Affinage

FGG

Fibrinogen gamma chain · UniProt P02679

Round 2 corrected
Length
453 aa
Mass
51.5 kDa
Annotated
2026-04-28
74 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FGG encodes the fibrinogen gamma chain, which assembles with the alpha and beta chains into the (AαBβγ)₂ hexamer that is the soluble precursor of fibrin and a key mediator of hemostasis, inflammation, and cell adhesion. The gamma-chain C-terminal globular domain contains the platelet integrin αIIbβ3 recognition site (γ400–411, with critical residues His400–401 and Lys406), a calcium-dependent polymerization pocket that accepts the Gly-Pro-Arg knob of fibrin monomers, and the factor XIIIa crosslinking site, as defined by peptide-inhibition studies and high-resolution crystal structures of fragment D and full-length fibrinogen (PMID:6326808, PMID:9333233, PMID:19296670). Beyond hemostasis, fibrinogen bridges leukocytes to endothelium via ICAM-1, forms a complex with FGF-2 to augment cancer-cell proliferation, and promotes hepatic stellate cell activation and M2 macrophage polarization in liver fibrosis (PMID:8100742, PMID:17949478, PMID:42001119). Loss-of-function FGG mutations cause congenital afibrinogenemia or hypofibrinogenemia through nonsense-mediated mRNA decay of truncated transcripts, intracellular retention of misfolded hexamers, or aberrant splicing, while the γA/γ' isoform ratio—regulated by a CstF polyadenylation-site polymorphism—modulates venous thrombosis risk (PMID:24011387, PMID:16141000, PMID:16144795).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1984 High

    Identifying the minimal platelet-binding determinant on the gamma chain (γ400–411) established that a short C-terminal peptide mediates fibrinogen recognition by activated platelets and that this site is shared with fibronectin and von Willebrand factor, defining the integrin αIIbβ3 ligand-recognition paradigm.

    Evidence Synthetic peptide competition of radiolabeled fibrinogen/fibronectin/vWF binding to ADP- and thrombin-stimulated platelets with structure–activity analysis

    PMID:6325435 PMID:6326808

    Open questions at the time
    • Full thermodynamic parameters for peptide–integrin interaction not determined
    • Three-dimensional structural basis of the γ-chain–αIIbβ3 interface unresolved at this stage
  2. 1993 High

    Demonstrating that fibrinogen binds endothelial ICAM-1 to bridge leukocytes to the vessel wall revealed an inflammation-relevant adhesion function of fibrinogen independent of its classical hemostatic integrin interactions.

    Evidence Affinity chromatography, direct binding to recombinant ICAM-1, and cell adhesion assays with ICAM-1 transfectants

    PMID:8100742

    Open questions at the time
    • Gamma-chain residues responsible for ICAM-1 binding not mapped
    • Contribution of each fibrinogen chain to ICAM-1 recognition not dissected
  3. 1997 High

    Crystal structures of the gamma-chain C-terminal fragment and of fragment D with a bound Gly-Pro-Arg-Pro peptide provided the atomic basis for fibrin polymerization, showing a deep 'hole' pocket in the gamma domain that accepts the complementary 'knob' from adjacent fibrin monomers.

    Evidence X-ray crystallography at 2.1–2.9 Å resolution with multiple crystal forms and a synthetic polymerization-site peptide ligand

    PMID:9016719 PMID:9333233

    Open questions at the time
    • Full-length hexamer structure not yet available at this point
    • Dynamics of polymerization pocket opening/closing not captured by static structures
  4. 2000 High

    Showing that the S. aureus adhesin FnbpA targets the same gamma-chain C-terminal site recognized by ClfA established that pathogens exploit the platelet-binding determinant of fibrinogen for host cell attachment.

