessibility during aging. Nature aging 4 41398392
2024 Total saponins from Panax japonicus mediate the paracrine interaction between adipocytes and macrophages to promote lipolysis in the adipose tissue during aging via the NLRP3 inflammasome/GDF3/ATGL axis. Phytomedicine : international journal of phytotherapy and phytopharmacology 4 39662098
2018 Functional and In Silico Assessment of GDF3 Gene Variants in a Chinese Congenital Scoliosis Population. Medical science monitor : international medical journal of experimental and clinical research 4 29735971
2017 A recurrent, non-penetrant sequence variant, p.Arg266Cys in Growth/Differentiation Factor 3 (GDF3) in a female with unilateral anophthalmia and skeletal anomalies. American journal of ophthalmology case reports 4 29260090
2025 Acute regulation of murine adipose tissue lipolysis and insulin resistance by the TGFβ superfamily protein GDF3. Nature communications 3 40360531
2022 Increased Serum Levels of Growth-Differentiation Factor 3 (GDF3) and Inflammasome-Related Markers in Pregnant Women during Acute Zika Virus Infection. Viruses 3 35632746
2024 GDF3 Protects Mice against Sepsis-Induced Acute Lung Injury by Suppression of Macrophage Pyroptosis. Pharmaceuticals (Basel, Switzerland) 2 38543054
2024 GDF3 promotes adipose tissue macrophage-mediated inflammation via altered chromatin accessibility during aging. bioRxiv : the preprint server for biology 2 39386655
2023 The GDF3-ALK7 signaling axis in adipose tissue: a possible therapeutic target for obesity and associated diabetes? Endocrine journal 2 37081691
2023 Temperature Sensing Properties of Biocompatible Yb/Er-Doped GdF3 and YF3 Mesocrystals. Journal of functional biomaterials 2 38248673
2022 Secreted key regulators (Fgf1, Bmp4, Gdf3) are expressed by PAC1-immunopositive retinal ganglion cells in the postnatal rat retina. European journal of histochemistry : EJH 1 35477223
2023 [Expression and significance analysis of GDF3 in testicular cancer based on TCGA and GTEx databases]. Zhonghua nan ke xue = National journal of andrology 0 38639949

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