Platelet adhesion & activation

P-selectin mediates platelet activation and adhesion to endothelium, driving thrombotic cascade in MI.

sCD40L released from activated platelets amplifies endothelial dysfunction and platelet–leukocyte thrombotic crosstalk.

PF4 is released upon platelet activation and serves as an early biomarker of platelet recruitment and thrombus formation in Type 1 MI.

Beta-thromboglobulin is released upon platelet activation and serves as an early AMI biomarker of platelet recruitment.

ITGA2B-encoded integrin αIIb subunit forms the αIIbβ3 receptor essential for platelet aggregation and coronary thrombus formation in Type 1 MI.

GPVI binds exposed collagen upon cap rupture or erosion, triggering platelet adhesion, activation, and thrombus propagation.

GPIb mediates platelet tethering to exposed von Willebrand factor at the site of endothelial rupture or erosion, initiating platelet adhesion and activation.

Phosphatidylserine exposure on activated platelets and microparticles promotes platelet aggregation and thrombin generation.

CD36 acts as a platelet scavenger receptor for oxidized LDL, amplifying platelet activation and microvesicle formation during acute thrombosis.

CD39 ectonucleotidase hydrolyzes ATP and ADP to adenosine monophosphate, attenuating platelet activation and arterial thrombosis.

Fibronectin mediates platelet adhesion to exposed matrix and fibroblast paracrine signaling; dysregulation marks plaque instability and thrombotic coronary even

ADP released from platelet dense granules activates P2Y receptors, sustaining platelet aggregation and thrombus propagation.

Integrin αIIbβ3 bridges platelets via fibrinogen binding, essential for platelet-dependent thrombus formation.

Phosphatidylethanolamine dysregulation in platelets and monocytes contributes to platelet dysfunction and pro-thrombotic extracellular vesicle release in Type 1

ATP depletion and extracellular accumulation drives platelet activation and signals myocardial ischemia during acute coronary occlusion.

CXCR4 mediates CXCL12-driven platelet activation and pro-thrombotic signaling, contributing to atherothrombotic cascade.

CD11b-mediated leukocyte activation and recruitment promote atherothrombotic plaque inflammation.

ITGB3 gene product (integrin β3) forms the fibrinogen receptor αIIbβ3, essential for platelet-platelet adhesion and thrombus consolidation.

AKT phosphorylation amplifies platelet activation via PI3K, while also promoting endothelial repair and cardiomyocyte survival through eNOS and mitochondrial pr

P2Y12 is the platelet ADP receptor central to platelet aggregation and thrombosis; therapeutic target for antiplatelet therapy.

CD63 exposure on platelet extracellular vesicles indicates granule secretion and platelet activation during thrombus formation.

Adenosine inhibits platelet activation and thrombus formation while promoting endothelial function and myocardial cardioprotection via ticagrelor-independent me

Growth arrest-specific 6 is a vitamin-K-dependent ligand of the TAM receptor family (AXL, MERTK, TYRO3). Released on platelet activation, it signals through platelet TAM receptors to potentiate degranulation, integrin αIIbβ3 activation and clot stabilization, linking platelet activation to thrombus growth in atherothrombotic MI. The Gas6/AXL axis is also upregulated in STEMI and implicated in vascular inflammation.

Neutrophil elastase activates both coagulation and platelet pathways, augmenting thrombus formation.

PSGL-1 engages P-selectin on activated platelets, driving platelet-leukocyte crosstalk and prothrombotic amplification at the site of plaque rupture.

Soluble TNF receptor 1 promotes platelet activation and correlates with thrombotic tendency at the site of plaque rupture.

CD73 5'-nucleotidase converts AMP to adenosine, which signals through adenosine receptors to inhibit platelet activation.

Heat shock protein 27 modulates platelet cytoskeletal dynamics and inhibits thrombotic responses, potentially stabilizing platelet function during atherothrombo

Serotonin is stored in and released from platelet α-granules during activation, promoting vasoconstriction and platelet–platelet recruitment at the thrombotic s

Annexin V enhances platelet and leukocyte microparticle–mediated thrombin generation during acute coronary thrombosis.

Beta-2-glycoprotein I complexes with oxidized LDL in atherosclerotic lesions and is targeted by antiphospholipid antibodies to activate thrombosis.

CAMP mediates antiplatelet signaling and immune regulation during acute myocardial injury.

CD42a-positive small extracellular vesicles are released during platelet activation and reflect early thrombus formation in acute MI.

