A short protein description with the molecular wheight, isoforms, etc...
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Wikigenes includes links to
- NCBI Gene
- NCBI SNP
- iHOP resource
CHEMICAL STRUCTURE AND IMAGES
When relevant for the function
- Primary structure
- Secondary structure
- Tertiary structure
- Quaternary structure
Protein Aminoacids Percentage
The Protein Aminoacids Percentage gives useful information on the local environment and the metabolic status of the cell (starvation, lack of essential AA, hypoxia)
Protein Aminoacids Percentage (Width 700 px)
SYNTHESIS AND TURNOVER
- Cell signaling and Ligand transport
- Structural proteins
It is released upon stimulation by vasopressin
[High concentration of coagulation factor VIII as a risk factor for thrombosis]. 2001
High factor VIII antigen levels increase the risk of venous thrombosis but are not associated with polymorphisms in the von Willebrand factor and factor VIII gene., 2001
In 301 thrombosis patients and 301 matched healthy controls, factor VIII antigen (VIII:Ag) levels > or = 150 IU/dl increased the thrombosis risk more than fivefold.
Cerebral venous thrombosis and plasma concentrations of factor VIII and von Willebrand factor: a case control study. 2007
Our study suggests that elevation of plasma factor VIII levels is the most common prothrombotic risk factor for CSVT. Elevation of VWF is also associated with an increased risk of CSVT but its effect seems to be partly mediated through FVIII.
von Willebrand factor and factor VIII as risk factors for arterial and venous thrombosis. 2005
The Hypercoagulable State in Cushing's Disease Is Associated with Increased Levels of Procoagulant Factors and Impaired Fibrinolysis, But Is Not Reversible after Short-Term Biochemical Remission Induced by Medical Therapy. 2012
Context:Cushing's disease (CD) is accompanied by an increased risk of venous thromboembolism. Surgery is the primary treatment of CD.Objective:The aim of the study was to compare hemostatic parameters between patients with CD and controls and to evaluate the effect of medical treatment of CD on hemostasis.Design and Setting:During 80 d, stepwise medical treatment was applied with the somatostatin analog pasireotide, the dopamine agonist cabergoline, and ketoconazole, which suppresses adrenocortical steroidogenesis, at four university medical centers in The Netherlands.Patients:Seventeen patients with de novo, residual, or recurrent CD were included.Main Outcome Measures:We measured urinary free cortisol and parameters of coagulation and fibrinolysis.Results:Patients with CD had significantly higher body mass index (P < 0.001), shortened activated partial thromboplastin time (P < 0.01), and higher levels of fibrinogen, Factor VIII, and protein S activity (P < 0.05) compared to healthy control subjects. In addition, fibrinolytic capacity was impaired in patients with CD as reflected by prolonged clot lysis time (P < 0.001) and higher levels of plasminogen activator inhibitor type 1, thrombin-activatable fibrinolysis inhibitor, and α2-antiplasmin (P < 0.01). There were no statistically significant differences in von Willebrand factor:antigen, antithrombin, and protein C activity. After 80 d, 15 of 17 patients had normalized urinary free cortisol excretion. Despite biochemical remission, only slight decreases in antithrombin (P < 0.01) and thrombin-activatable fibrinolysis inhibitor (P < 0.05) levels were observed. Other parameters of coagulation and fibrinolysis did not change significantly.Conclusions:The hypercoagulable state in patients with CD, which is explained by both increased production of procoagulant factors and impaired fibrinolysis, is not reversible upon short-term biochemical remission after successful medical therapy. This may have implications for the duration of anticoagulant prophylaxis in patients with (cured) CD.
Analysis of inflammation- and atherosclerosis-related gene polymorphisms in branch retinal vein occlusion. 2009
Furthermore, IL-6 promotes coagulation by upregulating the transcription of tissue factor, fibrinogen, and factor VIII.
Particulate Matter-Induced Lung Inflammation Increases Systemic Levels of PAI-1 and Activates Coagulation Through Distinct Mechanisms. 2011
We previously reported that PM-treated animals exhibited selective, IL-6 dependent increases in fibrinogen, FVIII and vWF .
IL6 Factor VIII
VRGF Factor VIII
Hepatic low-density lipoprotein receptor-related protein deficiency in mice increases atherosclerosis independent of plasma cholesterol. 2004
Lower plasma cholesterol in MX1Cre(+)LRP-LDLRAPOE mice coincided with increased plasma lipoprotein lipase (71.2 +/- 7.5 vs 19.1 +/- 2.4 ng/ml, P =.002), coagulation factor VIII (4.4 +/- 1.1 vs 1.9 +/- 0.5 U/mL, P =.001), von Willebrand factor (2.8 +/- 0.6 vs 1.4 +/- 0.3 U/mL, P =.001), and tissue-type plasminogen activator (1.7 +/- 0.7 vs 0.9 +/- 0.5 ng/ml, P =.008) compared with controls.
[Blood coagulation in normotensives and hypertensives in relation to their body mass index]. 2002
Pearson correlation showed a significant (p < 0.001) positive relationship between PAI-1 and body mass index (BMI) (0.539), triglycerides (0.512), blood pressure (0.388 to 0.534), fibrinogen (0.404, and a negative one with HDL-cholesterol (0.625). BMI also correlated with fibrinogen (0.509; p < 0.001) and factor VIII (0.337; p < 0.01).
The Factor VIII acute phase response requires the participation of NFkappaB and C/EBP. 2000
In this study, we have demonstrated that the human Factor VIII promoter is activated in cultured hepatocytes exposed to bacterial lipopolysaccharide (LPS).
Acquired inhibitor to factor VIII in small cell lung cancer: a case report and review of the literature. 2012
Vasopressin Factor VIII
The effect of DDAVP on plasma levels of von Willebrand antigen II in normal individuals and patients with von Willebrand's disease. 1984
The infusion of 1-deamino-(8-D-arginine)-vasopressin (DDAVP) causes not only an elevation in factor VIII-related antigen (FVIIIR:Ag), but also a marked elevation of plasma von Willebrand antigen II (vWAgII). vWAgII reaches a peak concentration at 60 min and is elevated 3-8-fold over basal levels in normal individuals and individuals with type I, IIA, and IIB von Willebrand's disease.