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Artykuły w czasopismach na temat „Factor XIII Val34Leu genetic polymorphism”

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Data publikacji: 2 czerwca 2025
Data aktualizacji: 31 lipca 2025

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1

Sucker, Christoph, Firuseh Farokhzad, Christine Kurschat, et al. "The Homozygous Leu Variant of the Factor XIII Val34Leu Polymorphism as a Risk Factor for the Manifestation of Thrombotic Microangiopathies." Clinical and Applied Thrombosis/Hemostasis 15, no. 2 (2007): 197–200. http://dx.doi.org/10.1177/1076029607304723.

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The 34 Leu (100T) variant of the factor XIII Val34Leu (G100T-) polymorphism slows down fibrinolysis and has been proposed as a thrombotic risk factor. In this pilot study, we enrolled 40 patients (mean age ± SD = 38 ± 11 years) and 728 controls to assess the role of this genetic variant for the manifestation of thrombotic microangiopathies. From the genotype prevalences, an increased manifestation risk for carriers of the TT genotype (homozygous Leu variant) of the factor XIII Val34Leu (G100T-) polymorphism was calculated (odds ratio [OR] = 2.44; 95% confidence interval [CI] = 0.8-7.6; P = .11
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2

Härtel, Christoph, Sören von Otte, Julia Koch, et al. "Polymorphisms of haemostasis genes as risk factors for preterm delivery." Thrombosis and Haemostasis 94, no. 07 (2005): 88–92. http://dx.doi.org/10.1160/th04-10-0653.

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SummaryClinical trials evaluating the potential benefit of anticoagulant treatment in pregnant women with inherited thrombophilia are based on the observation that a genetic predisposition to thrombosis is associated with frequent abortions and preterm birth. It was the aim of our study to delineate the impact of genetic polymorphisms with prothrombotic and antithrombotic effects on the occurrence of preterm birth in a large cohort of very-low-birth-weight (VLBW)-infants and their mothers. We examined the factor V Leiden and the prothrombin G20210A mutation, the factor VII 121del/ins and the f
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3

Sarecka-Hujar, Beata, Danuta Łoboda, Elżbieta Paradowska-Nowakowska, and Krzysztof S. Gołba. "Coagulation Factor XIII Val34Leu Polymorphism in the Prediction of Premature Cardiovascular Events—The Results of Two Meta-Analyses." Journal of Clinical Medicine 11, no. 12 (2022): 3454. http://dx.doi.org/10.3390/jcm11123454.

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Background: Polymorphisms within the gene that encodes for coagulation factor XIII (FXIII) have been suggested to be involved in the pathogeneses of ischemic stroke (IS) and myocardial infarction (MI). The Val34Leu polymorphism is one of the most commonly analysed FXIII polymorphisms. However, studies on the role of the Val34Leu polymorphism in the aetiology of vascular diseases often show contradictory results. In the present meta-analysis, we aimed to pool data from available articles to assess the relationship between the FXIII Val34Leu polymorphism and the susceptibilities to IS of undeter
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4

Reiner, Alexander P., Susan R. Heckbert, Hans L. Vos, et al. "Genetic variants of coagulation factor XIII, postmenopausal estrogen therapy, and risk of nonfatal myocardial infarction." Blood 102, no. 1 (2003): 25–30. http://dx.doi.org/10.1182/blood-2002-07-2308.

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Abstract We hypothesized that possession of either of 2 functional coagulation factor XIII polymorphisms, one within subunit A (Val34Leu) and one within subunit B (His95Arg), might modulate the prothrombotic effects of estrogen and help to explain the variation in incidence of arterial thrombotic events among postmenopausal women using hormone replacement therapy. In a population-based case-control study of 955 postmenopausal women, we assessed the associations of factor XIII genotypes and their interactions with estrogen therapy on risk of nonfatal myocardial infarction (MI). The presence of
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5

Shafey, Mona, Josdalyne L. Anderson, Dimitrios Scarvelis, Steve P. Doucette, France Gagnon, and Philip S. Wells. "Factor XIII Val34Leu Polymorphism and the Risk of Myocardial Infarction: A Meta-Analysis." Blood 106, no. 11 (2005): 1637. http://dx.doi.org/10.1182/blood.v106.11.1637.1637.

