Gene Report

Basic Information

Approved Symbol	F5
Approved Name	coagulation factor V (proaccelerin, labile factor)
Location	1q23
Position	chr1:169481192-169555769 (-)
External Links	Entrez Gene: 2153 Ensembl: ENSG00000198734 UCSC: uc001ggg.1 HGNC ID: 3542
No. of Studies (Positive/Negative)	1(1/0)
Type	Literature-origin

Positive relationships between F5 and MDD (count: 0)

Positive relationships between F5 and other components at different levels (count: 1)

Genetic/epigenetic locus					Protein and other molecule			Cell and molecular pathway			Neural system			Cognition and behavior		Symptoms and signs			Environment

Name in Literature	Level	Approved Name (Name in Literature)	Type	Reference	Research Type	Statistical Result	Relation Description	All
Name in Literature	Related Components
F5		Depression-like behaviors from animal model(depressive-like behavior)	cognition and behavior	Andrus, 2010	animal model		Differentially expressed depression genes hippocampus, (fold...... Differentially expressed depression genes hippocampus, (fold change > 2). More...

Positive relationship network of F5 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 F5 and MDD (count: 0)

Negative relationships between F5 and other components at different levels (count: 0)

F5 related SNPs in MK4MDD (count: 0)

F5 related proteins in MK4MDD (count: 1)

Approved Name	UniportKB	No. of Studies (Positive/Negative)	Source
Coagulation factor V	P12259	0(0/0)	Gene mapped

F5 related GO terms (count: 11)

ID	Name	Type	Evidence
Gene mapped GO terms
GO:0005886	plasma membrane	cellular component	TAS
GO:0005515	protein binding	molecular function	IPI[9556620]
GO:0005507	copper ion binding	molecular function	IEA
GO:0031093	platelet alpha granule lumen	cellular component	TAS
GO:0002576	platelet degranulation	biological process	TAS
GO:0005615	extracellular space	cellular component	IEA
GO:0007155	cell adhesion	biological process	IEA
GO:0005576	extracellular region	cellular component	NAS[14718574]; TAS
GO:0030168	platelet activation	biological process	TAS
GO:0008015	blood circulation	biological process	IEA
GO:0007596	blood coagulation	biological process	TAS

F5 related KEGG pathways (count: 1)

ID	Name	Brief Description	Full Description
Gene mapped KEGG pathways
hsa04610	complement and_coagulation_cascades	Complement and coagulation cascades	Blood coagulation is a series of coordinated and calcium-dep...... Blood coagulation is a series of coordinated and calcium-dependent proenzyme-to-serine protease conversions likely to be localized on the surfaces of activated cells in vivo. It culminates in the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. The kallikrein-kinin system is an endogenous metabolic cascade, triggering of which results in the release of vasoactive kinins (bradykinin-related peptides). Kinin peptides are implicated in many physiological and pathological processes including the regulation of blood pressure and sodium homeostasis, inflammatory processes, and the cardioprotective effects of preconditioning. Complement is a system of plasma proteins that is activated by the presence of pathogens. There are three pathways of complement activation: the classical pathway, the lectin pathway, and the alternative pathway. All of these pathways generate a crucial enzymatic activity that, intern, generates the effector molecules of complement. The three main consequences of complement activation are the opsonization of pathogens, the recruitment of inflammatory and immunocompetent cells, and the direct killing of pathogens. More...

F5 related BioCarta pathways (count: 2)

ID	Name	Brief Description	Full Description
Gene mapped BioCarta pathways
EXTRINSIC_PATHWAY	extrinsic pathway	Extrinsic Prothrombin Activation Pathway	Blood coagulation or clotting takes place in 3 essential pha...... Blood coagulation or clotting takes place in 3 essential phases. The first phase is the activation of a prothrombin activator complex. The second phase is the activation of prothrombin. The third stage is clot formation as a result of fibrinogen cleavage by activated thrombin. The prothrombin activation complex is formed by two pathways each of which results in a different form of the prothrombin activator. The extrinsic mechanism of prothrombin activator formation begins with trauma to vascular walls or extravascular tissues. The damaged tissue releases tissue thromboplastin also known as tissue factor (TF). The formation of a clot by this mechanism usually takes as little as 15 seconds. This cascade is initiated by the activation of factor X by TF and factor VII. Activated factor X combined with factor V, factor VII and TF constitutes the prothrombin activator. Calcium (Ca++) is required for each of these steps. The prothrombin activator in the extrinsic pathway is very similar to the activator in the intrinsic pathway. Antithrombin III inhibits the activity of thrombin and also the step leading to the activation of factor X. Antithrombin III is a hundred to a thousand times more effective when bound by heparin. Protein C is activated by thrombin and with the Protein S cofactor provides a strong negative feedback in this phase of clot formation. Disease Significance: Most of the clotting factors are formed in the liver. Diseases of the liver or damage to the liver can depress the levels of these factors in the blood resulting in excessive bleeding. Vitamin K deficiency can also result in a similar condition since Vitamin K is essential for the formation of factor VII, IX, X and prothrombin. Vitamin K is synthesized in the intestinal tract by bacteria. More...
INTRINSIC_PATHWAY	intrinsic pathway	Intrinsic Prothrombin Activation Pathway	Blood coagulation or clotting takes place in 3 essential pha...... Blood coagulation or clotting takes place in 3 essential phases. The first phase is the activation of a prothrombin activator complex. The second phase is the activation of prothrombin. The third stage is clot formation as a result of fibrinogen cleavage by activated thrombin. The prothrombin activation complex is formed by two pathways each of which results in a different form of the prothrombin activator. The intrinsic mechanism of prothrombin activator formation begins with trauma to the blood or exposure of blood to collagen in a traumatized vessel wall. This usually also results in damage to fragile platelets. The formation of a clot by this mechanism usually takes 1 to 6 minutes. This cascade begins with the activation of factor XII and the release of platelet factor 3 (PF3) from damaged platelets. Activated factor XII cleaves and actives factor XI and prekallikrein (PK). Factor XII is also activated by activated prekallikrein (aPK) in an internal amplification loop. Calcium (Ca++) is required for the initial three steps. The prothrombin activator in the intrinsic pathway is very similar to the activator in the extrinsic pathway. Antithrombin III inhibits the activity of thrombin and also two of the steps in the formation of the activator. Protein C is activated by thrombin and with the Protein S cofactor provides a strong negative feedback in this phase of clot formation. When blood is collected, the intrinsic pathway is activated by contact with the collection devices causing damage to the platelets and activation of factor XII. Antithrombin III is a hundred to a thousand times more effective when bound by heparin. Use of nonwettable surface materials can increase the clot formation time to over an hour. Disease Significance: Most of the clotting factors are formed in the liver. Diseases of the liver or damage to the liver can depress the levels of these factors in the blood resulting in excessive bleeding. Vitamin K deficiency can also result in a similar condition since Vitamin K is essential for the formation of factor VII, IX, X and prothrombin. Vitamin K is synthesized in the intestinal tract by bacteria. More...

