Affinage

ITGB3

Integrin beta-3 · UniProt P05106

Round 2 corrected
Length
788 aa
Mass
87.1 kDa
Annotated
2026-04-28
130 papers in source corpus 43 papers cited in narrative 42 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ITGB3 (integrin β3/GPIIIa/CD61) is a transmembrane adhesion receptor subunit that heterodimerizes with αIIb or αV to form the major platelet fibrinogen receptor (αIIbβ3) and the vitronectin receptor (αVβ3), mediating cell adhesion, migration, hemostasis, angiogenesis, and outside-in signaling through RGD-containing and RGD-independent extracellular matrix ligands. Crystal structures of the αVβ3 ectodomain reveal a bent, low-affinity resting conformation stabilized by the long-range Cys5–Cys435 disulfide bond; RGD-ligand binding at the α/β subunit interface triggers divalent-cation rearrangements at the β3 MIDAS site and a piston-like displacement of the α7-helix that propagates through the hybrid and PSI domains to extend the integrin into a high-affinity state, while talin FERM-domain binding to the membrane-proximal NPxY motif of the β3 cytoplasmic tail constitutes the principal inside-out activation event (PMID:11546839, PMID:11884718, PMID:15378069, PMID:12535520, PMID:12200372). The β3 cytoplasmic tail constitutively associates with c-Src (via SH3 domain) and Csk; ligand-induced integrin clustering displaces Csk, activates Src, and sequentially recruits Syk, initiating FAK/PI3K/Akt signaling, Vav/SLP-76 phosphorylation, and actin cytoskeletal reorganization required for platelet spreading, cell migration, and survival (PMID:14593208, PMID:11940607, PMID:8837777). Loss-of-function mutations in ITGB3 cause Glanzmann thrombasthenia through impaired αIIbβ3 surface expression and fibrinogen binding (PMID:1967954, PMID:10233432).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1987 High

    Cloning the GPIIIa cDNA established the primary structure of β3 integrin — a cysteine-rich extracellular domain, single transmembrane segment, and short cytoplasmic tail — and revealed homology to the fibronectin receptor β subunit, placing it in the integrin superfamily.

    Evidence cDNA cloning and sequencing from endothelial cell library

    PMID:3494014

    Open questions at the time
    • No tertiary structure information
    • Functional role of individual cysteine-rich repeats unknown
  2. 1990 High

    Site-directed mutagenesis of Asp119 and identification of disease-causing ITGB3 mutations established that divalent-cation coordination in the β3 ectodomain is essential for ligand binding and that ITGB3 gene defects cause Glanzmann thrombasthenia through diverse molecular mechanisms.

    Evidence Mutagenesis with ligand-binding assays; Southern/Northern blotting in GT families; disulfide-bond mapping by mass spectrometry

    PMID:1967954 PMID:2001252 PMID:2392682

    Open questions at the time
    • Atomic-resolution structure of the ligand-binding site not yet available
    • No systematic genotype-phenotype correlation for GT variants
  3. 1996 High

    Functional studies defined αVβ3 as the critical integrin for smooth muscle cell and endothelial cell migration toward matrix ligands (vitronectin, osteopontin), with PAI-1 acting as a physiological competitor that regulates αVβ3-dependent motility.

    Evidence Boyden chamber migration assays with anti-αVβ3 blocking antibodies and PAI-1 variant competition

    PMID:7532190 PMID:8837777

    Open questions at the time
    • Intracellular signaling pathways downstream of αVβ3-dependent migration not yet dissected
    • Relative contributions of αVβ3 vs αVβ5 in different vascular beds unclear
  4. 1999 High

    Discovery that αVβ3 physically associates with VEGFR-2 and enhances its phosphorylation revealed integrin-growth factor receptor crosstalk (transactivation) as a mechanism amplifying angiogenic signaling.

    Evidence Co-immunoprecipitation of β3 with phospho-VEGFR-2 plus anti-β3 antibody blockade in endothelial cells

    PMID:10022831

    Open questions at the time
    • Structural basis for β3–VEGFR-2 association unknown
    • Whether transactivation extends to other RTKs not tested
  5. 2001 High

    The crystal structure of the αVβ3 ectodomain revealed the severely bent resting conformation and the MIDAS site in the βA domain, providing the first atomic framework for understanding integrin conformational regulation.