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Abstract Genetic factors involving blood coagulation are thought to contribute to the pathogenesis of myocardial infarction. A common polymorphism of Factor XIII, Factor XIII Val34Leu, may be protective against developing an acute myocardial infarction, but various studies show conflicting results. We performed a meta-analysis to determine whether the Factor XIII Val34Leu polymorphism is associated with a decreased risk of myocardial infarction. 93 articles were reviewed after a MEDLINE search of the literature (1966 through April Week 1 2005) and 12 case-control studies were selected. We incl
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6

Dossenbach-Glaninger, Astrid, Michael van Trotsenburg, Martin Dossenbach, et al. "Plasminogen Activator Inhibitor 1 4G/5G Polymorphism and Coagulation Factor XIII Val34Leu Polymorphism: Impaired Fibrinolysis and Early Pregnancy Loss." Clinical Chemistry 49, no. 7 (2003): 1081–86. http://dx.doi.org/10.1373/49.7.1081.

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Abstract Background: A successful outcome of pregnancy depends on proper placental formation. In the very beginning of this process, trophoblast invasion and fibrin deposition into the wall of the decidual veins play an important part. Two polymorphisms, coagulation factor XIII (FXIII) Val34Leu and plasminogen activator inhibitor 1 (PAI-1) 4G/5G, interfere with fibrin cross-linking and regulation of fibrinolysis and may therefore contribute to early pregnancy loss. Methods: We enrolled 49 unrelated Caucasian women with a history of two consecutive or three to six nonconsecutive early pregnancy
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7

Pintao, Maria C., Dayse M. Lourenço, Francisco H. A. Maffei, et al. "New Interactive Effects Involving Factor XIII Gene Polymorphisms in Venous Thrombotic Disease." Blood 104, no. 11 (2004): 2590. http://dx.doi.org/10.1182/blood.v104.11.2590.2590.

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Abstract Venous thrombosis (VT) is considered to be a multifactorial disorder in which several genetic and acquired risk factors interact dynamically. Coagulation factor XIII (FXIII) is an enzyme that participates in the final steps of the coagulation cascade. A number of gene variations have been described in both FXIII A and B subunits. FXIIIA Val34Leu, Tyr204Phe and Pro564Leu polymorphisms have been associated to increased specific activity of FXIII, and FXIIIA Val34Leu has been claimed to be protective against VT in several studies. In the FXIII B subunit, two common polymorphisms (His95Ar
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8

Schwedler, Christian, Guido Heymann, Larisa Bukreeva та Berthold Hoppe. "Association of Genetic Polymorphisms of Fibrinogen, Factor XIII A-Subunit and α2-Antiplasmin with Fibrinogen Levels in Pregnant Women". Life 11, № 12 (2021): 1340. http://dx.doi.org/10.3390/life11121340.

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Fibrinogen synthesis is stimulated by proinflammatory triggers and depends on α-, β- and γ-fibrinogen (FGA, FGB, FGG) genotypes. Constellations of fibrinogen, factor XIII A-subunit (F13A) and α2-antiplasmin (A2AP) genotypes predisposing for dense fibrin gels with high antifibrinolytic capacity (e.g., FGB rs1800790 A-allele carriage in F13A 34Val/Val or A2AP 6Arg/Arg wildtypes) are related with reduced inflammation. As both relationships are likely to influence each other, we tested whether the association of fibrinogen genotypes with fibrinogen levels is influenced by F13A and A2AP genotypes i
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9

Ladenvall, Claes, Ludvig Csajbok, Karin Nylén, Katarina Jood, Bengt Nellgård, and Christina Jern. "Association between factor XIII single nucleotide polymorphisms and aneurysmal subarachnoid hemorrhage." Journal of Neurosurgery 110, no. 3 (2009): 475–81. http://dx.doi.org/10.3171/2008.7.jns08272.

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Object Family studies have suggested a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (aSAH), but the underlying genetic risk factors remain poorly defined. There is an activation of the fibrinolytic system in aSAH, and fibrinolytic markers may be useful in predicting outcome. The authors investigate associations between putative functional variants in genes of importance for fibrinolysis and aSAH and/or outcome following aSAH. Methods One hundred eighty-three patients presenting with aSAH at a neurointensive care unit were consecutively recruited. Two healthy
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10

Ivanova, Nevena Georgieva. "A Rare Case of Pulmonary Embolism, Deep Vein Thrombosis, Bilateral Avascular Necrosis of the Femoral Head, and Miscarriage following COVID-19 in a Patient with Multiple Genetic Coagulation Factor Deficiency—A Case Report." Life 13, no. 12 (2023): 2240. http://dx.doi.org/10.3390/life13122240.

