genes significantly affected in female MDD subjects
genes significantly affected in female MDD subjects
Positive relationships between P2RY12 and other components at different levels (count: 0)
Positive relationship network of P2RY12 in MK4MDD
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Note:
1. The different color of the nodes denotes the level of the nodes.
Genetic/Epigenetic Locus
Protein and Other Molecule
Cell and Molecular Pathway
Neural System
Cognition and Behavior
Symptoms and Signs
Environment
MDD
2. Besides the component related relationships from literature, gene mapped protein and protein mapped gene are also shown in the network.
If the mapped gene or protein is not from literature, square node would be used instead of Circle node.
Accordingly, the relationship is marked with dot line.
2. User can drag the nodes to rearrange the layout of the network. Click the node will enter the report page of the node.
Right-click will show also the menus to link to the report page of the node and remove the node and related edges.
Hover the node will show the level of the node and hover the edge will show the evidence/description of the edge.
3. The network is generated using Cytoscape Web
Negative relationships between P2RY12 and MDD (count: 0)
Negative relationships between P2RY12 and other components at different levels (count: 0)
Hemostasis is a physiological response that culminates in th......
Hemostasis is a physiological response that culminates in the arrest of bleeding from an injured vessel. Acute vessel injury results in its constriction to reduce the loss of blood. Under normal conditions vascular endothelium supports vasodilation, inhibits platelet adhesion and activation, suppresses coagulation, enhances fibrin cleavage and is anti-inflammatory in character. Under acute vascular trauma vasoconstrictor mechanisms predominate and the endothelium becomes prothrombotic, procoagulatory and proinflammatory in nature. This is achieved by a reduction of endothelial dilating agents: adenosine, NO and prostacyclin; and the direct action of ADP, serotonin and thromboxane on vascular smooth muscle cells to elicit their contraction. The chief trigger for the change in endothelial function that leads to the formation of haemostatic thrombus is the loss of the endothelial cell barrier between blood and ECM components. Circulating platelets identify and discriminate areas of endothelial lesions; here, they adhere to the exposed sub endothelium. Their interaction with the various thrombogenic substrates and locally generated or released agonists results in platelet activation. This process is described as possessing two stages, firstly, adhesion - the initial tethering to a surface, and secondly aggregation - the platelet-platelet cohesion.More...
Purinergic receptors are a family of newly characterized pla......
Purinergic receptors are a family of newly characterized plasma membrane molecules involved in several cellular functions such as vascular reactivity, apoptosis and cytokine secretion. The functions of these receptors are as yet only partially characterized. The family includes the GPCR P2Y purinergic receptors and adenosine P1 receptors. A third family member, the P2X receptor, is a ligand-gated ion channel.More...
G protein-coupled receptors. The beta:gamma G-protein dimer ......
G protein-coupled receptors. The beta:gamma G-protein dimer is also involved in downstream signaling , and some receptors form part of metastable complexes of receptor and accessory proteins such as the arrestins. GPCRs are involved in many diverse signaling events , using a variety of pathways that include modulation of adenylyl cyclase, phospholipase C, the mitogen activated protein kinases (MAPKs), extracellular signal regulated kinase (ERK) c-Jun-NH2-terminal kinase (JNK) and p38 MAPK.More...
Two principal mechanisms limit blood loss after vascular inj......
Two principal mechanisms limit blood loss after vascular injury. Initially, platelets are activated, adhere to the site of the injury, and aggregate into a plug that limits blood loss. Proteins and small molecules released from activated platelets stimulate the plug formation process, and fibrinogen from the plasma forms bridges between activated platelets. These events allow the initiation of the clotting cascade, the second mechanism to limit blood loss. Negatively charged phospholipids exposed on cell surfaces at the site of injury and on activated platelets interact with tissue factor, setting off a cascade of reactions leading to generation of fibrin and the formation of an insoluble fibrin clot that strengthens the platelet plug.More...
Platelet activation begins with the initial binding of adhes......