    Evidence X-ray crystallography at 3.1 Å resolution

    PMID:11546839

    Open questions at the time
    • No ligand-bound structure yet
    • Relationship between bent conformation and activation state on the cell surface unresolved
  6. 2002 High

    The RGD-ligand co-crystal structure and mutagenesis of the Cys5–Cys435 disulfide bond together defined the structural basis for ligand recognition and allosteric activation: RGD contacts both subunits and induces cation rearrangements, while disruption of the long-range disulfide constitutively activates αIIbβ3, linking redox regulation to integrin affinity.

    Evidence X-ray crystallography of αVβ3–RGD complex; Cys-to-Ala mutagenesis with PAC-1 binding and FAK phosphorylation assays

    PMID:11884718 PMID:12200372

    Open questions at the time
    • Full-length integrin structure including transmembrane and cytoplasmic domains unavailable
    • How thiol-disulfide exchange occurs on the platelet surface in vivo not established
  7. 2002 High

    Dissection of the Src-Csk-Syk signaling cascade on the β3 cytoplasmic tail — Src and Csk constitutively bound, Csk displaced upon fibrinogen engagement, Syk recruited sequentially — established the molecular order of outside-in signaling events leading to platelet spreading.

    Evidence Co-immunoprecipitation in Src-family and Syk-deficient platelets with phosphorylation and spreading assays

    PMID:11940607 PMID:14593208

    Open questions at the time
    • Stoichiometry of kinase occupancy on individual β3 tails unknown
    • Role of additional adaptor proteins (e.g. Gab1, Grb2) at this complex not characterized
  8. 2003 High

    The crystal/NMR structure of the talin FERM domain bound to the β3 cytoplasmic tail NPxY motif defined the structural basis for inside-out activation and enabled engineering of dominant-negative talin variants, establishing talin binding as the final common step in integrin activation.

    Evidence Crystal structure and NMR of talin FERM–β3 tail complex plus structure-based mutagenesis with PAC-1 activation assays

    PMID:12535520 PMID:17218263

    Open questions at the time
    • How kindlin cooperates with talin at the β3 tail not structurally resolved
    • Membrane lipid contributions to activation not fully defined
  9. 2004 High

    Crystal structures of multiple αIIbβ3 conformational states and drug complexes revealed the full allosteric pathway: α7-helix piston displacement, 62° hybrid-domain swing, and 70 Å knee separation converting bent-to-extended conformations, and defined the binding modes of clinical antiplatelet drugs eptifibatide and tirofiban.

    Evidence X-ray crystallography of αIIbβ3 in multiple conformers and drug co-crystals

    PMID:15378069

    Open questions at the time
    • Dynamics of conformational change on live platelet membranes not captured
    • How transmembrane domain separation couples to ectodomain extension unresolved
  10. 2007 High

    The uPAR–αVβ3 axis was shown to activate Cdc42/Rac1 in podocytes, causing foot process effacement and proteinuria, extending β3 integrin function beyond hemostasis and migration to kidney pathobiology.

    Evidence Plaur−/− mice, constitutively active β3 knockin, small GTPase activation assays, proteinuria measurements

    PMID:18084301

    Open questions at the time
    • Lipid-dependent mechanism of uPAR-mediated β3 activation not structurally defined
    • Whether this pathway operates in human glomerular disease not directly tested
  11. 2019 Medium

    An ITGB3 promoter variant (rs55827077) was shown to enhance transcription during megakaryocyte differentiation, increasing platelet β3 levels and SERT trafficking to the plasma membrane, thereby elevating blood serotonin — linking ITGB3 regulatory variation to serotonin homeostasis and autism-related phenotypes.

    Evidence Luciferase reporter assays in differentiating hematopoietic cell lines, SERT trafficking assay, cohort analysis in 176 autistic individuals

    PMID:30535103

    Open questions at the time
    • Causal relationship in autism not demonstrated by Mendelian genetics
    • Molecular mechanism linking β3 surface level to SERT trafficking incompletely defined
    • Independent replication in larger cohorts needed
  12. 2020 Medium

    In melanoma tumor-repopulating cells, ITGB3 activates a c-Src/STAT3 axis that transcriptionally represses RIG-I, conferring resistance to IFN-α-induced apoptosis — revealing a non-adhesive, immune-evasion function for β3 integrin in tumors.