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The coronavirus disease (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The most common symptoms of COVID-19 are respiratory symptoms, but some patients develop severe thrombotic complications. Studies have looked into the association between the disease severity in COVID-19 patients and polymorphisms in the genes encoding prothrombotic and cardiovascular risk factors. The presented rare case describes inflammatory and acute thrombotic complications with musculoskeletal involvement in a patient with combined coagulation genetic defects. A 37-year-old w
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11

Березовская, Г. А., Е. С. Клокова та Н. Н. Петрищев. "Genetic predictors for symptoms recurrenсe in coronary artery disease after percutaneous coronary intervention". ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», № 4(61) (19 грудня 2017): 81–86. http://dx.doi.org/10.25557/igpp.2017.4.8527.

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Гены тромбообразования и фолатного обмена играют важную роль в развитии и прогрессии ишемической болезни сердца (ИБС). Однако о возможной роли полиморфных маркеров в рецидиве ИБС после чрескожного коронарного вмешательства (ЧКВ) известно недостаточно. Цель исследования: Оценить роль генетических факторов системы тромбообразования и фолатного обмена (полиморфных маркеров генов F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB ), в возобновление клиники ИБС после ЧКВ. Методика: Исследование проводили с использованием выборки из 90 больных ИБС в возрасте от 40 до 75 лет: 75 пациентов после планового ЧКВ (60
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12

Undas, Anetta, Kathleen E. Brummel-Ziedins, and Kenneth G. Mann. "Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions." Blood 109, no. 6 (2006): 2285–92. http://dx.doi.org/10.1182/blood-2006-01-010645.

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Abstract Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A2 production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as
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13

Tolou, Farzaneh, Thomas Dörner, Holger Kiesewetter, Abdulgabar Salama, and Berthold Hoppe. "Gene polymorphisms implicated in influencing susceptibility to venous and arterial thromboembolism: Frequency distribution in a healthy German population." Thrombosis and Haemostasis 96, no. 10 (2006): 465–70. http://dx.doi.org/10.1160/th06-06-0312.

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SummaryEvolvement and progression of cardiovascular diseases affecting the venous and arterial system are influenced bya multitude of environmental and hereditary factors. Many of these hereditary factors consist of defined gene polymorphisms, such as single nucleotide polymorphisms (SNPs) or insertion-deletion polymorphisms, which directly or indirectly affect the hemostatic system. The frequencies of individual hemostatic gene polymorphisms in different normal populations are well defined. However, descriptions of patterns of genetic variability of a larger extent of different factors of her
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14

Silvain, Johanne, Ana Pena, Jean-Baptiste Vignalou, et al. "FXIII-A Leu34 genetic variant in premature coronary artery disease: A genotype – phenotype case control study." Thrombosis and Haemostasis 106, no. 09 (2011): 511–20. http://dx.doi.org/10.1160/th11-01-0027.

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SummaryThe FXIII-A Leu34 genetic variant increases and accelerates fibrin stabilisation; however, its association with premature coronary artery disease (CAD) and thrombotic events remains controversial. FXIII Val34Leu genotype was determined in 242 young individuals (<45 years old) who survived a myocardial infarction (MI) and 242 healthy controls matched for age and gender. We evaluated its effect on longterm clinical outcome defined as a composite of cardiovascular death, recurrent MI and urgent revascularisation. In addition, fibrin clot stiffness (elastic modulus or EM) and response to
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15

Wang, Dawei, Liang Tang, Wei Shi, et al. "A Novel Nonsense Mutation of F13A1 Gene Causing Inherited Factor XIII Deficiency in a Chinese Han Family." Blood 118, no. 21 (2011): 4661. http://dx.doi.org/10.1182/blood.v118.21.4661.4661.

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Abstract Abstract 4661 Introduction: Coagulation factor XIII (FXIII) is a protransglutaminase that has a major role in the final stage of blood coagulation process by forming cross-links between γ-glutamyl and ε-lysine residues of fibrin chains. The plasma FXIII (pFXIII) circulates in plasma as a heterotetramer (FXIII-A2B2) consisting of two catalytic A subunits (FXIII-A2) and two carrier B subunits (FXIII-B2). Inherited FXIII deficiency is a rare autosomal recessive disease with lifelong bleeding. Most cases of FXIII deficiency are heterogeneous due to mutations in the F13A gene. Currently, m
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16

Francis, Charles W. "Factor XIII Polymorphisms and Venous Thromboembolism." Archives of Pathology & Laboratory Medicine 126, no. 11 (2002): 1391–93. http://dx.doi.org/10.5858/2002-126-1391-fxpavt.