DPP-4 regulates GLP-1 stability and directly modulates platelet aggregation and endothelial function in MI.

GP5 downregulation in NSTEMI reflects enhanced platelet activation, consumption, and thrombin-driven coagulation.

GPV is a thrombin-activated platelet membrane protein released during platelet activation, indicating both thrombin generation and platelet responsiveness at th

Mean platelet volume reflects platelet function and predicts thrombotic recurrence in acute coronary syndromes.

miR-21 is elevated during acute MI, promoting platelet activation and aggregation while amplifying cardiomyocyte injury responses.

MAPK14 (p38α) regulates platelet activation and inflammatory responses, contributing to thrombotic amplification post-plaque rupture.

PAC-1 is a monoclonal antibody probe binding the activated (ligand-receptive) conformation of platelet integrin GPIIb-IIIa, directly reporting platelet activati

PAGln derived from microbiota metabolism promotes platelet activation and thrombotic response, increasing MI risk in rupture-prone plaques.

PLCG2 transduces GPVI-collagen signaling amplifying platelet activation and aggregation.

PAF amplifies platelet activation and recruits leukocytes in coronary thrombogenesis.

Platelet-derived vesicles released during platelet activation that propagate tissue-factor-driven thrombus formation.

Syk tyrosine kinase transduces GPVI-collagen signaling driving platelet activation and adhesion.

SRC mediates platelet activation and platelet-leukocyte crosstalk via downstream phosphorylation, amplifying thrombotic response at the ruptured atherosclerotic

Vimentin is released from the platelet cytoskeleton during activation and reflects both platelet involvement and vascular inflammation.

CYP2C19 genetic variants regulate clopidogrel activation, modulating platelet aggregation inhibition and stent thrombosis risk after coronary intervention.

ALDH2 controls acetaldehyde and reactive-aldehyde detoxification, regulating platelet activation state and thrombotic predisposition in acute coronary events.

Cathepsin G amplifies platelet recruitment and thrombin generation via ADP release and coagulation cascade activation.

Citrullinated histone H3 from neutrophil extracellular traps drives platelet activation and thrombus formation in STEMI.

Platelet surface receptor mediating collagen recognition and activation during thrombus formation.

C5a recruits neutrophils and activates platelets, amplifying thromboinflammatory response in acute MI.

Fc receptor on platelets mediating immune-complex-driven platelet aggregation and thrombotic amplification.

FERMT3 is a focal adhesion protein that mediates platelet integrin activation and firm adhesion, with elevated expression marking plaque erosion and thrombosis.

GLP-1 exerts anti-thrombotic and anti-inflammatory effects, reducing platelet aggregation and endothelial activation in MI pathogenesis.

Integrin mediating platelet adhesion to collagen on exposed vessel wall; critical for thrombus formation.

miRNA modulating platelet function and ventricular remodeling following acute ischemic injury.

miR-223 dysregulation in acute coronary events amplifies platelet activation and leukocyte recruitment, predicting post-MI mortality.

Cardiac signaling kinase whose cAMP-dependent activity suppresses platelet activation and thrombus formation through anti-aggregatory pathways.

Vinculin is released from platelet cytoskeleton during activation and aggregation, marking platelet involvement in acute coronary thrombosis.

Released hemoglobin amplifies oxidative stress and promotes platelet activation and thrombosis in acute coronary occlusion.

12-HETE is an eicosanoid mediator that activates platelets and amplifies oxidative stress during acute MI.

12-LOX catalyzes arachidonic acid metabolism toward pro-thrombotic lipid mediators that amplify platelet response.

Beta-actin is essential for platelet shape change, cytoskeletal reorganization during activation, and the adhesion-molecule-mediated tethering to exposed collag

ADAMTS family protease mediating ectodomain shedding of platelet and endothelial activation markers.

ADAMTS family protease releasing soluble forms of adhesion receptors and modulating platelet-endothelial interactions.

ACKR3 dampens platelet activation and thromboinflammatory signaling, protecting against thrombus amplification.

CD66b-positive neutrophil microparticles and extracellular traps amplify platelet activation and thrombus propagation in STEMI.

CD84 mediates platelet-to-platelet adhesion and thrombus stabilization during coronary occlusion.

Cell-adhesion molecule functioning as a negative regulator of platelet activation and correlating with aggregation capacity.

Collagen exposure following fibrous-cap rupture or endothelial erosion triggers GPVI-mediated platelet adhesion and the initiation of thrombosis in Type 1 MI.