    Evidence Co-immunoprecipitation, ChIP-qPCR of STAT3 at RIG-I promoter, siRNA knockdown, in vivo tumor model

    PMID:32152220

    Open questions at the time
    • Whether this signaling axis operates in non-melanoma tumor types unknown
    • Direct binding partner mediating ITGB3-Src engagement in these tumor cells not mapped
  13. 2022 Medium

    Itgb3 haploinsufficiency was shown to shift mGluR5 from synaptic to extra-synaptic signaling, impairing cortical network excitability; CRISPR-mediated Itgb3 restoration rescued the phenotype, establishing ITGB3 gene dosage as a determinant of glutamatergic synapse function relevant to ASD.

    Evidence Itgb3 heterozygous mice, electrophysiology, mGluR5 signaling assays, CRISPR activation, pharmacological rescue with MPEP

    PMID:36035754

    Open questions at the time
    • Physical interaction between β3 integrin and mGluR5 not structurally defined
    • Translation to human ASD not validated
    • Mechanism by which β3 controls mGluR5 synaptic localization unknown
  14. 2024 Medium

    Transient CD61 (β3 integrin) expression on tumor-infiltrating T cells was found to pair with CD103 at TCR synaptic microclusters, modulating TCR signaling and enhancing antitumor cytotoxicity — extending β3 function to adaptive immune synapse regulation.

    Evidence Flow cytometry, confocal imaging of synaptic microclusters, TCR signaling and cytotoxicity assays, in vivo tumor models

    PMID:38561495

    Open questions at the time
    • α-subunit partner for β3 on T cells not conclusively identified
    • Mechanism of transient β3 upregulation on TILs undefined
    • Independent confirmation in human clinical samples needed

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length structure of αIIbβ3 or αVβ3 including transmembrane and cytoplasmic domains in a lipid bilayer, the precise mechanism by which β3 integrin controls mGluR5 synaptic localization, and whether β3's immune-modulatory functions on T cells are therapeutically targetable remain unresolved.
  • No full-length integrin structure in a membrane environment
  • Molecular basis of β3-mGluR5 interaction uncharacterized
  • Clinical relevance of CD61 on tumor-infiltrating T cells not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098631 cell adhesion mediator activity 8 GO:0005198 structural molecule activity 3 GO:0060089 molecular transducer activity 3
Localization
GO:0005886 plasma membrane 6 GO:0005576 extracellular region 3
Pathway
R-HSA-162582 Signal Transduction 8 R-HSA-109582 Hemostasis 6 R-HSA-1474244 Extracellular matrix organization 5 R-HSA-1500931 Cell-Cell communication 3 R-HSA-1643685 Disease 2 R-HSA-168256 Immune System 1
Partners
CSKPLAURSRCSYKTGM2THY1TLN1VEGFR2
Complex memberships
αIIbβ3 (GPIIb-IIIa)αVβ3 (vitronectin receptor)