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Abstract Objective.—To review the relationship between factor XIII polymorphisms and venous thromboembolism. Methods.—Review of the medical literature using computerized databases and secondary sources identified through reviews of bibliographies. Data Synthesis.—Plasma factor XIII is the precursor of a transglutaminase that cross-links fibrin, thereby altering its properties, including resistance to fibrinolysis. It is, therefore, biologically plausible that alterations in factor XIII activity could affect thrombosis risk. There are 4 common polymorphic forms of factor XIII that differ among
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17

Mikkola, H., G. Szôke, G. Haramura, et al. "Effect of Val34Leu Polymorphism on the Activation of the Coagulation Factor XIII-A." Thrombosis and Haemostasis 84, no. 10 (2000): 595–600. http://dx.doi.org/10.1055/s-0037-1614073.

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SummaryCoagulation factor XIII (FXIII) is a protransglutaminase involved in the last step of the coagulation cascade by stabilising the fibrin clot. Recently, a common variation (FXIII Val34Leu) has been associated with a decreased risk of myocardial infarction and deep venous thrombosis. Val34Leu is critically located near the thrombin activation site of FXIII-A. In this study we investigated its effects on the activation of FXIII. Both recombinant and platelet-derived FXIII Val34Leu variants were shown to be more susceptible to thrombin cleavage than the wild type FXIII. The rate of enzymati
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18

Attié-Castro, Flávia, Marco Zago, João Lavinha, et al. "Ethnic Heterogeneity of the Factor XIII Val34Leu Polymorphism." Thrombosis and Haemostasis 84, no. 10 (2000): 601–3. http://dx.doi.org/10.1055/s-0037-1614074.

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SummaryA polymorphism in the coagulation factor XIII gene (FXIII Val34Leu) has been recently described to confer protection for arterial and venous thrombosis and to predispose to intracerebral hemorrhage. At present it is known that FXIII Val34Leu is prevalent in Caucasians, but information upon its distribution in different ethnic groups is scarce. We investigated the prevalence of FXIIIVal34Leu in 450 unrelated subjects of four ethnic groups: 97 Caucasians (Brazilians of European descent and Portuguese), 149 Blacks (Brazilians, and Africans from Cameroon, Zaire and Angola), 40 Asians (Japan
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19

Catto, Andrew J., Hans P. Kohler, Julie Coore, Michael W. Mansfield, Max H. Stickland, and Peter J. Grant. "Association of a Common Polymorphism in the Factor XIII Gene With Venous Thrombosis." Blood 93, no. 3 (1999): 906–8. http://dx.doi.org/10.1182/blood.v93.3.906.

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Abstract We have shown an association between a common mutation in the factor XIII a-subunit gene, coding for an amino acid change, 3 amino acids from the thrombin activation site (factor XIII Val34Leu) that may protect against myocardial infarction and predisposes to intracranial hemorrhage. To investigate the possible role of factor XIII Val34Leu in the pathogenesis of venous thromboembolism (VTE) and potential interactions with factor V Leiden (FV:Q506) and prothrombin G → A 20210, we studied 221 patients with a history of VTE and 254 healthy controls. Patients with VTE showed an increased
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20

Catto, Andrew J., Hans P. Kohler, Julie Coore, Michael W. Mansfield, Max H. Stickland, and Peter J. Grant. "Association of a Common Polymorphism in the Factor XIII Gene With Venous Thrombosis." Blood 93, no. 3 (1999): 906–8. http://dx.doi.org/10.1182/blood.v93.3.906.403k24_906_908.

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We have shown an association between a common mutation in the factor XIII a-subunit gene, coding for an amino acid change, 3 amino acids from the thrombin activation site (factor XIII Val34Leu) that may protect against myocardial infarction and predisposes to intracranial hemorrhage. To investigate the possible role of factor XIII Val34Leu in the pathogenesis of venous thromboembolism (VTE) and potential interactions with factor V Leiden (FV:Q506) and prothrombin G → A 20210, we studied 221 patients with a history of VTE and 254 healthy controls. Patients with VTE showed an increased frequency
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21

Corral, Javier, Juan Antonio Iniesta, Rocio González-Conejero, Marino Villalón, Jose Rivera, and Vicente Vicente. "Factor XIII Val34Leu polymorphism in primary intracerebral haemorrhage." Hematology Journal 1, no. 4 (2000): 269–73. http://dx.doi.org/10.1038/sj.thj.6200043.

