Recombinant Human Coagulation factor XI(F11),partial

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Code CSB-EP007916HU
Size US$2466Purchase it in Cusabio online store
(only available for customers from the US)
  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.

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Product Details

Purity Greater than 90% as determined by SDS-PAGE.
Target Names F11
Uniprot No. P03951
Research Area Cardiovascular
Alternative Names coagulation factor XI; Coagulation factor XIa light chain; F11; FA11_HUMAN; FXI; MGC141891; Plasma thromboplastin antecedent; Platelet coagulation factor XI ; PTA
Species Homo sapiens (Human)
Source E.coli
Expression Region 19-387aa
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 45.2kDa
Protein Length Partial
Tag Info N-terminal 6xHis-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Basically, we can dispatch the products out in 3-7 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

Target Data

Function Factor XI triggers the middle phase of the intrinsic pathway of blood coagulation by activating factor IX.
Gene References into Functions
  1. Direct DNA sequencing analysis of the F11 genes revealed that all of the 14 patients had a F11 gene mutation. Eight different mutations were identified in the apple 1, apple 2 or serine protease domains, except one which was a splice site mutation. Six of the mutations were recurrent. PMID: 27723456
  2. The aim of the current study was to analyze, for the first time in the Portuguese population, five well known and replicated venous thromboembolism - associated single nucleotide polymorphisms in genes ABO (rs2519093 and rs8176719), F11 (rs2036914 and rs2289252) and FGG (rs2066865), and to determine its possible association with risk for venous thromboembolism. PMID: 29995659
  3. Data indicate four new factor XI (FXI) gene defects potentially causing a functional deficiency and the duplication of 1653 bp involving exons 8 and 9. PMID: 28960694
  4. In this prospective cohort of elderly adults, there was no statistically significant association of higher FXI levels with incident coronary heart disease and stroke. PMID: 28009647
  5. High molecular weight kininogen has an inhibitory effect on nucleic acid-supported fXI activation and may function as a negative regulator of fXI activation. PMID: 28124063
  6. FXI has a role in promoting a vascular coagulation-inflammatory circuit in arterial hypertension PMID: 28148841
  7. thrombin activatable fibrinolysis inhibitor pathway impairment, largely caused by a hitherto unknown TAFIa resistance, appears to be one main cause of decreased fibrinolytic resistance in FXI deficiency PMID: 27094709
  8. factor XI has a role in procoagulant microparticle-promoted coagulation in human endotoxemia PMID: 26857798
  9. Three loci showed robust, replicating association with circulating FXI levels: KNG1 (rs710446, P-value = 2.07 x 10-302), F11 (rs4253417, P-value = 2.86 x 10-193), and a novel association in GCKR (rs780094, P-value = 3.56 x10-09), here for the first time implicated in FXI regulation. The two first SNPs (rs710446 and rs4253417) also associated with partial thromboplastin time PMID: 28053049
  10. The rs710446 and five low-frequency variant sets in KNG1 with FXI level variation of Factor XI were significant after multiple testing correction and permutation. PMID: 28445521
  11. Exploring the global landscape of genetic variation in coagulation factor XI deficiency PMID: 28615222
  12. Structures of FXI in complex with the laminin-derived peptide EFPDFP and a DFP peptide from the random screen demonstrated binding in the same pocket, although in a slightly different conformation, thus revealing some flexibility in the molecular interactions of the FXI apple 2 domain. PMID: 27006387
  13. inhibition of FXI and FXII distinctly alter the biophysical properties of fibrin. PMID: 27933406
  14. Data show that among the studied polymorphisms, only coagulation factor XI (F11) single nucleotide polymorphism rs2289252 was significantly associated with venous thrombosis (VT) and the F11 rs2289252-A allele was associated with a 1.6-fold increased risk of VT PMID: 27414984
  15. Thus in conclusion, the bleeding manifestations in FXI deficiency are varied and unpredictable; neither correlates with FXI levels nor with the mutations. Comprehensive analysis of all the factors including both plasma and platelet FXI, global hemostatic factors like thrombin generation potential may indicate a potential laboratory indicator for FXI deficiency related bleeding manifestations. PMID: 27710856
  16. Fasudil reduced LPS-mediated TF and PAI-1 expression and activity in PBMCs. These effects may partially be relevant to the clinical benefits of fasudil in the treatment of CAPD patients. PMID: 27756191