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1987 Protein sequence of GPIIIa (ITGB3) was derived from an endothelial cell cDNA clone, establishing identity between endothelial and platelet forms of GPIIIa and revealing structural features: a long extracellular domain with cysteine-rich tandem repeats, a 29-residue transmembrane segment, and a short cytoplasmic domain, with 47% homology to the integrin fibronectin receptor. cDNA cloning and sequencing, oligonucleotide probing of cDNA library The Journal of biological chemistry High 3494014
1989 The PlA1/PlA2 (HPA-1a/1b) alloantigenic system on GPIIIa is caused by a single C-to-T polymorphism at base 196 of the GPIIIa cDNA, resulting in a leucine33/proline33 amino acid polymorphism near the N-terminus. PCR amplification and nucleotide sequencing of GPIIIa cDNA from PlA1 and PlA2 homozygous individuals, followed by NciI restriction enzyme analysis The Journal of clinical investigation High 2565345
1990 A point mutation causing Asp119→Tyr119 substitution in the β3 subunit abolishes ligand binding and alters divalent cation-dependent conformation of αIIbβ3, implicating this residue—in a conserved oxygenated-residue region analogous to EF-hand calcium-binding motifs—in divalent cation-mediated ligand recognition. Site-directed mutagenesis, ligand binding assay, conformational antibody binding assay Science (New York, N.Y.) High 2392682
1990 GPIIIa (but not GPIIb) is phosphorylated on tyrosine by pp60c-src in platelet membranes; a synthetic peptide from the cytoplasmic domain of GPIIIa was phosphorylated by immunopurified pp60c-src, identifying a tyrosine phosphorylation site in the cytoplasmic tail. In vitro phosphorylation of platelet subcellular fractions, anti-phosphotyrosine immunoprecipitation, synthetic peptide phosphorylation assay with immunopurified pp60c-src FEBS letters Medium 2119315
1990 GPIIb and GPIIIa amino acid sequences confirmed from megakaryocyte cDNA libraries, establishing that megakaryocyte-derived sequences differ at specific nucleotide positions from HEL cell-derived sequences, with one difference in GPIIb at position 633 (Cys in megakaryocyte vs. Ser in HEL cells). cDNA library screening and sequencing from human megakaryocytes Molecular biology reports Medium 2345548
1991 Complete disulfide bond assignment of human GPIIIa identified distinct structural domains: an N-terminal domain (residues 1–62), an adhesive-protein-binding domain (101–422), a cysteine-rich proteinase-resistant core (423–622), and a C-terminal domain; two long-range disulfide bonds join Cys5–Cys435 and Cys406–Cys655, linking the N-terminus to the core and the fibrinogen-binding domain to the extracellular C-terminal domain, providing a structural basis for the integrin β-subunit fold applicable to all β-subunit family members. Protein chemical analysis (peptide mapping, disulfide bond mapping by mass spectrometry/amino acid sequencing) The Biochemical journal High 2001252
1990 Identification of an insertional mutation in the GPIIIa gene causing absence of GPIIIa mRNA in Glanzmann's thrombasthenia, demonstrating that ITGB3 gene defects cause GT through diverse mechanisms and that platelet RNA can be used for mRNA analysis. Southern blotting with GPIIIa cDNA probes, Northern blotting, restriction fragment length polymorphism analysis Blood High 1967954
1994 The Sra alloantigen system of GPIIIa is caused by a C2004→T substitution leading to an Arg636→Cys polymorphism within the cysteine-rich region; the unpaired cysteine alters N-linked glycosylation of the extracellular domain but does not affect GPIIb-IIIa surface expression or adhesive function. PCR amplification and sequencing of GPIIIa mRNA, recombinant allele-specific GPIIIa expression, alloantibody reactivity assays, glycosylation analysis (EndoH treatment) The Journal of biological chemistry High 8132570
2001 Crystal structure of the extracellular segment of integrin αVβ3 at 3.1 Å revealed that its 12 domains assemble into an ovoid head and two tails; the main inter-subunit interface lies between the αV β-propeller and the β3 βA (A) domain bearing a MIDAS (metal ion-dependent adhesion site); the ectodomain adopts a severely bent conformation suggesting flexibility linked to regulation. X-ray crystallography at 3.1 Å Science (New York, N.Y.) High 11546839
2002 Crystal structure of the extracellular segment of αVβ3 in complex with an Arg-Gly-Asp cyclic peptide showed that the ligand binds at the αV/β3 subunit interface making contacts with both subunits; ligand binding induces acquisition of two cations in the βA (β3) domain—one contacting the ligand Asp directly—and causes tertiary rearrangements in the βA domain and small quaternary changes in αV–β3 orientation. X-ray crystallography of αVβ3–RGD ligand co-crystal Science (New York, N.Y.) High 11884718
2002 Disruption of the long-range Cys5–Cys435 disulfide bond in GPIIIa (β3) by Cys5Ala or Cys435Ala substitution produces constitutively active αIIbβ3 complexes that bind LIBS antibodies, fibrinogen-mimetic antibodies (PAC-1, Pl-55), and soluble fibrinogen without activation, and that mediate FAK phosphorylation on adhesion; this provides a molecular basis for reduction-mediated activation of αIIbβ3. Site-directed mutagenesis, CHO cell transfection, conformational antibody binding (LIBS, PAC-1), soluble fibrinogen binding, immobilized fibrinogen adhesion, FAK phosphorylation assay Blood High 12200372