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Politou, Marianna, Christoforos Komporozos, Demosthenes Panagiotakos, et al. "Factor XIII Val34Leu polymorphism and the risk of myocardial infarction under the age of 36 years." Thrombosis and Haemostasis 99, no. 06 (2008): 1085–89. http://dx.doi.org/10.1160/th07-12-0755.

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SummaryThere are limited and controversial data regarding the impact of factor XIII (FXIII) Val34Leu polymorphism in the pathogenesis of premature myocardial infarction (MI). We examined whether FXIII Val34Leu polymorphism is associated with the development of early MI.We recruited 159 consecutive patients who had survived their first acute MI under the age of 36 years (mean age=32.1 ± 3.6 years, 138 were men). The control group consisted of 121 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease (CHD). FXIII Val34Leu polymorphis
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23

Ariëns, Robert A. S., Helen Philippou, Chandrasekaran Nagaswami, John W. Weisel, David A. Lane, and Peter J. Grant. "The factor XIII V34L polymorphism accelerates thrombin activation of factor XIII and affects cross-linked fibrin structure." Blood 96, no. 3 (2000): 988–95. http://dx.doi.org/10.1182/blood.v96.3.988.

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Abstract Factor XIII on activation by thrombin cross-links fibrin. A common polymorphism Val to Leu at position 34 in the FXIII A subunit is under investigation as a risk determinant of thrombosis. Because Val34Leu is close to the thrombin cleavage site, the hypothesis that it would alter the function of FXIII was tested. Analysis of FXIII subunit proteolysis by thrombin using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and high-performance liquid chromatography showed that FXIII 34Leu was cleaved by thrombin more rapidly and by lower doses than 34Val. Mass spectrometry of isolat
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Ariëns, Robert A. S., Helen Philippou, Chandrasekaran Nagaswami, John W. Weisel, David A. Lane, and Peter J. Grant. "The factor XIII V34L polymorphism accelerates thrombin activation of factor XIII and affects cross-linked fibrin structure." Blood 96, no. 3 (2000): 988–95. http://dx.doi.org/10.1182/blood.v96.3.988.015k57_988_995.

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Factor XIII on activation by thrombin cross-links fibrin. A common polymorphism Val to Leu at position 34 in the FXIII A subunit is under investigation as a risk determinant of thrombosis. Because Val34Leu is close to the thrombin cleavage site, the hypothesis that it would alter the function of FXIII was tested. Analysis of FXIII subunit proteolysis by thrombin using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and high-performance liquid chromatography showed that FXIII 34Leu was cleaved by thrombin more rapidly and by lower doses than 34Val. Mass spectrometry of isolated activa
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25

Gerardino, L., P. Papaleo, A. Flex, et al. "Coagulation factor XIII Val34Leu gene polymorphism and Alzheimer's disease." Neurological Research 28, no. 8 (2006): 807–9. http://dx.doi.org/10.1179/016164106x110454.

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Bereczky, Zsuzsanna, Éva Katona, Róza Ádány, László Muszbek, and Zoltán Vokó. "Factor XIII Val34Leu variant protects against coronary artery disease." Thrombosis and Haemostasis 97, no. 03 (2007): 458–63. http://dx.doi.org/10.1160/th06-11-0676.

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SummarySeveral studies suggested that Val34Leu variant of factor XIII (FXIII) might have a protective effect against coronary artery disease (CAD), but studies not supporting these findings have also been published. The authors performed a meta-analysis of 16 studies on 5,346 cases and 7,053 controls that investigated the association between Val34Leu polymorphism and CAD defined as history of myocardial infarction or significant stenosis on a coronary artery assessed by coronary angiography. Because of the heterogeneity of the study-specific results, the pooled effect estimates were calculated
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Reitsma, P. H., D. Lourenço, F. H. Maffei, et al. "Factor XIII Val34Leu Is a Genetic Factor Involved in the Aetiology of Venous Thrombosis." Thrombosis and Haemostasis 81, no. 05 (1999): 676–79. http://dx.doi.org/10.1055/s-0037-1614552.