  17. rs2289252 and rs2036914 polymorphisms have important role in development of venous thromboembolism in the white race PMID: 28353616
  18. High activity of factor XI indicates a risk of occurrence of deep vein thrombosis in post-trauma patients with fractures. F11 rs2089252 and rs2036914 (single nucleotide polymorphisms) are associated with activity of factors XI in such patients despite prophylaxis. PMID: 27627722
  19. this study confirms the significant associations between polymorphism of 25264C.T in FXI and its activity and the risk of deep vein thrombosis after artificial joint replacement surgery PMID: 26934731
  20. F11 genetic variants are associated with the risk of incident venous thrombosis among women PMID: 26631918
  21. This study characterized FXI deficiency mutation spectrum in Chinese population with a high frequency of the W228*, G400V, Q263* and c.1136-4delGTTG mutations, which is distinct from that of other populations including Korean, Jewish or European populations. PMID: 27067486
  22. factor XI is localized to GPIb in membrane rafts and that this association is important for promoting the activation of factor XI by thrombin on the platelet surface PMID: 12517745
  23. higher basal factor XI concentration in the general population is not a risk marker for stroke or coronary heart disease PMID: 26386215
  24. Factor XI and factor XII activities were significantly higher in patients with slow coronary flow than in controls, and could be associated with enhanced procoagulant state present in these patients. PMID: 24509324
  25. FXI-thrombin axis contributes to distal platelet activation and procoagulant microaggregate formation in the blood flow downstream of the site of thrombus formation. PMID: 26769048
  26. F11 gene variant rs2289252 contributes to inherited forms of deep vein thrombosis incidence in Latvian population. PMID: 25091233
  27. These studies enhance understanding on the first allosteric inhibitor of FXIa and highlight its value as a promising anticoagulant. PMID: 25935648
  28. ROTEM assays failed to distinguish bleeding from non-bleeding patients but could do so between different FXI activity levels and genotypes. PMID: 26160656
  29. increased activity of FXI may be a potential risk factor for miscarriage; high activity of FXI diagnosed in women with history of miscarriage is not probably caused by the presence of SNPs rs2289252 and rs2036914 PMID: 25517908
  30. Data indicate that the mean factor XI (FXI) was not significantly different in laboratories using the same method on both exercises, suggesting good intralaboratory precision over time. PMID: 25976967
  31. Identification of a novel c.290G>A mutation in the F11 gene that is associated with mild Factor XI deficiency in a Dutch Caucasian family. PMID: 25618263
  32. In whites, the FXI variant was associated with both factor XI concentration and venous thromboembolism (VTE) incidence (1.15-fold greater incidence of VTE per risk allele), whereas In African-Americans, these associations were absent. PMID: 26260105
  33. Mass spectrometry analyses of FXI revealed full occupation of two of the three heavy-chain glycosites and almost full-site occupancy of the light chain. Analysis of FXI glycopeptides by LC-MS/MS enabled site-specific glycan profiling and occupancy. PMID: 25092234
  34. This study presents the first application of a new thrombin generation based factor XIa assay. PMID: 25288467
  35. study determined the molecular basis of FXI deficiency in 6 unrelated severely deficient patients in China; reported 8 mutations in FXI gene leading to FXI deficiency; functional consequences of a novel mutation leading to FXI deficiency have been elucidated PMID: 25681615
  36. FXI expression is directly regulated by a specific miRNA, miR-181a-5p, in the human liver PMID: 25379760
  37. FXI may have a role in risk of ischemic stroke, but not myocardial infarct; FXII and prekallikrein may not have a role in either PMID: 24977287
  38. We suggested that the minor allele of rs3756008 in the promoter of FXI gene could reduce its expression in kidney. PMID: 24420855
  39. at variance with other populations, no single major founder effect is present in Italian patients with FXI deficiency. PMID: 24112640
  40. Genetic variants of coagulation factor XI show association with ischemic stroke up to 70 years of age. PMID: 24086496
  41. Identification of a novel candidate F11 gene mutation associated with a cross-reacting material positive plasma FXI deficiency. PMID: 23571684
  42. Studies indicate that in the past two decades, more than 220 mutations in the factor XI (FXI) gene have been reported in patients with FXI deficiency, of which 7 showed a founder effect. PMID: 23929304