2003 c-Src binds constitutively and selectively to β3 integrins (not β1, β2) via an interaction involving the c-Src SH3 domain and the carboxyl-terminal region of the β3 cytoplasmic tail; integrin β3 clustering activates c-Src and induces Tyr-418 phosphorylation, which drives adhesion-dependent Syk phosphorylation. Co-immunoprecipitation, domain mapping with SH2/SH3 mutants, in-cell kinase activation assays, phosphorylation assays in CHO and platelet systems Proceedings of the National Academy of Sciences of the United States of America High 14593208
2003 Talin FERM domain binds the membrane-proximal segment of the β3 integrin cytoplasmic tail via a PTB-domain/NPxY motif interaction; specific contacts identified by crystal structure and NMR; structure-based mutations that retain binding but abolish activation were used to engineer dominant-negative talin, establishing this interaction as the structural basis for talin-mediated integrin activation. Crystal structure of talin FERM–β3 tail complex, NMR, mutagenesis, integrin activation assays Molecular cell High 12535520
2004 Crystal structures of αIIbβ3 ectodomain defined the atomic basis for allosteric regulation: allostery in the β3 I (βA) domain alters three metal-binding sites and associated loops, causing 62° reorientation between the β3 I and hybrid domains; piston-like α7-helix displacement propagates through the PSI domain to cause 70 Å separation between α and β leg knees, converting the integrin from bent low-affinity to extended high-affinity conformation. Fibrinogen-mimetic therapeutics (eptifibatide, tirofiban) bind at the ligand-binding interface. X-ray crystallography of multiple αIIbβ3 conformational states and drug complexes Nature High 15378069
2007 Talin activates integrins through a specific interaction between the talin PTB domain and the membrane-proximal segment of the β3 cytoplasmic domain; NMR structure of the talin–β3 complex and structure-based mutagenesis identified key contacts required for activation, and talin variants engineered to bind β3 without activating it blocked activation by competing with endogenous talin. NMR structure determination of talin–β3 complex, site-directed mutagenesis, integrin activation assay (PAC-1 binding) Cell High 17218263
2002 Quinine-dependent drug-dependent antibodies (DDAbs) that cause immune thrombocytopenia bind at a specific 17-amino acid sequence within the hybrid and PSI homology domains of GPIIIa (β3), and disulfide bonds are required to stabilize the target epitope; this region is a favored target for quinine-dependent DDAbs. Human/rat GPIIIa chimeras, site-directed mutagenesis, monoclonal antibody blocking with AP3, drug-dependent antibody binding assays Blood High 12393510 17959856
1998 Truncation of GPIIIa at residue 616 (Glu616→Stop) prevents its heterodimerization with GPIIb and surface expression; pulse-chase and immunoprecipitation in cotransfected cells showed no maturation of GPIIb and no complex formation, establishing that the GPIIIa sequence from Glu616 to Thr762 is essential for αIIbβ3 complex formation. Pulse-chase metabolic labeling, co-immunoprecipitation, cell surface expression assay in transiently transfected cells Blood High 9845537
1999 αVβ3 integrin on the platelet surface mediates serotonin transporter (SERT) trafficking; ITGB3 Leu33Pro (PlA1/A2) polymorphism is associated with increased platelet aggregability to epinephrine, implicating molecular variants of GPIIIa in regulating platelet reactivity in vivo. Population-based genotyping (PCR-RFLP), Born method platelet aggregation phenotyping in 1422 subjects with covariate adjustment Arteriosclerosis, thrombosis, and vascular biology Medium 10195947
1996 Active PAI-1 blocks αVβ3-mediated smooth muscle cell migration by competing for the αVβ3 binding site on vitronectin; PAI-1 inactivation (upon complex formation with plasminogen activators) restores cell migration, establishing that αVβ3/vitronectin interaction is required for cell motility and is regulated by PAI-1. Cell migration assays (Boyden chamber), adhesion blocking with anti-αVβ3 antibodies, competition binding assays with PAI-1 variants Nature High 8837777
1999 αVβ3 integrin (β3-containing) physically associates with VEGFR-2 (KDR) in VEGF-A165-stimulated endothelial cells; this interaction enhances VEGFR-2 phosphorylation, downstream PI3K activation, and mitogenicity when cells are plated on vitronectin; anti-β3 antibody reduces VEGFR-2 activation without blocking cell adhesion. Co-immunoprecipitation of β3 with phospho-VEGFR-2, anti-β3 antibody blockade, adhesion-specific signaling assays The EMBO journal High 10022831
2002 Coordinated interactions of Src, Csk, and Syk with αIIbβ3 initiate integrin signaling to the actin cytoskeleton: Src and Csk are constitutively associated with αIIbβ3; fibrinogen binding causes Csk dissociation and Src activation (Tyr-418 phosphorylation), followed by Syk recruitment to αIIbβ3 and Syk-dependent phosphorylation of Vav1, Vav3, and SLP-76 required for platelet spreading. Co-immunoprecipitation of kinases with αIIbβ3, Src-family kinase-deficient platelets, Syk-deficient platelets, phosphorylation assays, fibrinogen adhesion spreading assays The Journal of cell biology High 11940607