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SummaryA mutation in the factor XIII gene (FXIII Val34Leu) gene was recently reported to confer protection against myocardial infarction, but its relationship with venous thrombosis is unknown. In addition, a mutation in the 5’-untranslated region of the FXII gene (46 C→T) was identified which is associated with low plasma levels of the protein. Its prevalence in patients with venous thrombosis is also unknown. We investigated the frequency of the FXIII Val34Leu and FXII 46 C→T mutations in 189 patients with deep venous thrombosis and in 187 age-, gender- and race-matched controls. FXIII Val34
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Elbaz, Alexis, Odette Poirier, Sandrine Canaple, François Chédru, François Cambien, and Pierre Amarenco. "The association between the Val34Leu polymorphism in the factor XIII gene and brain infarction." Blood 95, no. 2 (2000): 586–91. http://dx.doi.org/10.1182/blood.v95.2.586.

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Factor XIII catalyzes the formation of covalent bounds between fibrin monomers, thus stabilizing the fibrin clot and increasing its resistance to fibrinolysis. The frequency of a frequent Val34Leu polymorphism in the FXIII A-subunit gene has been shown to be lower in patients with myocardial infarction or venous thrombosis than in controls, whereas it was higher in patients with hemorrhagic stroke than in controls. Our aim was to study the relation between brain infarction (BI) and the FXIII Val34Leu polymorphism in 456 patients consecutively recruited with a BI confirmed by MRI, and 456 match
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Bossone, Anna, Vincenzo Brancaccio, Antonio Ciampa, Giovanni Di Minno, and Maurizio Margaglione. "Factor XIII Val34Leu Polymorphism and Risk of Deep Vein Thrombosis." Thrombosis and Haemostasis 84, no. 12 (2000): 1118–19. http://dx.doi.org/10.1055/s-0037-1614181.

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Saibeni, Simone, Maurizio Vecchi, Elena M. Faioni, Franca Franchi, Emanuele Rondonotti, and Roberto de Franchis. "Val34Leu factor XIII polymorphism in patients with inflammatory bowel diseases." Digestive and Liver Disease 33 (November 2001): A30. http://dx.doi.org/10.1016/s1590-8658(01)80274-7.

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Antalfi, B., E. Pongrácz, Z. Csiki, Z. A. Mezei, and A. H. Shemirani. "Factor XIII-A subunit Val34Leu polymorphism in fatal hemorrhagic stroke." International Journal of Laboratory Hematology 35, no. 1 (2012): 88–91. http://dx.doi.org/10.1111/j.1751-553x.2012.01465.x.

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Weger, Martin, Wilfried Renner, Olaf Stanger, et al. "Role of Factor XIII Val34Leu Polymorphism in Retinal Artery Occlusion." Stroke 32, no. 12 (2001): 2759–61. http://dx.doi.org/10.1161/hs1201.99889.

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33

Undas, Anetta, Wojciech J. Sydor, Kathleen Brummel, Jacek Musial, Kenneth G. Mann, and Andrew Szczeklik. "Aspirin Alters the Cardioprotective Effects of the Factor XIII Val34Leu Polymorphism." Circulation 107, no. 1 (2003): 17–20. http://dx.doi.org/10.1161/01.cir.0000047062.03282.a3.

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Hancer, Veysel Sabri, Reyhan Diz-Kucukkaya, Ahmet Kaya Bilge, et al. "The Association Between Factor XIII Val34Leu Polymorphism and Early Myocardial Infarction." Circulation Journal 70, no. 3 (2006): 239–42. http://dx.doi.org/10.1253/circj.70.239.

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35

Saibeni, S., M. Vecchi, E. M. Faioni, et al. "Val34Leu factor XIII polymorphism in Italian patients with inflammatory bowel disease." Digestive and Liver Disease 35, no. 1 (2003): 32–36. http://dx.doi.org/10.1016/s1590-8658(02)00008-7.

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36

Shemirani, Amir-Houshang, Bálint Antalfi, Endre Pongrácz, Zoltán András Mezei, Zsuzsanna Bereczky, and Zoltán Csiki. "Factor XIII-A subunit Val34Leu polymorphism in fatal atherothrombotic ischemic stroke." Blood Coagulation & Fibrinolysis 25, no. 4 (2014): 364–68. http://dx.doi.org/10.1097/mbc.0000000000000055.

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37

Chen, Fei, Qi Qiao, Peng Xu, Bing Fan, and Zaoping Chen. "Effect of Factor XIII-A Val34Leu Polymorphism on Myocardial Infarction Risk." Clinical and Applied Thrombosis/Hemostasis 20, no. 8 (2013): 783–92. http://dx.doi.org/10.1177/1076029613504130.

