F7
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Official Full Name
coagulation factor VII (serum prothrombin conversion accelerator)
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Overview
Factor VII (formerly known as proconvertin) is one of the proteins that causes blood to clot in the coagulation cascade. It is an enzyme (EC 3.4.21.21) of the serine protease class. A recombinant form of human factor VIIa (NovoSeven, eptacog alfa [activated]) has U.S. Food and Drug Administration approval for uncontrolled bleeding in hemophilia patients. It is often used unlicensed in severe uncontrollable bleeding, although there has been safety concerns. -
Synonyms
F7; coagulation factor VII; SPCA; eptacog alfa; proconvertin; OTTHUMP00000018733; OTTHUMP00000018734; FVII coagulation protein; serum prothrombin conversion accelerator; factor VII;
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Fig1. Schema showing factor VII activation, activity and inhibition. (Francesco Bernardi, 2021)
What is F7 Protein?
Factor VII, or F7 protein, is crucial for blood clotting. Made mainly in the liver, it jumps into action when there's an injury, partnering with tissue factor to kickstart clot formation. This process turns fibrinogen into fibrin, which forms the clot. The F7 gene on chromosome 13 guides its production, and any mutation here can lead to a rare bleeding disorder known as Factor VII deficiency. Folks with this condition might experience anything from nosebleeds to severe internal bleeding. Interestingly, Factor VII's activity relies on vitamin K, and medications like warfarin can reduce its levels by affecting its synthesis in the liver.
What is the Function of F7 Protein?
F7 protein is like a key player in our body's way of stopping cuts from bleeding too much. It's kind of like the starter in a relay race for blood clotting. When we get hurt, F7 changes into its active form, F7a, especially when it meets up with another protein called tissue factor, which shows up at the injury site. Once F7a and tissue factor join forces, they get other clotting factors, like X and IX, moving in the right direction. This whole process ends up turning prothrombin into thrombin, which helps make a strong fibrin clot. That clot is like a plug that stops the bleeding and helps our body heal the wound. If F7 isn't working right, we might have trouble with bleeding, which shows just how important it is for keeping our blood balanced.
F7 Related Signaling Pathway
Factor VII, or F7, is vital in the coagulation cascade, helping in blood clotting. When there's damage to blood vessels, F7 becomes activated and partners with tissue factor (TF) to set off a chain of events that eventually form a blood clot. This activation of F7 is part of the extrinsic pathway, a rapid-response mechanism to minimize bleeding by converting prothrombin to thrombin. Thrombin then transforms fibrinogen into fibrin, weaving a stable clot to safeguard the wound. Beyond its primary role, F7's interactions can influence inflammation and even cell signaling in various pathological conditions.
F7 Related Diseases
Factor VII, or F7, is connected to a variety of blood-related diseases primarily due to its integral role in clotting. If there's too little F7, it can cause bleeding disorders since the blood doesn't clot properly. Conversely, too much F7 activity might lead to excessive clotting, which can result in conditions like thrombosis. This delicate balance makes F7 an important factor in maintaining normal circulatory health and preventing both bleeding and clotting complications.
Bioapplications of F7
Recombinant F7 protein finds extensive use across research and industrial sectors because of its key role in exploring blood clotting processes. In scientific studies, it is a significant instrument for dissecting clotting mechanisms and formulating treatments for bleeding conditions. The protein is also instrumental in devising diagnostic tests to assess bleeding dangers and is used in the production of pharmaceuticals to ensure the safety and effectiveness of blood-thinning drugs. Offering a dependable and uniform protein source, recombinant F7 boosts progress in medical research and biotechnology applications.
High Purity
Fig1. SDS-PAGE (F7-3908H)
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Fig2. SDS-PAGE (F7-3622H)
Case Study 1: Sarai Pongjantarasatian, 2019
Human mesenchymal stem cells (hMSCs) can transform into liver-like cells, which might make them useful for making biopharmaceuticals. Our team developed an immortalized hepatocyte-like cell line from these stem cells, which shows some liver-specific features. We checked if these cells could produce coagulation proteins and found that they could generate a small amount of human factor VII (FVII) using a lentiviral system, releasing about 22 ng/mL into a culture medium. The coagulation activity of FVII from these cells was nearly the same as that from HEK293T cells, as shown by testing. This is the first indication that these cells can produce FVII, showcasing a distinct quality of liver cells.