C3a activates complement-driven platelet recruitment and thromboinflammatory cascade in coronary thrombosis.

Circulating dsDNA from neutrophil extracellular traps marks platelet-leukocyte activation and correlates with myocardial injury magnitude.

ERK1 participates in platelet activation signaling and integrates with p38 pathways to amplify platelet recruitment and aggregation.

FYN amplifies platelet activation via GPVI signaling and supports platelet-leukocyte crosstalk, driving thrombotic occlusion.

Glycocalicin is the soluble ectodomain of platelet GPIbα shed during platelet activation, reflecting vWF-mediated platelet tethering and adhesion to injured end

GNAQ encodes a Gαq protein essential for platelet signaling and thrombus formation, directly driving the thrombotic occlusion phase of Type 1 MI.

Platelet glycoprotein integrin mediating fibrinogen-dependent platelet–platelet aggregation and thrombus propagation.

L-tryptophan dysregulation reflects platelet activation and thrombotic stress in acute coronary syndrome.

P-selectin (CD62P) mediates platelet–leukocyte adhesion and tethering, amplifying thromboinflammation in Type 1 MI.

PI3K signaling drives platelet activation and endothelial progenitor cell mobilization, regulating thrombotic and reparative responses.

PIK3CB promotes phosphatidylinositol-3-kinase signaling downstream of CD40L, enhancing platelet activation and thrombus formation.

PDGF-BB released from activated platelets amplifies plaque inflammation and predicts microvascular thrombosis and no-reflow in acute coronary occlusion.

PDGF-A from activated platelets promotes vascular inflammation and plaque destabilization, amplifying thrombotic response in STEMI.

RhoA GTPase mediates platelet activation and endothelial dysfunction in Type 1 MI.

Sema7A bridges platelet activation and monocyte recruitment, amplifying thrombo-inflammatory responses during acute MI and reperfusion injury.

SAP mediates platelet activation and platelet–leukocyte aggregation, amplifying thrombotic and inflammatory responses during acute coronary thrombosis.

SLP-76 scaffolds GPVI signaling to couple collagen recognition to platelet secretion and aggregation.

TAGLN2 dysregulation in ACS platelets reflects aberrant cytoskeletal remodeling in atherothrombotic activation.

β-Thromboglobulin is released during platelet activation and aggregation, marking the initiation of thrombotic cascade in acute MI.

LIGHT (TNFSF14) promotes platelet adhesion and endothelial activation, facilitating leukocyte recruitment and thromboinflammatory cascade.

miR-126 released from activated platelets modulates adhesion and aggregation, reflecting thrombotic MI burden.

PGD2 is an anti-platelet prostanoid whose post-PCI reduction indicates resolution of acute thrombus-associated inflammation.

Platelet-derived extracellular vesicles released during activation amplify thrombin generation and fibrin formation, contributing to occlusive thrombus propagat

Platelet-derived thromboinflammatory RNA signature that integrates platelet activation and inflammatory signals associated with MI risk.

12-HETrE is a lipid metabolite that suppresses platelet adhesion and activation in response to vessel injury.

13-HODE, an oxidized linoleic acid metabolite, suppresses platelet aggregation and protects against thrombosis in Type 1 MI.

18-HEPE, derived from eicosapentaenoic acid, exerts antiplatelet effects limiting platelet-driven thrombosis.

5-oxo-ETE is an arachidonic-acid-derived eicosanoid that promotes leukocyte infiltration and myocardial injury during acute myocardial infarction.

9-HODE, an oxidized linoleic acid metabolite, inhibits platelet aggregation and reduces thrombotic burden in acute coronary events.

ACAD10 controls platelet mitochondrial homeostasis and activation state, modulating the thrombotic response to vascular injury.

Gamma-actin is critical for platelet contractile responses, morphological changes during activation, and stable adhesion to thrombogenic surfaces.

ADRA2A signaling transduces PAGln-driven platelet activation and leukocyte recruitment in atherothrombotic cascades.

ADRA2B signaling transduces PAGln effects on platelet response and vascular inflammation.

ATP1A1 encodes Na/K-ATPase α1, which maintains platelet ion homeostasis and contractility, supporting but not directly driving thrombotic activation.

Vacuolar H+ ATPase subunit correlating with platelet aggregation capacity via granule acidification.

Aurora kinase B elevated in STEMI platelets, regulating platelet cytokinesis and activation dynamics.