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38

Ehrenforth, Silke, and M. von Depka. "The Role of Factor XIII Val34Leu Polymorphism in Thrombofic Disease. Die Rolle des Faktor XIII Val34Leu Polymorphismus bei thrombotischen Erkrankungen." LaboratoriumsMedizin 25, no. 7-8 (2001): 254–61. http://dx.doi.org/10.1515/labm.2001.25.7-8.254.

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39

Balogh, István, Gabriella Szôke, Levente Kárpáti, et al. "Val34Leu polymorphism of plasma factor XIII: biochemistry and epidemiology in familial thrombophilia." Blood 96, no. 7 (2000): 2479–86. http://dx.doi.org/10.1182/blood.v96.7.2479.

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Abstract Val34Leu polymorphism of the A subunit of coagulation factor XIII (FXIII-A) is located in the activation peptide (AP) just 3 amino acids away from the thrombin cleavage site. This mutation has been associated with a protective effect against occlusive arterial diseases and venous thrombosis; however, its biochemical consequences have not been explored. In the current study it was demonstrated that the intracellular stability and the plasma concentration of FXIII of different Val34Leu genotypes are identical, which suggests that there is no difference in the rate of synthesis and exter
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40

Balogh, István, Gabriella Szôke, Levente Kárpáti, et al. "Val34Leu polymorphism of plasma factor XIII: biochemistry and epidemiology in familial thrombophilia." Blood 96, no. 7 (2000): 2479–86. http://dx.doi.org/10.1182/blood.v96.7.2479.h8002479_2479_2486.

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Val34Leu polymorphism of the A subunit of coagulation factor XIII (FXIII-A) is located in the activation peptide (AP) just 3 amino acids away from the thrombin cleavage site. This mutation has been associated with a protective effect against occlusive arterial diseases and venous thrombosis; however, its biochemical consequences have not been explored. In the current study it was demonstrated that the intracellular stability and the plasma concentration of FXIII of different Val34Leu genotypes are identical, which suggests that there is no difference in the rate of synthesis and externalizatio
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41

Carter, Angela M., Andrew J. Catto, Hans P. Kohler, Robert A. S. Ariëns, Max H. Stickland та Peter J. Grant. "α-Fibrinogen Thr312Ala polymorphism and venous thromboembolism". Blood 96, № 3 (2000): 1177–79. http://dx.doi.org/10.1182/blood.v96.3.1177.

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Abstract The A-fibrinogen Thr312Ala polymorphism, which occurs in a region involved in factor XIII (FXIII)-dependent cross-linking processes, is associated with poststroke mortality in subjects with atrial fibrillation, suggesting an influence either on intraatrial clot formation or embolization. We have determined the association of Thr312Ala with deep vein thrombosis (DVT) and pulmonary embolism (PE) and have assessed the interaction of Thr312Ala with the FXIII Val34Leu polymorphism in 122 patients with DVT, 99 patients with PE, and 254 healthy control subjects. The genotype distribution of
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42

Carter, Angela M., Andrew J. Catto, Hans P. Kohler, Robert A. S. Ariëns, Max H. Stickland та Peter J. Grant. "α-Fibrinogen Thr312Ala polymorphism and venous thromboembolism". Blood 96, № 3 (2000): 1177–79. http://dx.doi.org/10.1182/blood.v96.3.1177.015k25_1177_1179.

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The A-fibrinogen Thr312Ala polymorphism, which occurs in a region involved in factor XIII (FXIII)-dependent cross-linking processes, is associated with poststroke mortality in subjects with atrial fibrillation, suggesting an influence either on intraatrial clot formation or embolization. We have determined the association of Thr312Ala with deep vein thrombosis (DVT) and pulmonary embolism (PE) and have assessed the interaction of Thr312Ala with the FXIII Val34Leu polymorphism in 122 patients with DVT, 99 patients with PE, and 254 healthy control subjects. The genotype distribution of patients
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43

Anderson, Josdalyne L., Dimitrios Scarvelis, Steven Doucette, and Philip S. Wells. "Factor XIII Val34Leu Polymorphism Is Protective Against Venous Thromboembolism; a Meta-Analysis." Blood 104, no. 11 (2004): 3512. http://dx.doi.org/10.1182/blood.v104.11.3512.3512.