2000 Tissue transglutaminase binds directly to β3 integrin (and other β1/β3 integrins but not β2) at the cell surface, forming complexes during biosynthesis; these complexes act as coreceptors to mediate adhesion and spreading on fibronectin via its 42-kD gelatin-binding domain (which lacks integrin-binding RGD motifs), amplifying focal adhesion kinase phosphorylation. Co-immunoprecipitation, cell adhesion/spreading assays, FAK phosphorylation assay, overexpression studies The Journal of cell biology High 10684262
2007 uPAR signaling in podocytes activates αVβ3 integrin in a lipid-dependent manner, promoting podocyte foot process effacement and proteinuria; uPAR-dependent αVβ3 activation drives Cdc42 and Rac1 GTPase activation and podocyte motility; constitutively active β3 integrin reproduces the phenotype in Plaur-/- mice. Genetic mouse models (Plaur-/-, constitutively active β3 knockin), gene transfer, αVβ3 blockade, in vitro podocyte motility assays, small GTPase activation assays Nature medicine High 18084301
2003 Tumstatin, derived from the α3 chain of type IV collagen, binds αVβ3 (β3-containing integrin) in an RGD-independent manner and inhibits endothelial cell proliferation and promotes apoptosis by suppressing FAK/PI3K/Akt/mTOR/4E-BP1 cap-dependent translation; this is mechanistically distinct from endostatin's action via α5β1. Integrin binding assays, competition with RGD cyclic peptide, cell proliferation and apoptosis assays, PI3K/Akt/mTOR pathway analysis with anti-αVβ3 blockade Proceedings of the National Academy of Sciences of the United States of America High 12682293
1995 αVβ3 (CD51/CD61) integrin is specifically required for smooth muscle cell migration toward osteopontin (but not adhesion alone); migration is αVβ3-dependent while adhesion can also be mediated by αVβ5 and αVβ1. Migration assays (Boyden chamber) with αVβ3-deficient cell populations, anti-integrin antibody blocking The Journal of clinical investigation High 7532190
2005 αVβ3 integrin on melanoma cells specifically binds human Thy-1 expressed on activated endothelial cells; this Thy-1/αVβ3 interaction mediates melanoma cell adhesion to and transmigration across activated endothelium under both static and flow conditions. Binding of purified Thy-1 protein to αVβ3-transfected cells and purified αVβ3, melanoma cell adhesion to Thy-1 transfectants, blocking of transmigration with αVβ3/Thy-1 inhibitors Oncogene High 15897908
2004 Platelet F11R (JAM-1/JAM-A) associates with integrin GPIIIa (β3) in a complex upon platelet activation; F11R crosslinking activates PI3K-dependent actin filament assembly, platelet aggregation and secretion, with F11R dimerization and phosphorylation occurring concomitantly with its co-immunoprecipitation with GPIIIa and CD9. Co-immunoprecipitation, actin polymerization assays, PI3K inhibition (wortmannin), calcium measurement, aggregation/secretion assays Journal of receptor and signal transduction research Medium 15344881
2011 ROS upregulate ITGB3 expression in colorectal cancer cells; ITGB3 (functioning as surface αVβ3 heterodimer) promotes migration and invasion via upregulation of STMN1 and activation of the PI3K-Akt-mTOR pathway; ITGB3 knockdown reduces migration/invasion with concomitant STMN1 downregulation. 2D-electrophoresis proteomics, Western blot, siRNA knockdown, Transwell invasion/migration assays, H2O2 treatment Molecular & cellular proteomics : MCP Medium 21622897
2017 ITGB3 is translationally (not transcriptionally) activated under hypoxia in breast cancer cells; ITGB3 knockdown increased apoptosis and reduced survival and migration under hypoxia, and was required for sustained TGF-β pathway activation and induction of Snail-associated EMT markers; ITGB3 downregulation significantly reduced lung metastasis in vivo. Polysomal RNA-Seq (translatome analysis), siRNA knockdown, apoptosis assays, TGF-β pathway analysis (phospho-SMAD), EMT marker expression, in vivo mouse metastasis model Oncotarget Medium 29383126
2018 G9A histone methyltransferase promotes ITGB3 expression in gastric cancer by forming a transcriptional activator complex with P300 and GR at the ITGB3 promoter (in response to dexamethasone/Reg IV/ERK/SP1 signaling); importantly, this transcriptional activation is independent of G9A's SET domain methyltransferase activity. ChIP assay, promoter luciferase assays, co-immunoprecipitation of G9A-P300-GR complex, SET domain deletion/mutation analysis, invasion assays Cell death & disease Medium 29449539
2019 ITGB3 promoter variant rs55827077 (C allele) enhances ITGB3 transcription specifically during megakaryocyte differentiation; higher ITGB3 expression increases platelet integrin β3 protein levels and enhances SERT trafficking from cytosol to the platelet plasma membrane, thereby elevating serotonin blood levels in autistic individuals. ITGB3 promoter sequencing, luciferase reporter assays in K-562 and HEL 92.1.7 hematopoietic cell lines during differentiation, quantitative SERT trafficking assay, association analysis in 176 autistic individuals Human molecular genetics Medium 30535103
2019 In podocytes, miR-30 family deficiency activates calcineurin-NFATC signaling, which in turn activates uPAR-ITGB3 signaling; activated ITGB3 drives Rho GTPase activation, synaptopodin downregulation and podocyte injury/proteinuria; miR-30, calcineurin inhibitors, and ITGB3 inhibitors all converge to prevent podocyte injury in vitro and in vivo. Podocyte-specific miR-30 knockdown/transgenic mice, ITGB3 inhibitor treatment, Rho GTPase activation assay, synaptopodin Western blot, proteinuria measurement Cell death & disease Medium 31127093