Fig1. FVII levels secreted in culture media supernatant.
Fig2. FVII coagulant activity from each cell line determined by chromogenic assay.
Case Study 2: Prafull S Gandhi, 2024
Dealing with serious bleeding disorders like Glanzmann thrombasthenia (GT) can be tough since there's no standard preventive treatment available. Right now, people handle severe bleeding with blood transfusions or by frequently giving recombinant activated factor VII (rFVIIa) intravenously. Researchers have come up with HMB-001, a bispecific antibody that attaches to the body's natural FVIIa, aiming to direct it to areas of blood vessel damage using a special receptor found on activated platelets. In studies with healthy nonhuman primates, HMB-001 extended the lifespan of FVIIa, leading to its build-up. Tests on mice and ex vivo models of GT showed that this antibody boosts FVIIa's effectiveness by targeting it to activated platelets, promoting clotting. These findings suggest that HMB-001 could become a new subcutaneous treatment option, potentially preventing bleeding episodes in GT and similar disorders with less frequent dosing.
Fig3. rFVIIa-equivalent activity was measured in PRP from healthy controls supplemented with d-RGDW to obtain GT-like platelets.
Fig4. Fibrin-dependent platelet pseudoaggregation was measured in washed platelets from healthy donors supplemented with d-RGDW.
F7 involved in several pathways and played different roles in them. We selected most pathways F7 participated on our site, such as Complement and coagulation cascades, which may be useful for your reference. Also, other proteins which involved in the same pathway with F7 were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.
Pathway Name | Pathway Related Protein |
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Complement and coagulation cascades | PLAT;TFPI;PLAUR;C4A;F11;SERPIND1;SERPINA1A;Serpina1b;CD59 |
F7 has several biochemical functions, for example, calcium ion binding, glycoprotein binding, protein binding. Some of the functions are cooperated with other proteins, some of the functions could acted by F7 itself. We selected most functions F7 had, and list some proteins which have the same functions with F7. You can find most of the proteins on our site.
Function | Related Protein |
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calcium ion binding | PCDH1G3;ACTN3A;DGKG;CHP2;PKD2L1;CD69;DGKA;S100A11;MGP |
glycoprotein binding | CALR;AZGP1;VWF;PLAT;TFR2;ERBB2;TGFB1;B2M;ITGB2 |
protein binding | TBC1D10C;MED28;ZBTB49;PCK2;FAP;DTX3;CST3;HORMAD1;RECK |
receptor binding | NRG3;PEX14;WNT11R;CADM2A;HLA-F;ASIP;PVR;CSK;ANGPTL1 |
serine-type endopeptidase activity | F9B;HTRA4;PRSS57;TPP1;PRSS59.1;GZMA;TMPRSS2;KLK1B22;CFI |
serine-type peptidase activity | DPP7;PRSS28;TMPRSS12;GZME;MCPT1;ELA3L;PRSS44;PLAUB;TMPRSS11B |
F7 has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with F7 here. Most of them are supplied by our site. Hope this information will be useful for your research of F7.
F3; capsh_ade05; DMWD; USP49; UIMC1; IKBKG; RCHY1; ALB; BECN1; SLX4; GABARAPL1
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Q&As (5)
Ask a questionFactor VII's role in the coagulation cascade ensures rapid initiation of clot formation, preventing excessive bleeding and contributing to hemostasis.
Factor VII is a key player in the extrinsic pathway, where it forms a complex with tissue factor to activate factor X, initiating the cascade leading to thrombin generation.
Factor VII is activated through a proteolytic cleavage, converting it into its active form (VIIa). This activation is regulated by tissue factor and other coagulation factors.
F7 deficiency results in impaired blood clotting, leading to a bleeding disorder known as coagulation factor VII deficiency. This condition can manifest in varying degrees of severity.
Factor VII is activated to its enzymatically active form (factor VIIa) and initiates the coagulation cascade by activating factor X, ultimately leading to the formation of a stable blood clot.
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