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Abstract Controversy over whether the factor XIII Val34Leu polymorphism confers protection against venous thromboembolism (VTE) is a persistent debate in the current thrombosis literature. If an accurate estimate of the protective effect were established, routine screening for this mutation in patients with VTE could provide more precise individual risk-profiling, but presently, it remains undetermined whether it is worthwhile to screen for this polymorphism. We performed a meta-analysis to determine whether the 34Leu allele of the factor XIII gene is associated with a decreased risk of VTE. S
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44

Shemirani, Amir H., Endre Pongrácz, Bálint Antalfi, Róza Ádány, and László Muszbek. "Factor XIII A subunit Val34Leu polymorphism in patients suffering atherothrombotic ischemic stroke." Thrombosis Research 126, no. 2 (2010): 159–62. http://dx.doi.org/10.1016/j.thromres.2010.06.012.

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Wells, Philip S., Josdalyne L. Anderson, Marc A. Rodger, Nancy Carson, Rebecca L. Grimwood, and Steve P. Doucette. "The factor XIII Val34Leu polymorphism: is it protective against idiopathic venous thromboembolism?" Blood Coagulation & Fibrinolysis 17, no. 7 (2006): 533–38. http://dx.doi.org/10.1097/01.mbc.0000245295.79891.86.

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Muszbek, L., A. H. Shemirani, and G. Haramura. "Activation of factor XIII in whole plasma: the influence of Val34Leu polymorphism." Journal of Thrombosis and Haemostasis 1 (July 2003): OC171. http://dx.doi.org/10.1111/j.1538-7836.2003.tb04552.x.

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Van Hylckama Vlieg, Astrid, Nantarat Komanasin, Robert A. S. Ariëns, et al. "Factor XIII Val34Leu polymorphism, factor XIII antigen levels and activity and the risk of deep venous thrombosis." British Journal of Haematology 119, no. 1 (2002): 169–75. http://dx.doi.org/10.1046/j.1365-2141.2002.03797.x.

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48

Iniesta, JA, J. Corral, R. González-Conejero, A. Díaz Ortuño, ML Martínez Navarro, and V. Vicente. "Role of Factor Xiii Val 34 Leu Polymorphism in Patients with Migraine." Cephalalgia 21, no. 8 (2001): 837–41. http://dx.doi.org/10.1046/j.0333-1024.2001.00273.x.

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At present, it is contradictory to determine if the combination of certain prothrombotic polymorphisms and migraine increases the risk to develop ischaemic cerebrovascular disease. Recently, the common Val34Leu polymorphism of the A-chain factor XIII gene, associated with variations in factor XIII activity, has been suggested to play a significant role in the development of arterial and venous thrombotic disorders. We analysed the prevalence of this polymorphism in 17 patients with coexisting ischaemic cerebrovascular disease and migraine (5 with aura, and 12 without aura), 89 patients with mi
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49

Mansfield, Michael, Peter Grant, and Joseph Mills. "Factor XIII – Circulating Levels and the Val34Leu Polymorphism in the Healthy Male Relatives of Patients with Severe Coronary Artery Disease." Thrombosis and Haemostasis 87, no. 03 (2002): 409–14. http://dx.doi.org/10.1055/s-0037-1613018.

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SummaryWe aimed to investigate whether increased levels of FXIII and/or a low prevalence of the protective Leu allele (of the Val34Leu FXIII polymorphism) occur in relatives of patients with severe CAD. 185 healthy male relatives aged 65 or less were recruited from 125 patients with multi-vessel CAD and compared to 185 healthy, agematched controls. The relatives and controls were similar in terms of clinical parameters. FXIII B-subunit levels were elevated in relatives, 1.11 µg/mL (1.08-1.14), compared with controls, 1.00 µg/mL (0.97-1.04), P<0.0001 but FXIII A2B2 levels did not differ betw
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50

Tammen, Harald, Thomas Möhring, Markus Kellmann, Andreas Pich, Hans H. Kreipe, and Rüdiger Hess. "Mass Spectrometric Phenotyping of Val34Leu Polymorphism of Blood Coagulation Factor XIII by Differential Peptide Display." Clinical Chemistry 50, no. 3 (2004): 545–51. http://dx.doi.org/10.1373/clinchem.2003.028209.

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Abstract Background: The Val34Leu mutation in the activation peptide of factor XIII (FXIIIA) correlates with a lower incidence of myocardial infarction and ischemic stroke but an increased risk for hemorrhagic stroke. We describe mass spectrometric detection of the activation peptide variants in human serum. Methods: We used differential peptide display (DPD) to compare comprehensive peptide maps from pairs of serum samples from healthy volunteers. Peptides were separated by liquid chromatography, and fractions were subjected to mass spectrometry. Mass spectra of all fractions were combined, g
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