    Evidence SPR, fluorescence polarization, and competitive binding assays using recombinant FnbpA domains and gamma-chain peptides in ClfA/ClfB-null S. aureus

    PMID:10788510

    Open questions at the time
    • Atomic structure of FnbpA–gamma chain complex not solved
    • Relative in vivo contribution of FnbpA vs. ClfA to fibrinogen-dependent pathogenesis unclear
  5. 2005 Medium

    Functional studies of the FGG-H2 haplotype (rs2066865) linked a polyadenylation-site SNP to altered γA/γ' chain ratio and DVT risk, providing a molecular mechanism connecting fibrinogen gamma-chain isoform regulation to thrombin's antithrombin-1 activity and thrombotic disease.

    Evidence Population case-control study (Leiden Thrombophilia Study) with haplotype-tagging SNPs and fibrinogen γ' quantification

    PMID:16144795

    Open questions at the time
    • Direct in vitro demonstration that the SNP alters CstF binding and polyadenylation not yet provided
    • Replication in diverse populations not reported in this study
  6. 2004 High

    Characterization of FGG loss-of-function mutations—including nonsense, missense, and splice-site variants—established that congenital afibrinogenemia and hypofibrinogenemia arise through at least three distinct pathogenic mechanisms: NMD of truncated transcripts, intracellular retention of assembled but secretion-incompetent hexamers, and aberrant mRNA splicing.

    Evidence COS-7/CHO cell transfection, co-expression of mutant and wild-type chains, cycloheximide NMD inhibition, minigene splicing assays, ELISA and immunoblot across multiple mutations

    PMID:15284111 PMID:16141000 PMID:20580695 PMID:24011387 PMID:34196169 PMID:38233949

    Open questions at the time
    • Structural basis for ER retention of specific missense mutants (e.g. W253C) not determined
    • Genotype–phenotype correlation across mutation classes remains incomplete
    • NMD efficiency for different PTC positions along FGG not systematically compared
  7. 2007 High

    Demonstrating that cancer cells endogenously synthesize fibrinogen and that FGG knockdown suppresses FGF-2-dependent proliferation—rescued by exogenous fibrinogen—established a non-hemostatic, autocrine growth-promoting role for the gamma chain through direct FGF-2–fibrinogen complex formation.

    Evidence RNAi knockdown of FGG in A549/PC-3 cells; thymidine incorporation; co-immunoprecipitation of FGF-2–fibrinogen; FGF-2 binding-deficient mutant control

    PMID:17949478

    Open questions at the time
    • Gamma-chain residues mediating FGF-2 binding not mapped
    • In vivo relevance of autocrine fibrinogen in tumor growth not demonstrated
  8. 2009 High

    The full-length human fibrinogen crystal structure at ~3.3 Å completed the atomic picture of the (AαBβγ)₂ hexamer, confirming gamma-chain domain orientation within the D region and revealing αC domain flexibility.

    Evidence X-ray crystallography of intact fibrinogen with post-diffraction biochemical validation

    PMID:19296670

    Open questions at the time
    • αC domains and γ' C-terminal extension not resolved
    • No structure of fibrinogen in complex with platelet integrin αIIbβ3
  9. 2019 Medium

    Showing that FGG overexpression promotes hepatocellular carcinoma invasion via Slug/ZEB1-driven EMT extended the cancer-relevant functions of FGG beyond proliferation to invasive behavior through a specific transcription-factor axis.

    Evidence FGG overexpression and siRNA knockdown in SK-HEP-1 cells; transwell invasion; Western blot for EMT markers

    PMID:30863175

    Open questions at the time
    • Upstream receptor or signaling pathway linking extracellular FGG to Slug/ZEB1 induction not identified
    • Findings limited to a single cell line
  10. 2026 Medium

    FGG was shown to drive cholestatic liver fibrosis through dual mechanisms—direct HSC activation and promotion of M2 macrophage polarization—with in vivo validation using targeted siFGG lipid nanoparticles, expanding FGG's pathological roles beyond hemostasis and cancer to fibrotic disease.