Autotaxin-LPA axis promotes platelet activation and plaque inflammation in atherothrombosis.

BAFF, released from activated platelets, amplifies B-cell and vascular inflammation in atherothrombotic coronary disease.

C4d deposition marks platelet activation and complement engagement in arterial thrombosis.

CACNA1I encodes a T-type calcium channel contributing to platelet activation signaling, though not a primary thrombotic driver in Type 1 MI.

CD226 upregulation enhances platelet-mediated thrombosis in clopidogrel-resistant ACS and Type 1 MI.

CD235a on erythrocyte-derived microparticles signals platelet activation and thrombus propagation during coronary occlusion.

CD41+ microparticles reflect platelet activation and contribute to thrombin generation and thrombus formation post-plaque rupture.

CD61 is a structural component of integrin αIIbβ3 and serves as a pan-platelet marker.

cGMP exerts inhibitory signaling that suppresses platelet aggregation and thrombus formation.

PRKG1 phosphorylates substrates that inhibit platelet activation, reducing thrombotic risk in atherothrombosis.

Circular RNAs are platelet-derived microvesicle markers released during platelet activation and thrombus formation.

Citrullinated histone H3 from neutrophil extracellular traps is incorporated into coronary thrombi, promoting platelet activation and coagulation.

cGAS senses platelet-associated dsDNA and drives thromboinflammatory platelet activation.

Cyclophilin D regulates platelet necrosis and activation, modulating thrombus formation and myocardial injury signaling.

DIDO1 is a circulating biomarker upregulated in STEMI plasma, reflecting platelet activation and thrombotic burden during acute coronary occlusion.

DHETs, the hydrolyzed metabolites of EETs, accumulate post-PCI and mark active eicosanoid-mediated vascular repair and endothelial recovery.

Diacylglycerol kinase dysregulation promotes platelet hyperreactivity in Type 1 MI.

Dok-2 fine-tunes GPVI-driven platelet activation, affecting thrombus propagation kinetics.

EETs are vasoprotective epoxyeicosatrienoic acids whose post-PCI elevation indicates restoration of endothelial-protective eicosanoid metabolism.

Metabolic enzyme elevated in STEMI platelets with undefined role in platelet function.

ERK1/2 kinases transduce activation signals driving platelet aggregation and thrombus formation.

ERM proteins organize platelet cytoskeleton and membrane dynamics during activation.

ERK2 transduces p38 signaling to promote platelet activation and thrombus formation in coronary thrombosis.

F-box ubiquitin ligase elevated in STEMI platelets, involved in platelet activation signaling.

FcRγ-chain couples GPVI collagen sensing to PLCγ2 and downstream platelet activation.

Immunophilin co-chaperone elevated in STEMI platelets, modulating stress response and protein folding.

FGD6, elevated during acute MI, may regulate small-GTPase signaling in platelet or endothelial dysfunction.

Glutathione-S-transferase reflects platelet antioxidant response and oxidative stress during acute coronary thrombosis.

GPIbα is the vWF-binding platelet receptor that initiates platelet tethering to exposed subendothelial collagen and injured endothelium, triggering downstream a

Glycoprotein Ib-V-IX mediates initial platelet adhesion to von Willebrand factor on exposed subendothelium, initiating thrombus formation.

GP1BB prothrombotic variants enhance platelet tethering to exposed collagen/vWF and increase thrombotic risk.

Glycoursodeoxycholic acid suppresses platelet activation, reducing Type 1 MI thrombus burden.

GPC5 is a surface proteoglycan regulating adhesion and coagulation; protective variants reduce sudden cardiac arrest risk in MI.

GPIb-alpha binds von Willebrand factor, initiating platelet adhesion and aggregation at sites of endothelial injury.

Gremlin-1, a platelet-derived cytokine, promotes platelet activation and vascular inflammation during acute coronary syndrome.

GNA12/13-coupled pathways drive shape change and aggregation responses to thrombin and other platelet agonists.

GNAI-coupled receptors transduce anti-aggregatory signals that suppress platelet activation during thrombus formation.

HDL2 exerts antiplatelet and antithrombotic effects, opposing platelet activation at the thrombotic phase of Type 1 MI.

Heparanase degrades subendothelial heparan sulfate, promoting platelet and leukocyte infiltration and thrombus expansion in STEMI.

Histamine dampens platelet activation and thromboinflammation, protecting against coronary microthrombosis in acute MI.