2020 In melanoma tumor-repopulating cells (TRCs), ITGB3 activates c-SRC, which phosphorylates STAT3; activated STAT3 suppresses RIG-I expression, thereby reducing STAT1 activation and conferring resistance to IFN-α-induced apoptosis; disruption of ITGB3/c-SRC/STAT3 signaling restores IFN-α sensitivity. Co-immunoprecipitation (ITGB3-c-SRC interaction), ChIP-qPCR (STAT3 at RIG-I promoter), siRNA knockdown of STAT3 and ITGB3, Western blot of phospho-signaling, apoptosis assays, in vivo tumor model Journal for immunotherapy of cancer Medium 32152220
2020 EGFL7 binds to ITGB3 on multiple myeloma cells acting as a functional receptor, inducing ITGB3 phosphorylation and focal adhesion kinase (FAK) activation; ITGB3 overexpression upregulates the transcription factor KLF2, which further enhances EGFL7 transcription, establishing an EGFL7-ITGB3-KLF2-EGFL7 positive feedback loop supporting MM cell survival and proliferation. Co-IP/binding assays (EGFL7-ITGB3), phosphorylation assays (FAK), overexpression/knockdown studies, KLF2 promoter analysis, in vivo xenograft model, neutralizing antibody treatment Blood advances Medium 32191808
2018 ITGB3 depletion sensitizes mesenchymal lung cancer cells to conventional chemotherapeutic drugs by modulating NF-κB signaling; ITGB3 knockdown reduces NF-κB pathway activity; atorvastatin mimics the transcriptome-level changes caused by ITGB3 knockdown and was identified as a candidate to overcome ITGB3-dependent chemoresistance. siRNA knockdown, NF-κB pathway analysis, large-scale transcriptome + drug-response dataset analysis, in silico drug screening Molecular cancer Medium 30563517
2021 ITGB3 knockdown in ovine conceptus trophectoderm (via morpholino antisense oligonucleotides) does not prevent conceptus elongation or implantation but reduces embryo growth, and decreases conceptus expression of SPP1 and NOS3, implicating ITGB3-dependent SPP1/NOS3 signaling in placental allantoic vascular development. Morpholino antisense oligonucleotide knockdown in utero, quantitative RT-PCR, immunolocalization of SPP1 and NOS3 Biology of reproduction Medium 33232974
2017 Osteocytes sense extracellular matrix stiffness via integrin αVβ3 (ITGB3-containing), which interacts with focal adhesion kinase (FAK); FAK activation triggers cytoplasmic β-catenin signaling and nuclear translocation, thereby regulating gap junction function and mineralization activity of osteocytes. PDMS substrates of varying stiffness, integrin αVβ3 blocking antibodies, FAK inhibitor, β-catenin signaling analysis, gap junction assays, mineralization assays ACS applied bio materials Medium 34996170
2022 Itgb3 haploinsufficiency in mice impairs cortical network excitability by promoting extra-synaptic over synaptic signaling of mGluR5; CRISPR activation to restore Itgb3 gene dosage rebalances network excitability as effectively as mGluR5 antagonist MPEP, establishing an ITGB3–mGluR5 functional interaction relevant to ASD pathophysiology. Itgb3 KO and heterozygous mouse models, electrophysiology (network excitability), mGluR5 signaling assays, CRISPR activation in vivo, pharmacological rescue with MPEP Molecular therapy. Nucleic acids Medium 36035754
2021 IL1RN (interleukin-1 receptor antagonist) interacts with integrin β3 (ITGB3) to activate β-catenin signaling, which regulates osteoblast differentiation; IL1RN silencing attenuates osteogenic differentiation induced by osteogenic medium, while IL1RN overexpression promotes osteogenic marker expression. Co-immunoprecipitation (IL1RN–ITGB3 interaction), β-catenin signaling analysis, siRNA knockdown, overexpression studies, osteogenic differentiation assays (ALP, alizarin red) Acta biochimica et biophysica Sinica Medium 33493267
2024 CD61 (ITGB3/β3 integrin) is transiently expressed on tumor-infiltrating T cells, where it pairs with CD103 at synaptic microclusters; CD61 colocalization with the TCR modulates downstream TCR signaling, enhancing antitumor cytotoxicity and promoting physiological control of tumor growth. Flow cytometry, confocal microscopy (synaptic microcluster imaging), TCR signaling assays, cytotoxicity assays, in vivo tumor models Nature immunology Medium 38561495
2008 A single-nucleotide polymorphism (C622>T) in exon 5 of ITGB3, causing Thr195→Met substitution in mature β3, underlies the HPA-17bw (Va) platelet alloantigen; recombinant β3 carrying Met195 specifically reacted with the original maternal Va alloantiserum. ITGB3 genomic sequencing, recombinant β3 expression in S2 cells, serological reactivity assays Transfusion Medium 18484951
1999 A homozygous Cys542→Arg substitution in GPIIIa (in exon 11) causes type I Glanzmann's thrombasthenia; this mutation disrupts disulfide bond formation within the cysteine-rich core region, resulting in trace amounts of slowly migrating GPIIIa, nearly absent surface αIIbβ3, and also reduced αVβ3 expression, linking ITGB3 structural integrity to both integrin complexes. Western blotting, flow cytometry, PCR-SSCP and direct sequencing, restriction enzyme analysis, family study British journal of haematology Medium 10233432