    Evidence BDL mouse model; LX2/THP-1 co-culture; FGG overexpression and siRNA knockdown in vivo via AEAA-LNP; RNA-seq and macrophage polarization assays

    PMID:42001119

    Open questions at the time
    • Receptor on HSCs through which FGG signals is not identified
    • Molecular mechanism linking FGG to M2 macrophage polarization not delineated
    • Findings from a single lab and model system

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of the gamma chain–αIIbβ3 integrin complex, the receptor and signaling pathway by which secreted FGG activates EMT and HSCs, and how oxidative post-translational modifications of fibrinogen modulate clot structure and disease risk.
  • No co-crystal structure of gamma chain bound to integrin αIIbβ3
  • No receptor identified for FGG on hepatic stellate cells or cancer cells driving EMT
  • Functional significance of oxidative PTMs on fibrinogen gamma chain in vivo undetermined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0048018 receptor ligand activity 3 GO:0098631 cell adhesion mediator activity 3
Localization
GO:0005576 extracellular region 5 GO:0031012 extracellular matrix 2
Pathway
R-HSA-109582 Hemostasis 5 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 1
Complex memberships
FGF-2–fibrinogen complexFibrinogen hexamer (AαBβγ)₂

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1984 The carboxy-terminal segment of the fibrinogen gamma chain (residues γ400–411, sequence HHLGGAKQAGDV) constitutes the platelet receptor recognition site. Synthetic peptides corresponding to this region inhibit fibrinogen binding to ADP- and thrombin-stimulated platelets in a dose-dependent manner; the lysine at γ406 and the histidines at γ400–401 are required for full inhibitory activity. Synthetic peptide inhibition of 125I-fibrinogen binding to ADP/thrombin-stimulated platelets; platelet aggregation assays Biochemistry High 6325435 6326808
1984 The γ-chain C-terminal peptide γ402–411 (GGAKQAGDV core) defines a common recognition site on activated platelets shared by fibrinogen, fibronectin, and von Willebrand factor; blocking the ε-amino group of lysine 406 abolishes inhibitory activity, demonstrating that this residue is critical for receptor recognition. Competitive inhibition of 125I-fibrinogen, 125I-fibronectin, and 125I-von Willebrand factor binding to thrombin/ADP-stimulated fixed platelets using synthetic gamma-chain peptides The Journal of biological chemistry High 6325435
1993 Fibrinogen mediates leukocyte adhesion to vascular endothelium through a novel pathway: fibrinogen binds ICAM-1 on endothelial cells (identified by affinity chromatography and direct binding to recombinant ICAM-1) and simultaneously engages leukocyte receptors, thereby bridging leukocytes to endothelium. This pathway is independent of the classical integrin αIIbβ3 platelet receptor. Affinity chromatography purification, genetically engineered transfectants expressing ICAM-1, direct binding studies to isolated recombinant ICAM-1, cell adhesion assays Cell High 8100742
1997 Crystal structure of a 30 kDa C-terminal fragment of the fibrinogen gamma chain resolved to 2.1–2.5 Å reveals three domains including a C-terminal fibrin-polymerization domain (P) containing a single calcium-binding site and a deep binding pocket that forms the polymerization surface. The C-terminal residues (containing the factor XIIIa crosslinking site and platelet receptor recognition site) are highly flexible, and the structure has a pronounced dipole moment proposed to electrostatically steer fibrin monomer alignment. X-ray crystallography (multiple isomorphous replacement, molecular replacement); three crystal forms Structure High 9016719
1997 Crystal structure of fragment D from human fibrinogen (2.9 Å) and its crosslinked double-D counterpart from fibrin (with Gly-Pro-Arg-Pro ligand mimicking the donor polymerization site) defined the structural basis of fibrin polymerization: the coiled-coil and two homologous globular entities of the D fragment are oriented at ~130° to each other, and the Gly-Pro-Arg-Pro peptide docks into a specific pocket in the gamma-chain globular domain. X-ray crystallography; molecular replacement with GPRPam peptide ligand Nature High 9333233