HDC catalyzes histamine synthesis, modulating platelet activation and plaque inflammation in atherothrombotic disease.

Circulating histone H1 from NETs activates platelets and endothelium, amplifying thrombus formation.

HPS3 controls platelet dense-granule biogenesis and release, modulating ADP-driven platelet activation during thrombotic events.

Integrin alpha subunits heterodimerize with integrin beta-2 to mediate platelet adhesion and aggregation in thrombosis.

Integrin β1 mediates leukocyte and platelet recruitment to inflamed and eroding plaques.

Ion-channel auxiliary subunit elevated in STEMI platelets, potentially modulating platelet physiology.

LAT mediates downstream signaling from GPVI collagen receptor, propagating platelet activation and adhesion to exposed subendothelial matrix.

LYN phosphorylates adapter proteins downstream of GPVI collagen receptor, initiating the signaling cascade that drives platelet activation and thrombus formatio

Exposed on the platelet surface upon α-granule exocytosis during platelet activation and thrombus formation.

Manganese superoxide dismutase reflects platelet antioxidant defense and oxidative stress during acute coronary activation.

MAPKAPK2 amplifies p38-mediated platelet activation and α-granule release driving thrombotic response.

miR-143-3p targets vascular proteins involved in smooth-muscle contractility and platelet adhesion, modulating the thrombotic response to plaque rupture.

miR-145-5p suppresses vascular targets that regulate endothelial barrier function and platelet activation during thromboinflammation.

microRNA regulating platelet activation and aggregation signals in thrombotic cascade.

microRNA regulating platelet activation and aggregation signals in thrombotic cascade.

miR-199a-3p is a circulating microRNA biomarker of platelet activation that regulates genes governing thromboinflammatory responses.

Mitochondrial DNA methylation in platelets indicates altered energy metabolism and platelet activation status in MI.

MT-CO1 methylation changes reflect platelet activation and mitochondrial stress in acute MI.

MT-CO2 methylation status serves as a marker of platelet mitochondrial dysfunction in MI.

MT-CO3 methylation reflects platelet metabolic activation and oxidative stress in acute MI.

Mitochondrial DNA methylation in platelets serves as a marker of platelet metabolic status and activation during thrombotic events.

Mitochondrial tRNA methylation patterns in platelets reflect mitochondrial function during thrombotic activation.

MOB3C may regulate platelet–leukocyte interactions and vascular cell adhesion in thrombotic response.

MST1R (RON) promotes platelet activation and leukocyte recruitment in atherothrombotic cascades.

MYH9 is a focal adhesion protein that mediates platelet contractility and firm adhesion to exposed collagen/vWF during coronary thrombus formation.

Neutrophil Activating Protein-2 is a platelet-derived chemokine promoting platelet activation and leukocyte recruitment.

Platelet-intrinsic protein mediating platelet activation and membrane perturbation during thrombus formation.

Nucleosome complexes released in neutrophil extracellular traps promote platelet activation and thrombus formation at the site of plaque rupture.

Oligophrenin-1 transduces Rev-erb α signaling to enhance platelet activation in MI.

OXE-R (oxoeicosanoid receptor) transduces 5-oxo-ETE signaling to promote leukocyte recruitment and myocardial damage; a candidate cardioprotective target.

P-selectin+ microparticles are released during platelet activation and mediate leukocyte adhesion at sites of arterial injury.

P2X1 receptor mediates ATP-dependent rapid platelet activation and calcium influx during thrombus formation.

P2Y1 receptor mediates ADP-dependent platelet activation and thrombus formation at the site of plaque rupture.

PAR4 is a thrombin-activated platelet receptor whose signaling drives platelet shape change, aggregation, and secretion during coronary thrombosis.

PARVA is a focal adhesion protein that anchors the actin cytoskeleton in platelets, supporting firm adhesion and thrombotic response at the injury site.

Platelet-derived growth factor subunit correlating with platelet aggregation and involved in vascular responses to injury.

PGE2 is an anti-platelet prostanoid whose post-intervention decline reflects resolution of acute platelet activation in STEMI.

PAGly augments platelet activation and adhesion in response to exposed plaque substrate.

PC18:0 activates platelet adhesion and aggregation during acute thrombotic events.

PLCγ2 activation is a critical branch point in collagen/GPVI-triggered platelet activation and thrombus formation.

Platelet factor 4 released during platelet activation promotes further platelet recruitment and enhances tissue-factor-driven coagulation.

