Recombinant Human F2

• Cat.No.: F2-170H
• Product Overview: Recombinant human F2 protein was expressed in E.coli.

Specification

• Description: Coagulation factor II is proteolytically cleaved to form thrombin in the first step of the coagulation cascade which ultimately results in the stemming of blood loss. F2 also plays a role in maintaining vascular integrity during development and postnatal life. Mutations in F2 leads to various forms of thrombosis and dysprothrombinemia.
• Source: E.coli
• Species: Human
• Form: Liquid. In 20mM Tris-HCl buffer (pH 8.0) containing 0.4M urea, 10% glycerol.
• Molecular Mass: 33.9kDa (296aa)
• AA Sequence: MTFGSGEADC GLRPLFEKKS LEDKTERELL ESYIDGRIVE GSDAEIGMSP WQVMLFRKSP QELLCGASLI SDRWVLTAAH CLLYPPWDKN FTENDLLVRI GKHSRTRYER NIEKISMLEK IYIHPRYNWR ENLDRDIALM KLKKPVAFSD YIHPVCLPDR ETAASLLQAG YKGRVTGWGN LKETWTANVG KGQPSVLQVV NLPIVERPVC KDSTRIRITD NMFCAGYKPD EGKRGDACEG DSGGPFVMKS PFNNRWYQMG IVSWGEGCDR DGKYGFYTHV FRLKKWIQKV IDQFGE
• Purity: > 80% by SDS - PAGE
• Storage: Can be stored at +4C short term (1-2 weeks). For long term storage, aliquot and store at -20C or -70C. Avoid repeated freezing and thawing cycles.
• Concentration: 1.0 mg/ml (determined by Bradford assay)

Gene Information

• Gene Name: F2 coagulation factor II (thrombin) [ Homo sapiens (human) ]
• Official Symbol: F2
• Synonyms: F2; coagulationfactor II (thrombin); PT; prothrombin;serine protease; OTTHUMP00000197117; OTTHUMP00000233661; prothrombin B-chain
• Gene ID: 2147
• mRNA Refseq: NM_000506
• Protein Refseq: NP_000497
• MIM: 176930
• UniProt ID: P00734
• Chromosome Location: 11p11-q12
• Pathway: Angiopoietinreceptor Tie2-mediated signaling; BloodClotting Cascade; Cell surfaceinteractions at the vascular wall; CommonPathway; Diabetes pathways; G alpha (q) signalling events; GPCR downstream signaling
• Function: calciumion binding; growth factor activity; peptidase activity; protein binding;receptor binding; contributes_to receptor binding; serine-type endopeptidaseactivity; thrombospondin receptor activity

Reviews

01/01/2022

Quality control is evident. This product ensures accuracy in our studies.

01/27/2019

Our lab swears by this protein. Fast shipping is a definite bonus.

12/18/2018

Consistently reliable. The shipping speed is appreciated in our fast-paced lab.

Q&As

Can you discuss the role of the F2 gene in the synthesis of vitamin K-dependent clotting factors, and how disruptions in this process may lead to coagulation disorders?

The F2 gene plays a crucial role in the synthesis of vitamin K-dependent clotting factors, including prothrombin. Disruptions in this process, often due to genetic or nutritional factors, can contribute to coagulation disorders, impacting hemostasis and blood clotting.

How is the F2 gene regulated at the transcriptional level, and what factors influence prothrombin synthesis in hepatocytes?

Transcriptional regulation of the F2 gene involves factors like vitamin K-dependent gamma-carboxylation. Hepatocytes synthesize prothrombin under the influence of vitamin K and other coagulation factors.

The F2 gene encodes prothrombin, a crucial factor in blood coagulation. Prothrombin is converted to thrombin, a key enzyme in the clotting cascade, facilitating fibrin formation.

The F2 gene encodes prothrombin, a crucial factor in blood coagulation. Prothrombin is converted to thrombin, a key enzyme in the clotting cascade, facilitating fibrin formation.

What are the implications of genetic variations in the F2 gene, particularly polymorphisms, on prothrombin function and susceptibility to thrombotic or bleeding disorders?

Genetic variations in F2, including polymorphisms, can influence prothrombin function. Certain variants may predispose individuals to thrombotic or bleeding disorders.

How does genetic variation in the F2 gene impact prothrombin levels, and what are the consequences for an individual's risk of thrombotic events?

Genetic variations in the F2 gene can influence prothrombin levels, affecting an individual's propensity for thrombotic events. Certain variants may predispose individuals to a higher or lower risk of abnormal blood clot formation.