2000 The S. aureus MSCRAMM FnbpA is a bifunctional protein that binds fibrinogen in addition to fibronectin; the fibrinogen-binding activity resides in the N-terminal A region of FnbpA, which recognizes the C-terminal residues of the fibrinogen gamma chain — the same site targeted by ClfA. Surface plasmon resonance and fluorescence polarization quantified the dissociation constants for recombinant FnbpA with intact immobilized fibrinogen and with a synthetic C-terminal gamma-chain peptide. Recombinant protein expression, competitive binding assays, surface plasmon resonance, fluorescence polarization, overexpression in ClfA/ClfB-null S. aureus The Journal of biological chemistry High 10788510
2004 A nonsense mutation in FGG (Arg134Xaa), encoded by a split codon spanning exon 4–intron 4–exon 5, causes congenital afibrinogenemia in Lebanese patients. Expression studies in COS-7 cells showed the mutation does not affect mRNA splicing or stability but produces a severely truncated gamma chain that is unstable and not incorporated into the fibrinogen hexamer. Cell transfection (COS-7), RT-PCR (mRNA splicing/stability analysis), protein expression analysis Blood High 15284111
2005 A missense mutation W253C in the C-terminal globular domain of the fibrinogen gamma chain (fibrinogen Bratislava) causes hypofibrinogenemia by allowing intracellular hexamer assembly but completely blocking secretion. Co-expression of mutant FGG with wild-type FGA and FGB cDNAs in cells showed that mutant-containing hexamers assemble normally but are not secreted, demonstrating that the gamma-chain globular domain contributes to the secretion step independently of hexamer assembly. Co-expression of mutant and wild-type fibrinogen chain cDNAs in mammalian cells; ELISA of conditioned medium and cell lysates Journal of medical genetics High 16141000
2005 The FGG-H2 haplotype (tagged by SNP 10034C/T, rs2066865) reduces DVT risk through a specific molecular mechanism: the T allele strengthens a CstF polyadenylation site, favoring production of the γA chain over the γ' chain. Reduced fibrinogen γ' levels (which contains a unique high-affinity nonsubstrate thrombin-binding site critical for antithrombin-1 activity during fibrin formation) increases thrombosis risk ~2.4-fold in homozygotes. Population-based case-control study (Leiden Thrombophilia Study) with haplotype-tagging SNPs; fibrinogen γ' quantification; multivariate analysis Blood Medium 16144795
2007 Cancer cells (prostate DU-145, PC-3; lung A549) synthesize fibrinogen endogenously; fibrinogen augments FGF-2-stimulated cell proliferation through direct FGF-2–fibrinogen interaction. RNAi-mediated knockdown of FGG in A549 and PC-3 cells reduced fibrinogen protein production and inhibited DNA synthesis by ~60%, which was rescued by exogenous fibrinogen. FGF-2 and fibrinogen were co-immunoprecipitated from conditioned medium as a soluble complex. RNAi knockdown of FGG; [3H]-thymidine incorporation proliferation assay; co-immunoprecipitation; metabolic labeling with fluorography; FGF-2 mutant lacking fibrinogen-binding affinity Journal of thrombosis and haemostasis High 17949478
2009 Crystal structure of full-length human fibrinogen determined at ~3.3 Å resolution, revealing the complete hexameric (AαBβγ)2 architecture including coiled-coil regions, D and E domains. The structure adds to understanding of γ-chain domain orientation and shows prominent carbohydrate groups on β chains; αC domains lacked resolvable electron density, indicating flexibility in solution. X-ray crystallography; SDS-PAGE and N-terminal sequencing of post-diffraction crystals Biochemistry High 19296670
2010 An FGG IVS3-2A>G splice-site mutation causes hypofibrinogenemia by generating aberrant mRNA transcripts: the major aberrant product retains intron 3, while a minor product uses a cryptic splice site in exon 4. These aberrant transcripts are predicted to be degraded before translation or to yield variant chains that undergo intracellular quality-control degradation. Minigene transfection into CHO cells; RT-PCR with agarose gel electrophoresis; nucleotide sequencing of aberrant transcripts Clinica chimica acta Medium 20580695
2013 Nonsense-mediated mRNA decay (NMD) is the primary mechanism underlying hypofibrinogenemia caused by FGG truncating mutations. For both γ23X (frameshift, exon 3) and γ376X (nonsense, exon 9) mutations, mRNA levels were reduced compared to wild-type; cycloheximide (NMD inhibitor) dose-dependently restored mutant mRNA levels. The γ376X truncated chain was detectable in cell lysates but not in secreted fibrinogen, while γ23X chain was undetectable (fully NMD-degraded). Minigene transfection into CHO cells; real-time quantitative RT-PCR; cycloheximide NMD inhibition assay; ELISA of medium and cell lysates; immunoblot Thrombosis research High 24011387
