Transfected Stable Cell Lines
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Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC005176 | Panoply™ Human F7 Knockdown Stable Cell Line | Inquiry |
| CSC-SC005176 | Panoply™ Human F7 Over-expressing Stable Cell Line | Inquiry |
| CLOE-0880 | Human F7 HEK293 Cell Lysate | Inquiry |
| CLOE-2965 | Mouse F7 (His) CHO stable Cell Lysate | Inquiry |
| CLOE-2968 | Mouse F7 (His) CHO Cell Lysate | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| LV12090L | human F7 (NM_000131) lentivirus particles | Inquiry |
| LV12091L | human F7 (NM_019616) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHW004955 | shRNA set against Chicken F7 (NM_204442) | Inquiry |
| SHW015216 | shRNA set against Danio rerio F7 (NM_131819) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDCB160358 | Human F7 ORF clone (NM_019616.2) | Inquiry |
| CDFR014564 | Rat F7 cDNA Clone(NM_152846.1) | Inquiry |
| MiUTR1R-01804 | F7 miRNA 3'UTR clone | Inquiry |
| MiUTR3H-13057 | F7 miRNA 3'UTR clone | Inquiry |
| MiUTR3H-13058 | F7 miRNA 3'UTR clone | Inquiry |
| CDCB157332 | Mouse F7 ORF clone (NM_010172.2) | Inquiry |
| CDCB159351 | Human F7 ORF clone (NM_000131.3) | Inquiry |
| CDCB166430 | Chicken F7 ORF Clone (NM_204442) | Inquiry |
| CDCB176691 | Danio rerio F7 ORF Clone (NM_131819) | Inquiry |
| CDCB180485 | Rabbit F7 ORF clone (NM_001082679.1) | Inquiry |
| CDCG001149 | Mouse F7 ORF clone(NM_010172.3) | Inquiry |
| CDCR278603 | Human F7 ORF Clone(NM_000131.4) | Inquiry |
| CDCR381651 | Rat F7 ORF Clone(NM_152846.1) | Inquiry |
| CDCS405445 | Human F7 ORF Clone (BC130468) | Inquiry |
Coagulation factor VII (F7) is a vitamin k-dependent serine protease, which exists in the humans in the form of 406 amino acids, and is involved in the coagulation process with activated F7 (F7a).
Figure 1. Structure and domain of F7.
Clinical Application
As an important coagulation factor, F7a is mainly used to treat the bleeding of hemophilia. Currently, F7a becomes the most common medicine for both hemophilia A and B patients. Besides, F7a is also used to treat the clinical bleeding, especially maternal bleeding.
Otherwise, F7 has the shortest half-life and low plasma content, so it can be used as an early diagnostic index for protein synthesis dysfunction in patients with liver disease. It was found that the expression of F7 was negatively correlated with the grading of hepatic fibrosis in patients with chronic liver disease through orthotopic hybridization in liver biopsy, which could be used as an index to predict the degree of fibrosis. The activity of coagulation factor VII is also closely related to prognosis, which is an early predictor of the prognosis in patients with cirrhosis and can better identify candidates for liver transplantation. The F7 deficiency can lead to the change of platelet activity, combined with the decrease of platelet count to prolong the bleeding time, so patients with invasive diagnosis and treatment should also use coagulation factor VII activity to evaluate the risk of hemorrhage. In addition to diagnosis, recombinant coagulation factor VII can effectively correct coagulation abnormalities in patients with liver disease and facilitate invasive examinations.
F7 and Hemophilia
Hemophilia is a coagulation disorder caused by a lack of relevant factors in the coagulation pathway. Prothrombin complicated concentrate (PCC) has a therapeutic effect on hemophilia. When studying PCC for the treatment of hemophilia, it was found that some components of PCC may be the key to the treatment. Analysis of this component shows that F7 is a key component of coagulation. By comparing the therapeutic effects of plasma derived from F7 (pd-F7) and PCC, it was found that pd-F7 had the better therapeutic effects on both type A and B hemophilia, and also for hemophilia patients with antibody inhibitors.
In the absence of the VIII/FIX complex, activated factor VII can still be activated on the surface of platelets, producing a small amount of factor Xa, resulting in a large amount of thrombin. At the same time, coagulation can be achieved by increasing the activity of thrombin-activated fibrinolytic inhibitors (TAFI) or restoring the permeability of fibrin. Meanwhile, no other side effects are produced during the treatment, which has caused concern in the research related to hemophilia treatment.
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