  43. a novel mutations in family with inherited factor XI deficiency PMID: 23494098
  44. Propose that long polyphosphates promote FXII-mediated blood coagulation bypassing FXI. PMID: 23659638
  45. The rather rare type I mutation in the FXI gene is a third founder mutation in Ashkenazi Jews with factor XI deficiency. PMID: 23332144
  46. For activation by thrombin, or during autoactivation, the data support a cis-activation mechanism in which the activating protease binds to and activates the same fXI subunit. PMID: 23515926
  47. F11 gene mutational screening revealed 11 different DNA variations, 3 of which had not yet been described PMID: 23305485
  48. Factor XI is a substrate for oxidoreductases: enhanced activation of reduced FXI is found in antiphospholipid syndrome thrombosis. PMID: 22704541
  49. A novel amino acid substitution in the serine protease catalytic domain (Ile463Ser) appears to be responsible for the congenital factor XI deficiency in a Swiss family. PMID: 22322133
  50. The F11 rs2289252 polymorphism is associated with FXI activity levels and APTT ratio in women with thrombosis. PMID: 22633531
  51. Circulating active TF and FXIa can occur in patients with cerebrovascular ischemic events >/=6 months after the events. The presence of these factors is associated with worse functional outcomes, persistent hypercoagulable state in cerebrovascular disease. PMID: 21820158
  52. The high frequency of the Q263X mutation in Korean patients with FXI deficiency and the presence of significant difference in the frequency of the mutation-bearing haplotype between the control and patient groups revealed a founder effect of the mutation. PMID: 21668437
  53. two structures of FXIa in complex with nonbasic inhibitors that occupy both the prime and nonprime sides of the active site are presented PMID: 22505407
  54. analysis of nine new mutations and an original large 4qTer deletion in western Brittany (France) with a possible role in factor XI deficiency PMID: 22159456
  55. The new mutation (Ile 436 Lys) was present in five patients with FXI deficiency at the homozygote level and in one patient as a compound heterozygote with an already known mutation namely Glu 117 stop. PMID: 21999818
  56. present findings define a new mechanism of mutations in F11 and underscore the need to perform expression studies and mRNA analysis of point mutations before stating that they are missense mutations PMID: 21718436
  57. Molecular analysis of whole coding region and splice junctions of F11 gene in three FXI deficient patients and their family members. PMID: 21649796
  58. In a Chinese family two new mutations were found: a heterozygous missense mutation in the Factor XI gene; and a deletion of two nucleotides resulting in frameshift mutation and premature termination of transcription in the Factor XII gene. PMID: 21192253
  59. Suggest that severe FXI deficiency provides protection against deep vein thrombosis. PMID: 21057700
  60. Coagulation factor XI has a role in thrombosis and it may be a novel target for antithrombotic treatment [review] PMID: 20727068
  61. TAFI plays an important role in platelet mediated resistance to fibrinolysis via feedback activation of factor XI. PMID: 20961395
  62. Molecular characterization of FXI deficiency. PMID: 20308231
  63. two novel mutations (Cys118Arg and Trp497Gly)in patients from Southern Italy with FXI deficiency PMID: 20491955
  64. molecular basis (ie. FIX mutations) of FXI deficiency in 16 patients from 12 families originating from the Marseilles area in the south of France was studied PMID: 20523169
  65. FXIa inhibitor did not prevent tissue factor-induced platelet aggregation. PMID: 20589316
  66. the pathogenic mechanism underlying the Thr33Pro and Gly217Ser mutations in patients with FXI deficiency PMID: 20015217
  67. 4 "apple domains" for a disk structure with extensive interfaces at the base of the catalytic domain. The characterization of this structure & its mutations provide new insight into F11 activation, interaction with F9, & platelet binding. Review. PMID: 20110423
  68. The coupling of alternative splicing and nonsense-mediated mRNA decay may play a role in regulating F11 expression, and point to the existence of a novel FXI isoform. PMID: 20042724
  69. The FXI gene mutations Trp228stop, Glu323Lys and Leu172Pro attribute to the pathogenesis of the factor XI deficiency in Chinese. PMID: 15182578
  70. Two SNPs, rs2289252 and rs2036914 in F11, appear to independently contribute to the risk of DVT, a contribution that is explained at least in part by an association with FXI levels. PMID: 19583818