2016 Compound heterozygous FGG mutations (IVS-8 deep intronic deletion and Ex-9 deletion affecting the γ' splice variant) cause hypodysfibrinogenemia through distinct mechanisms: the IVS-8 deletion produces both normal and unspliced transcripts, with unspliced products likely degraded by NMD leading to hypofibrinogenemia; the Ex-9 deletion abolishes normal γA and γ' chain production but generates an aberrant γ'409ΔA chain that is secreted more efficiently than normal fibrinogen, contributing to dysfibrinogenemia. Minigene transfection into CHO cells; RT-PCR; establishment of stable CHO cell line expressing γ'409ΔA recombinant variant; secretion assay Thrombosis research Medium 27837696
2019 FGG promotes hepatocellular carcinoma cell migration and invasion through activation of the epithelial-to-mesenchymal transition (EMT) signaling pathway, specifically by upregulating the transcription factors Slug and ZEB1. Overexpression of FGG in SK-HEP-1 cells enhanced migration and invasion, while FGG knockdown inhibited these phenotypes; EMT marker expression (E-cadherin, vimentin, Slug, ZEB1) changed concordantly. FGG overexpression and siRNA knockdown in SK-HEP-1 cells; transwell invasion assay; wound-healing assay; Western blot for EMT markers (Slug, ZEB1, E-cadherin, vimentin) Cancer management and research Medium 30863175
2020 FGG contributes to anthracycline (epirubicin) chemoresistance in breast cancer cells through the JAK2/STAT3 signaling pathway. Ligustrazine reversed epirubicin resistance by inhibiting JAK2/STAT3 signaling and reducing FGG expression; FGG-expressing tumor cells showed decreased response to anthracycline-based chemotherapy, and the compound eliminated cancer stem cells in resistant cells. Cell viability/drug resistance assays; JAK2/STAT3 pathway inhibition; FGG knockdown; cancer stem cell assays; clinical correlation in breast cancer tissues American journal of cancer research Low 32266101
2022 A novel FGG c.8G>A mutation in the gamma-chain signal peptide causes hypofibrinogenemia associated with thrombosis. Functional analysis showed normal fibrin polymerization kinetics but reduced maximal absorbance, prolonged fibrinolysis, and structurally altered clot architecture by scanning electron microscopy. Mass spectrometry identified multiple oxidative post-translational modifications of fibrinogen in the patient, suggesting a combined effect of the signal peptide mutation and oxidative PTMs on fibrinogen function. Fibrin polymerization assay; fibrinolysis assay; scanning electron microscopy; mass spectrometry (PTM analysis); reptilase clotting assay Blood coagulation & fibrinolysis Medium 35067535
2022 A 403 bp duplication of the FGG exon 8–intron 8 junction causes congenital afibrinogenemia by disrupting mRNA splicing. Because the duplication duplicates the intron 8 donor splice site, it generates multiple aberrant FGG transcripts containing premature termination codons, as demonstrated by minigene transfection analysis. Whole exome sequencing; PCR amplification and sequencing; minigene transfection into mammalian cells; mRNA splicing analysis Haematologica Medium 34196169
2024 A novel heterozygous missense mutation FGG c.1168G>T impairs fibrinogen synthesis, secretion, and polymerization. Recombinant fibrinogen expression in CHO cells showed reduced protein in medium (impaired secretion) and cell lysates (impaired synthesis); thrombin-catalyzed polymerization was defective. In silico analysis indicated the mutation disrupts a hydrogen bond and impairs the 'A:a' polymerization knob-hole interaction. Recombinant CHO cell expression system; Western blotting; ELISA of medium and lysates; thrombin-catalyzed fibrin polymerization assay; in silico molecular modeling Hereditas Medium 38233949
2026 FGG promotes cholestatic liver fibrosis through two parallel mechanisms: direct activation of hepatic stellate cells (HSCs) and promotion of macrophage polarization toward the M2 phenotype. In BDL mice, FGG was upregulated and localized to activated HSCs. FGG overexpression promoted liver fibrosis in vivo; co-culture experiments showed FGG drove M2 macrophage polarization. Targeted delivery of siFGG via AEAA-modified lipid nanoparticles inhibited HSC activation and HSC–M2 macrophage crosstalk, alleviating BDL-induced fibrosis. BDL mouse model; LX2/THP-1 co-culture; FGG overexpression in vivo; siRNA knockdown via AEAA-LNP nanoparticles; RNA-seq; qRT-PCR; Western blot; immunofluorescence; macrophage polarization assays Journal of nanobiotechnology Medium 42001119

