anti-Coagulation Factor XIII, A1 Polypeptide (F13A1) Antikörper

Cow (Bovine) Coagulation Factor XIII, A1 Polypeptide (F13A1) Interaktionspartner

1. kinetic and structural analysis of interactions between thrombin and the Factor XIII activation peptide

Human Coagulation Factor XIII, A1 Polypeptide (F13A1) Interaktionspartner

1. Inflammatory monocytes highly express Factor XIIIA, which promotes fibrin cross-linking to create a scaffold for lung squamous carcinomas cell invasion and metastases.

2. Effect of factor XIII levels and polymorphisms on the risk of myocardial infarction in young patients

3. Polymorphisms of F2, PROC, PROZ, and F13A1 Genes are Associated With Recurrent Spontaneous Abortion in Chinese Han Women.

4. Coagulation factor FXIII-A (FXIIIA) was found to express specifically in the fetal beta islets but not in the alpha/delta islets.

5. Factor XIIIa (AC-1A1) is a sensitive and specific nuclear marker for sebaceous differentiation...which can be utilized to aid in the diagnosis of sebaceous neoplasms.

6. Our meta-analysis supports an association between F13A1 Val34Leu and recurrent pregnancy loss.

7. A brief history of some key events in the conversion of fibrinogen to fibrin has been reviewed. (Review)

8. The results of this study suggest that these biomarker F13A1 can serve as a potential non-invasive early diagnosis platform reflecting PiB-PET imaging for Mild Cognitive Impairment and Alzheimer's Disease.

9. F13A1 gene mutations in 73 patients treated with recombinant FXIII-A2

10. Results show that the missense mutations-causing mild FXIII de fi ciency influence different aspects of FXIII function and can be functionally categorized on the basis of their expression phenotype.

11. These findings provide insight into assembly of the fibrinogen/FXIII-A2B2 complex in both physiologic and therapeutic situations.

12. FXIIIa exhibits a preference for Q237 in crosslinking reactions within fibrinogen alphaC (233-425) followed by Q328 and Q366.

13. factor XIII Val34Leu polymorphism is associated with coronary artery diseases risk, especially myocardial infarction. Age and sex did not affect the relationship between factor XIII Val34Leu polymorphism and diseases risk (Meta-Analysis)

14. Mounting evidence now suggests that platelet FXIII-A modulates hemostasis by several different mechanisms. This condensed review discusses recent advances in the understanding of the novel intracellular and extracellular functions of platelet FXIII-A. [review]

15. It is a unique case showing the combination of a highly aggressive angiosarcoma and presence of inherited FXIII deficiency. It is also a rare example demonstrating the benefit of FXIII genotyping besides the expected acquired FXIII deficiency possibly due to neoplasm induced increased consumption by elevated crosslinking of fibrin fibers.

16. The Val34Leu polymorphism of FXIII was not found in Korean people, and compared with Caucasians, a noticeably low incidence of deep vein thrombosis was shown.

17. Genetic basis of severe factor XIII deficiency in a large cohort of Indian patients has been uncovered.

18. Our meta-analysis suggests that there is no evidence for strong association between FXIII Val34Leu polymorphisms and intracerebral hemorrhage--{review}

19. Deletion of 11 or more N-terminal amino acids disrupts intersubunit interactions, which may prevent FXIII-A2 homodimer formation. AP-FXIII plays an important role in the stability of the FXIII-A2 dimer.

20. Mutations in the activation peptide of full-length recombinant FXIII regulate activation rates by thrombin, and V34L influences in vivo thrombus formation by increased cross-linking of the clot.

Mouse (Murine) Coagulation Factor XIII, A1 Polypeptide (F13A1) Interaktionspartner

1. Factor XIII-A and TG2 regulate resorption, adipogenesis and plasma fibronectin homeostasis in bone and bone marrow.

2. Suggest that resident macrophages maintain plasma FXIII-A and exclude the platelet lineage as a major contributor.

3. These findings provide insight into assembly of the fibrinogen/FXIII-A2B2 complex in both physiologic and therapeutic situations.

4. Mast cells have the ability to produce and degrade FXIIIA depending on their chymase expression profile: mast cells expressing chymase degrade FXIIIA, whereas mast cells that do not express chymase mainly produce FXIIIA

5. A lack of factor XIII leads to prolonged clotting times, increased signs of inflammation, and elevated bacterial dissemination in streptococcal skin diseases.

6. FXIII is a significant determinant of mucosal healing and clinical outcome following inflammatory colitis induced mucosal injury

7. These findings expose a newly recognized, essential role for fibrin crosslinking during whole blood clot formation and consolidation and establish FXIIIa activity as a key determinant of thrombus composition and size.

8. related to islet dysfunction during the development of type 2 diabetes

9. 5-HT inhibits Factor XIII-A-mediated plasma fibronectin matrix assembly and crosslinking in osteoblast cultures via direct competition with transamidation

10. High Transglutaminase factor XIII promotes arthritis through mechanisms linked to inflammation and bone erosion.

11. Fibrinogen from mice harboring the Fibgamma390-396A mutation exhibited reduced binding to FXIII, and plasma from these mice exhibited delayed FXIII activation and fibrin crosslinking, indicating these residues mediate FXIII binding and activation.

12. FXIII-A serves as a preadipocyte-bound proliferation/differentiation switch that mediates effects of hepatocyte-produced circulating pFN.

13. Physiological significance of mouse TG2 and Factor XIII through identification of substrate proteins in MC3T3-E1 cells.

14. Studies indicate that in FXIII-A-knockout mice, tail-tip bleeding times are doubled and clot stability, assessed by thromboelastography, was impaired compared with wild-type mice.

15. FXIIIA mRNA was regulated by the MAP kinase pathway.

16. Data indicate that FXIIIa-targeted probe signals showed good overlap with immune-fluorescent fibrin staining images.

17. factor XIIIA transglutaminase activity regulates osteoblast matrix secretion and deposition by affecting microtubule dynamics

18. Inhibition of TG2 and FXIIIA during early development of lesions reduced the macrophage content in the media of atherosclerotic vessels, while not affecting lesion size or geometric remodeling

19. Knockout mouse studies suggest that plasma FXIII-A does not derive primarily (if at all) from circulating platelets and indeed may not derive from the megakaryocyte lineage.

20. All FXIII2/2 and FXIII2/+ mice died within 5 days after MI from left ventricular (LV) rupture and had locally reduced levels of FXIII.