  71. HK binding to FXI involves multiple apple domains, with F2 being most important. The findings demonstrate a similarity in mechanism for FXI and prekallikrein binding to HK PMID: 11733491
  72. role of HNF-4alpha in hepatocyte-specific expression PMID: 11891231
  73. interaction of coagulation factor XI with human umbilical vein endothelial cells (HUVEC) and with platelets PMID: 12029092
  74. plasma kallikrein and FXIa activate pro-HGF in vitro PMID: 12372819
  75. The frequency distributions of platelet polymorphisms and of prothrombotic polymorphisms were not different between patients with severe FXI deficiency who experienced or not an AMI. PMID: 12871398
  76. prekallikrein abolished Factor XI or -Factor XIa binding to vascular endothelial cell suspensions PMID: 12944405
  77. FXI has no effect on thrombin generation at 10 pm TF and physiological concentrations of Vitamin K-Dependent Proteins (VKDP); platelets and plasma FXI are able to compensate for the inhibitory effects of elevated VKDP PMID: 14521591
  78. The data indicate that FXI domains A2 and A3 make contributions to dimer formation and stabilize this dimeric conformation PMID: 14629467
  79. new ancient mutation in exon 4 resulting in Q88X, specific to patients from Nantes, France PMID: 14717969
  80. Data describe the structural role of glycine(193) in the serine protease, factor XIa. PMID: 15090552
  81. whole gene deletion as the causative mutation of factor XI deficiency, the result of unequal homologous recombination between flanking Alu repeat sequences PMID: 15226185
  82. binding of FXI to GPIbalpha is mediated by amino acids in the A3 domain in the presence or absence of HK. PMID: 15317813
  83. FXI binds to glycoprotein Ibalpha at sites comprising the leucine-rich repeat sequences within the NH2-terminal globular domain that are separate and distinct from the thrombin-binding site PMID: 15375170
  84. nature of possible platelet-associated FXI activity PMID: 15456479
  85. the platelets of both normal and FXI deficient individuals contain FXI mRNA that is identical to the mRNA found in liver; the FXI message is not alternatively spliced in platelets PMID: 15456480
  86. Crystal structures of the FXIa catalytic domain complexed to ecotin mutants PMID: 15545266
  87. structural characterization of FXI disease-causing mutations to complement phenotypic ata PMID: 15634276
  88. To provide a complete database of mutations and polymorphisms associated with factor XI deficiency, all available data on hereditary factor XI deficiency from main biological and medical databases were collected PMID: 15870541
  89. For optimal rates of factor IX activation in solution or on the physiologically relevant surface of activated platelets, a preformed dimer of factor XI is not required. PMID: 16042419
  90. Six novel missense mutations were identified in factor XI deficiency. PMID: 16079124
  91. Arg15, Phe34, Pro13, and Arg20 are important for FXIa inhibition by PN2 Kunitz protease inhibitor domain PMID: 16085935
  92. crystallographic analysis of Factor XI with mutated surface residues bound to benzamidine PMID: 16204896
  93. In 3 cases, the Glu117stop mutation caused a quantitative deficiency of factor XI by reducing mRNA levels. PMID: 16330457
  94. 31 novel mutations in the F11 gene are associated with Factor XI deficiency. PMID: 16835901
  95. The results demonstrate that basic amino acids in the autolysis loop of fXIa are important determinants of serpin specificity. PMID: 16878977
  96. coagulation factor XI (FXIP520L) has a proline to leucine substitution at residue 520, which results in a catalytic defect PMID: 17229051
  97. the F283L mutation leads to increased dimer dissociation by stabilizing a monomeric state with altered side-chain packing that is unfavorable for homodimer formation PMID: 17257616
  98. Report five missense mutations of Factor XI as being causative of factor XI deficiency. PMID: 17549289
  99. a novel mutation, a C-to-G transition at position 1394 in exon 12 in the FXI gene (F11 c.1394 C>G). This transition resulted in a missense mutation (Gln433Glu), which led to the disruption of the catalytic domain structure of the FXI molecule. PMID: 17581330
  100. review of the role of FXI in thrombosis and hemostasis, and the etiology and antithrombotic effect of FXI deficiency PMID: 17597996

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Involvement in disease Factor XI deficiency (FA11D)
Subcellular Location Secreted
Protein Families Peptidase S1 family, Plasma kallikrein subfamily
Tissue Specificity Isoform 2 is produced by platelets and megakaryocytes but absent from other blood cells.
Database Links

HGNC: 3529

OMIM: 264900

KEGG: hsa:2160

STRING: 9606.ENSP00000384957

UniGene: Hs.1430

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