Source papers

Stage 0 corpus · 74 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1999 Characterization of single-nucleotide polymorphisms in coding regions of human genes. Nature genetics 1381 10391209
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2008 Large-scale proteomics and phosphoproteomics of urinary exosomes. Journal of the American Society of Nephrology : JASN 607 19056867
1984 Fibrinogen and fibrin. Annual review of biochemistry 600 6383194
1984 Platelet receptor recognition site on human fibrinogen. Synthesis and structure-function relationship of peptides corresponding to the carboxy-terminal segment of the gamma chain. Biochemistry 464 6326808
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2007 Systematic analysis of the protein interaction network for the human transcription machinery reveals the identity of the 7SK capping enzyme. Molecular cell 367 17643375
1997 Crystal structures of fragment D from human fibrinogen and its crosslinked counterpart from fibrin. Nature 360 9333233
2005 Human plasma N-glycoproteome analysis by immunoaffinity subtraction, hydrazide chemistry, and mass spectrometry. Journal of proteome research 350 16335952
1993 Fibrinogen mediates leukocyte adhesion to vascular endothelium through an ICAM-1-dependent pathway. Cell 315 8100742
1980 Studies on synthetic peptides that bind to fibrinogen and prevent fibrin polymerization. Structural requirements, number of binding sites, and species differences. Biochemistry 294 7356959
2006 p130Cas: a versatile scaffold in signaling networks. Trends in cell biology 266 16581250
2009 Crystal structure of human fibrinogen. Biochemistry 258 19296670
1984 Evidence that three adhesive proteins interact with a common recognition site on activated platelets. The Journal of biological chemistry 253 6325435
1983 Covalent structure of fibrinogen. Annals of the New York Academy of Sciences 241 6575689
2000 The fibronectin-binding MSCRAMM FnbpA of Staphylococcus aureus is a bifunctional protein that also binds to fibrinogen. The Journal of biological chemistry 227 10788510
1999 Fibrinogen. The international journal of biochemistry & cell biology 223 10467729
2013 Congenital fibrinogen disorders: an update. Seminars in thrombosis and hemostasis 218 23852822
1997 Crystal structure of a 30 kDa C-terminal fragment from the gamma chain of human fibrinogen. Structure (London, England : 1993) 216 9016719
2005 Genetic variation in the fibrinogen gamma gene increases the risk for deep venous thrombosis by reducing plasma fibrinogen gamma' levels. Blood 211 16144795
2014 Extracellular matrix signatures of human primary metastatic colon cancers and their metastases to liver. BMC cancer 203 25037231
2007 Fibrinogen synthesized by cancer cells augments the proliferative effect of fibroblast growth factor-2 (FGF-2). Journal of thrombosis and haemostasis : JTH 187 17949478
2017 Characterization of the Extracellular Matrix of Normal and Diseased Tissues Using Proteomics. Journal of proteome research 185 28675934
1999 Signaling through platelet integrin alpha IIb beta 3: inside-out, outside-in, and sideways. Thrombosis and haemostasis 179 10605720
2001 Molecular analysis of the fibrinogen gene cluster in 16 patients with congenital afibrinogenemia: novel truncating mutations in the FGA and FGG genes. Human genetics 62 11354637
2020 Genetic Variants in the FGB and FGG Genes Mapping in the Beta and Gamma Nodules of the Fibrinogen Molecule in Congenital Quantitative Fibrinogen Disorders Associated with a Thrombotic Phenotype. International journal of molecular sciences 54 32610551