Platelet activation begins with the initial binding of adhesive ligands and of the excitatory platelet agonists. Intracellular signaling reactions will then enhance the adhesive and procoagulant properties of tethered platelets or of platelets circulating in the proximity. From the subendothelial adhesive substrates, collagen and possibly vWF are the main inducers of platelet activation. GP VI is the most potent collagen receptor initiating signal generation, an ability derived from its interaction with the FcRI gamma chain. This results in the phosphorylation of the gamma-chain by the non-receptor tyrosine kinases of the Src family. The phosphotyrosine motif is recognized by the SH2 domains of Syk, a tyrosine kinase. This association activates the Syk enzyme, leading to activation. Four PARs are identified, of which PARs 1 ,3 and 4 are substrates for thrombin. PAR 1 is the predominant thrombin receptor, PAR 3 is minimally expressed and PAR 4 is less responsive to thrombin. Platelets do not store PAR1, due to limited protein synthesis, they are capable of responding to thrombin only once. Platelet activation further results in the scramblase-mediated transport of negatively-charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by phosphatidylserine and phosphatidylethanolamine) for the tenase complex (formed by the activated forms of the blood coagulation factors factor VIII and factor I).More...
P2Y receptors are a family of purinergic receptors, G protei......
P2Y receptors are a family of purinergic receptors, G protein-coupled receptors stimulated by nucleotides such as ATP, ADP, UTP, UDP and UDP-glucose. To date, 12 P2Y receptors have been cloned in humans. P2Y receptors are present in almost all human tissues where they exert various biological functions based on their G-protein coupling. Purine nucleotides are involved in a large number of intermediate metabolic pathways, taking part as substrates, products or allosteric factors.More...
There are more than 800 G-protein coupled receptor. GPCRs ar......
There are more than 800 G-protein coupled receptor. GPCRs are receptors for a diverse range of ligands from large proteins to photons and have an equal diverstiy of ligand-binding mechanisms. Classical GPCR signaling involves signal transduction via heterotrimeric G-proteins, however many G-protein independent mechanisms have been reported.More...
The classical signalling mechanism for G alpha (i) is inhibi......
The classical signalling mechanism for G alpha (i) is inhibition of the cAMP dependent pathway through inhibition of adenylate cyclase. Decreased production of cAMP from ATP results in decreased activity of cAMP-dependent protein kinases.More...
In the initial response to injury, platelets adhere to damag......
In the initial response to injury, platelets adhere to damaged blood vessels, responding to the exposure of collagen from the vascular epithelium. Once adhered they degranulate, releasing agents such as serotonin and ADP and synthesize Thromboxane A2, all of which amplify the response, recruiting further platelets to the area and promoting platelet aggregation.More...
Co-activation of P2Y1 and P2Y12 is necessary for complete pl......
Co-activation of P2Y1 and P2Y12 is necessary for complete platelet activation. P2Y1 is coupled to Gq and helps trigger the release of calcium from internal stores, leading to weak and reversible platelet aggregation. P2Y12 is Gi coupled, and required for the amplification of aggregation induced by all platelet agonists including collagen, thrombin, thromboxane, adrenaline and serotonin. P2Y12 activation leads to irreversible platelet aggregation.More...
Rhodopsin-like receptors. They represent members which inclu......
Rhodopsin-like receptors. They represent members which include hormone, light and neurotransmitter receptors and encompass a wide range of functions including many autocrine, paracrine and endocrine processes.More...
In the initial response to injury, platelets adhere to damag......
In the initial response to injury, platelets adhere to damaged blood vessels, responding to the exposure of collagen from the vascular epithelium. Once adhered they degranulate, releasing agents such as serotonin and ADP and synthesize Thromboxane A2, all of which amplify the response, recruiting further platelets to the area and promoting platelet aggregation.More...
P2RY12 related interactors from protein-protein interaction data in HPRD (count: 1)
Basic Information
Positive relationships between P2RY12 and other components at different levels (count: 0)