Source papers

Stage 0 corpus · 130 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
2008 Genetic determinants of response to clopidogrel and cardiovascular events. The New England journal of medicine 1335 19106083
2002 Crystal structure of the extracellular segment of integrin alpha Vbeta3 in complex with an Arg-Gly-Asp ligand. Science (New York, N.Y.) 1311 11884718
2009 Integrins. Cell and tissue research 1256 19693543
2001 Crystal structure of the extracellular segment of integrin alpha Vbeta3. Science (New York, N.Y.) 1048 11546839
1990 An interaction between alpha-actinin and the beta 1 integrin subunit in vitro. The Journal of cell biology 777 2116421
2004 Structural basis for allostery in integrins and binding to fibrinogen-mimetic therapeutics. Nature 671 15378069
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1996 The serpin PAI-1 inhibits cell migration by blocking integrin alpha V beta 3 binding to vitronectin. Nature 589 8837777
1999 Role of alphavbeta3 integrin in the activation of vascular endothelial growth factor receptor-2. The EMBO journal 533 10022831
2007 Structural basis of integrin activation by talin. Cell 524 17218263
1991 GPIIb-IIIa: the responsive integrin. Cell 498 2018971
2011 Analysis of the myosin-II-responsive focal adhesion proteome reveals a role for β-Pix in negative regulation of focal adhesion maturation. Nature cell biology 490 21423176
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