2009 Abnormal expression of fibrinogen gamma (FGG) and plasma level of fibrinogen in patients with hepatocellular carcinoma. Anticancer research 52 19596924
2019 FGG promotes migration and invasion in hepatocellular carcinoma cells through activating epithelial to mesenchymal transition. Cancer management and research 41 30863175
2007 The fibrinogen gamma (FGG) 10034C>T polymorphism is associated with venous thrombosis. Thrombosis research 35 17445871
2019 FGB and FGG derived from plasma exosomes as potential biomarkers to distinguish benign from malignant pulmonary nodules. Clinical and experimental medicine 31 31576477
2004 Expression and analysis of a split premature termination codon in FGG responsible for congenital afibrinogenemia: escape from RNA surveillance mechanisms in transfected cells. Blood 26 15284111
2005 Hypofibrinogenaemia caused by a novel FGG missense mutation (W253C) in the gamma chain globular domain impairing fibrinogen secretion. Journal of medical genetics 25 16141000
2020 Ligustrazine reverts anthracycline chemotherapy resistance of human breast cancer by inhibiting JAK2/STAT3 signaling and decreasing fibrinogen gamma chain (FGG) expression. American journal of cancer research 14 32266101
2013 Nonsense-mediated mRNA decay was demonstrated in two hypofibrinogenemias caused by heterozygous nonsense mutations of FGG, Shizuoka III and Kanazawa II. Thrombosis research 14 24011387
1993 The gamma fibrinogen gene (FGG) maps to chromosome 17 in both cattle and sheep. Cytogenetics and cell genetics 14 8428520
2012 A novel regulatory element between the human FGA and FGG genes. Thrombosis and haemostasis 13 22836734
2016 Construction of supramolecular polymer by enzyme-triggered covalent condensation of CB[8]-FGG-based supramonomer. Chemical communications (Cambridge, England) 10 26686377
2017 The amplitude of coagulation curves from thrombin time tests allows dysfibrinogenemia caused by the common mutation FGG-Arg301 to be distinguished from hypofibrinogenemia. International journal of laboratory hematology 9 28318107
2010 In vitro transcription of compound heterozygous hypofibrinogenemia Matsumoto IX; first identification of FGB IVS6 deletion of 4 nucleotides and FGG IVS3-2A>G causing abnormal RNA splicing. Clinica chimica acta; international journal of clinical chemistry 9 20580695
2006 Fibrinogen Seoul (FGG Ala341Asp): a novel mutation associated with hypodysfibrinogenemia. Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis 8 16959688
2018 Cortical atrophy and hypofibrinogenemia due to FGG and TBCD mutations in a single family: a case report. BMC medical genetics 7 29769041
2016 Genetic analyses of novel compound heterozygous hypodysfibrinogenemia, Tsukuba I: FGG c.1129+62_65 del AATA and FGG c.1299+4 del A. Thrombosis research 7 27837696
2016 Thrombosis Related ABO, F5, MTHFR, and FGG Gene Polymorphisms in Morbidly Obese Patients. Disease markers 7 27999448
2023 Factor VII R353Q (rs6046), FGA A6534G (rs6050), and FGG C10034T (rs2066865) Gene Polymorphisms and Risk of Recurrent Pregnancy Loss in Iranian Women. Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion 6 38708173
2022 Thrombosis-associated hypofibrinogenemia: novel abnormal fibrinogen variant FGG c.8G>A with oxidative posttranslational modifications. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 6 35067535
2019 Polymorphism rs2066865 in the Fibrinogen Gamma Chain (FGG) Gene Increases Plasma Fibrinogen Concentration and Is Associated with an Increased Microvascular Thrombosis Rate. Medicina (Kaunas, Lithuania) 6 31484330