GPIb/V/IX mediates the initial catch-bond interaction between platelets and von Willebrand factor at sites of endothelial injury.

PDGFC promotes platelet activation and aggregation at the site of vascular injury.

Actin-nucleating protein released during platelet activation and thrombus formation.

PDI catalyzes disulfide bond formation in platelet integrins and coagulation factors, promoting thrombosis.

PDIA3 release during acute coronary events promotes platelet adhesion and thrombus propagation.

PKCα phosphorylates downstream effectors of platelet activation, promoting adhesion and thrombus formation.

PP2Cm activates branched-chain amino acid catabolism, altering amino-acid-driven signaling that modulates platelet activation and thrombotic risk.

RAP1B is a small GTPase that regulates platelet integrin activation and focal adhesion formation, enabling platelet tethering and stable adhesion during coronar

Rev-erb α controls circadian platelet reactivity, potentiating Type 1 MI thrombosis.

rLj-RGD3 inhibits platelet adhesion and aggregation by blocking integrin-mediated interaction with the thrombogenic substrate.

sC5b-9 (terminal complement complex) activates platelets and endothelium, bridging complement activation to thrombosis.

SCUBE1 is a soluble protein released from platelet α-granules during activation, serving as a marker of platelet secretion and thrombotic state initiation.

SGK1 promotes platelet activation and thrombotic responses in acute coronary syndromes.

Glucose transporter 3 correlating with platelet aggregation function through metabolic substrate availability.

SNAP29 orchestrates α-granule exocytosis and dense-granule release, amplifying platelet recruitment and thrombus stabilization.

Soluble semaphorin 4D, a platelet-derived mediator, predicts thrombus burden and major adverse cardiac events.

sTLT-1 shedding marks platelet activation and thrombotic burden in coronary disease.

Src family kinases transduce GPVI collagen-binding signals, driving platelet activation and thrombus propagation at the ruptured plaque.

ST3GAL6 regulates platelet adhesion molecule glycosylation, affecting platelet aggregation capacity.

ST6Gal-1 modulates platelet activation through sialic-acid glycosylation of adhesion ligands.

STING transduces cGAS-detected dsDNA signals to activate platelets and promote thrombus formation.

STX6 regulates intracellular calcium mobilization; variants influence platelet activation kinetics and thrombotic response.

SYT11 regulates exocytosis and cell–cell communication implicated in thromboinflammatory responses.

Serine-threonine kinase elevated in STEMI platelets, involved in platelet signaling cascades.

Thrombopoietin activates platelets and couples thrombosis to inflammation, driving coronary thrombus formation.

MPL signaling modulates platelet mass and functional state, influencing thrombotic response at coronary lesion.

TNFRSF10C acts as a TNF superfamily receptor contributing to inflammatory signaling and platelet-leukocyte crosstalk in coronary thrombus.

Tropomodulin-3 propionylation at lysine 255 couples branched-chain amino acid metabolism to platelet activation signaling.

VASP phosphorylation state reflects endothelial nitric oxide signaling and serves as a marker of platelet activation resistance.

VDR regulates platelet activation and inflammatory responses, modulating thrombosis in acute coronary syndrome.

Xanthine oxidoreductase activity modulates platelet function through redox-sensitive signaling pathways.

Y RNAs are platelet-derived RNA fragments released during platelet activation and aggregation at the thrombotic site.

β-tubulin is released from the platelet cytoskeleton during shape change and activation in acute coronary events.

ABI2 couples receptor signaling to actin remodeling; essential for platelet spreading and thrombus formation.

DOK proteins regulate platelet adhesion and integrin-mediated signaling in thrombosis.

NCK1 couples receptor tyrosine kinases to actin remodeling; regulates platelet activation and adhesion signaling.

Phospholipase C mediates platelet G-protein signaling and platelet activation/aggregation.

RAPH1 mediates Ras-dependent adhesion signaling; promotes integrin clustering and platelet-endothelial interaction.

RASGEF1B activates Rap1 GTPase, promoting integrin clustering and platelet/leukocyte adhesion.

TUBB1 is essential for megakaryocyte and platelet microtubule organization; mutations impair platelet granule cargo secretion and hemostasis.

TUBB4B maintains platelet cytoskeleton and granule architecture; variants affect platelet activation, aggregation, and thrombotic response.

VAMP5 mediates α-granule and dense-granule release in platelet activation; critical for thrombus formation.