F5 related Reactome pathways (count: 6)

ID	Name	Description
Gene mapped Reactome pathways
REACT_798	platelet activation	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...
REACT_20	formation of_platelet_plug	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...
REACT_2051	formation of_fibrin_clot_clotting_cascade	The formation of a fibrin clot at the site of an injury to t...... The formation of a fibrin clot at the site of an injury to the wall of a normal blood vessel is an essential part of the process to stop blood loss after vascular injury. The reactions that lead to fibrin clot formation are commonly described as a cascade, in which the product of each step is an enzyme or cofactor needed for following reactions to proceed efficiently. The entire clotting cascade can be divided into three portions, the extrinsic pathway, the intrinsic pathway, and the common pathway. The extrinsic pathway begins with the release of tissue factor at the site of vascular injury and leads to the activation of factor X. The intrinsic pathway provides an alternative mechanism for activation of factor X, starting from the activation of factor XII. The common pathway consists of the steps linking the activation of factor X to the formation of a multimeric, cross-linked fibrin clot. Each of these pathways includes not only a cascade of events that generate the catalytic activities needed for clot formation, but also numerous positive and negative regulatory events. More...
REACT_604	hemostasis	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...
REACT_1439	common pathway	The common pathway consists of the cascade of activation eve...... The common pathway consists of the cascade of activation events leading from the formation of activated factor X to the formation of active thrombin, the cleavage of fibrinogen by thrombin, and the formation of cleaved fibrin into a stable multimeric, cross-linked complex. Thrombin also efficiently catalyzes the activation of several factors required earlier in the clotting cascade, thus acting in effect as a positive regulator of clotting. At the same time, thrombin activates protein C, which in turn catalyzes the inactivation of several of these upstream factors, thereby limiting the clotting process. Thrombin can also be trapped in a stable, inactive complex with antithrombin-3, a circulating blood protein. The quantitative interplay among these positive and negative modulators is critical to the normal regulation of clotting, facilitating the rapid formation of a protective clot at the site of injury, while limiting and physically confining the process. These events are outlined in the drawing: black arrows connect the substrates (inputs) and products (outputs) of individual reactions, and blue lines connect output activated enzymes to the other reactions that they catalyze. More...
REACT_318	platelet degranulation	Platelets function as exocytotic cells, secreting a plethora...... Platelets function as exocytotic cells, secreting a plethora of effector molecules at sites of vascular injury. Platelets contain a number of distinguishable storage granules including alpha granules, dense granules and lysosomes. On activation platelets release a variety of proteins, largely from storage granules but also as the result of apparent cell lysis. These act in an autocrine or paracrine fashion to modulate cell signaling. Alpha granules contain mainly polypeptides such as fibrinogen, von Willebrand factor, growth factors and protease inhibitors that that supplement thrombin generation at the site of injury. Dense granules contain small molecules, particularly adenosine diphosphate (ADP), adenosine triphosphate (ATP), serotonin and calcium, all recruit platelets to the site of injury. More...

F5 related interactors from protein-protein interaction data in HPRD (count: 12)

Gene	Interactor	Interactor in MK4MDD?	Experiment Type	PMID
F5	CALR	No	in vivo	9525969
F5	F5	Yes	in vitro	10586886
F5	PROS1	No	in vitro	10593904 , 8428962
F5	PROC	No	in vitro	1615482 , 7989361 , 10026263
F5	CSNK2A1	No	in vivo	9525959
F5	CTSG	No	in vitro	9718313
F5	F10	No	in vitro	2303476
F5	ELANE	No	in vitro	9242537
F5	F2	No	in vitro;in vivo	9032460 , 10026263
F5	MMRN1	No	in vitro	15452129
F5	SERPINA3	No	in vitro	8216224
F5	EPR1	No	in vitro	9079657

Gene Report

Gene mapped GO terms

Gene mapped KEGG pathways

Gene mapped BioCarta pathways

Gene mapped Reactome pathways