2023 Spatial transcriptomics reveals the heterogeneity and FGG+CRP+ inflammatory cancer-associated fibroblasts replace islets in pancreatic ductal adenocarcinoma. Frontiers in oncology 5 37124494
2009 Recurrence of the 'deep-intronic' FGG IVS6-320A>T mutation causing quantitative fibrinogen deficiency in the Italian population of Veneto. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 4 19551918
2008 The role of weakly polar and H-bonding interactions in the stabilization of the conformers of FGG, WGG, and YGG: an aqueous phase computational study. Biopolymers 4 18615659
2004 [Cloning and identification of fibrinogen gamma polypeptide (FGG) gene differentially expressed in human hepatocellular carcinoma]. Ai zheng = Aizheng = Chinese journal of cancer 4 15025951
2024 The FGG c.952G>A variant causes congenital dysfibrinogenemia characterized by recurrent cerebral infarction: a case report. Frontiers in neurology 3 38327620
2024 A novel missense mutation (FGG c.1168G > T) in the gamma chain of fibrinogen causing congenital hypodysfibrinogenemia with bleeding phenotype. Hereditas 2 38233949
2022 A homozygous duplication of the <I>FGG</i> exon 8-intron 8 junction causes congenital afibrinogenemia. Lessons learned from the study of a large consanguineous Turkish family. Haematologica 2 34196169
2021 [Congenital Fibrinogen Deficiency Caused by Novel FGG Gene Mutation]. Zhongguo shi yan xue ye xue za zhi 2 33812435
2019 Fibrinogen Columbus II: A novel c.1075G>T mutation in the FGG gene causing hypodysfibrinogenemia and thrombosis in an adolescent male. Pediatric blood & cancer 2 31131962
2025 A familial study of a de novo FGG gene mutation causing congenital hypofibrinogenaemia and intervention during pregnancy and childbirth. Scientific reports 1 40025073
2025 Hereditary hepatic fibrinogen storage disease with a novel fibrinogen variant FGG c.1113T>A ( fibrinogen Seoul III ). Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 1 40501422
2025 Genetic Associations of ITGB3, FGG, GP1BA, PECAM1, and PEAR1 Polymorphisms and the Platelet Activation Pathway with Recurrent Pregnancy Loss in the Korean Population. International journal of molecular sciences 1 40806633
2024 A novel mutation in the FGG gene causes hypofibrinogenemia in a Chinese family. Hereditas 1 38374144
2026 Congenital hypofibrinogenemia with bleeding risk: mutations in the FGA, FGB, and FGG genes. Laboratory medicine 0 41233956
2026 Tuning the Viscoelasticity of Supramolecular Alginate Hydrogels via Homoternary FGG-Peptide-Cucurbit[8]uril Complexes. Biomacromolecules 0 41499360
2026 Targeting FGG alleviates cholestatic fibrosis by inhibiting hepatic stellate cell activation and regulating macrophage homeostasis. Journal of nanobiotechnology 0 42001119
2025 Implications of the c.1201C > G (p.Arg401Gly) mutation in FGG gene on fibrinogen stability and function. Frontiers in medicine 0 41030265
2024 Case Report: Laboratory detection of a thrombotic tendency in a family with hypodysfibrinogenemia and a novel FGG mutation. Frontiers in cardiovascular medicine 0 39473893
2023 [Genetic analysis of a Chinese pedigree affected with Congenital dysfibrinogenemia due to variant of FGG gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 37906135
2020 [A case of inherited afibrinogenemia caused by an IVS7-12A>G splice mutation of FGG gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 33306830
2018 [Mutation analysis of a FGG gene causing hereditary abnormal fibrinogen]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 30512152
2015 [Congenital hypofibrinogenemia associated with a novel mutation in FGG gene]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 26037343