This is a default text for your page Sandbox GGC6. Click above on edit this page to modify. Be careful with the < and > signs.
You may include any references to papers as in: the use of JSmol in Proteopedia [1] or to the article describing Jmol [2] to the rescue.
Function
protease thrombin cleaves fibrinogen into monomers. The formation of monomers, fibrinogen beta, and fibrinogen alpha is insoluble fibrin matrix. fibrin works as a binding or trapping agent in the coagulation process, which creates blood clot.
For small wounds, the polymerized fibrin with platelets forms a hemostatic plug over the wounds site. Fibrin is also anti inflammatory which it protects against IFNG- mediated hemorrhage.
Afibrinogenemic pregnant patients will result in spontaneous miscarriage. Fibrinogen supplemental will allow the patients to sustain the pregnancy, therefore, maternal fibrinogen plays a important role for successful pregnancy.[3]
Disease
Congenital afibrinogenemia (CAFBN)
This is an inherited blood disorder where the blood does not clot normally. This disease is caused by truncating mutations. Changing in position Arg-35 when Thrombin cleaves the site of Fibrinopeptide leads to alpha- Dysfibrinogenemias. [4]
Nosebleeds, bleeding from the gums and tongue are commons after a minor trauma for people with this disease. bleedings in the brain and internal organs can occur for affected individuals which can lead to be fatal. However, it's rare. Women with this disease can experience an abnormal heavy menstrual bleeding, they could also have a difficult time carrying a pregnancy, and could result in miscarriages. Newborn with this disease can experience bleeding from the umbilical cord stump after birth. The treatment for this disease includes cryoprecipitate, fibrinogen, and plasma (contains clotting factors). [5]
Amyloidosis 8 (AMYL8)
This is hereditary disease which insoluble amyloid proteins deposits in body tissues and organs. This tends to abnormal protein build-up and leads to damaged organs and deaths. The disease is caused by a mutation fibrinogen alpha chain.[6]
Relevance
Structural highlights
This is a sample scene created with SAT to color by Group, and another to make a transparent representation of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. this shows polar and unpolar structure of 1XKT
- ↑ Hanson, R. M., Prilusky, J., Renjian, Z., Nakane, T. and Sussman, J. L. (2013), JSmol and the Next-Generation Web-Based Representation of 3D Molecular Structure as Applied to Proteopedia. Isr. J. Chem., 53:207-216. doi:https://dx.doi.org/10.1002/ijch.201300024
- ↑ Herraez A. Biomolecules in the computer: Jmol to the rescue. Biochem Mol Biol Educ. 2006 Jul;34(4):255-61. doi: 10.1002/bmb.2006.494034042644. PMID:21638687 doi:10.1002/bmb.2006.494034042644
- ↑ Iwaki T, Castellino FJ. Maternal fibrinogen is necessary for embryonic development. Curr Drug Targets. 2005 Aug;6(5):535-9. doi: 10.2174/1389450054546006. PMID:16026273 doi:https://dx.doi.org/10.2174/1389450054546006
- ↑ Asselta R, Plate M, Robusto M, Borhany M, Guella I, Solda G, Afrasiabi A, Menegatti M, Shamsi T, Peyvandi F, Duga S. Clinical and molecular characterisation of 21 patients affected by quantitative fibrinogen deficiency. Thromb Haemost. 2015 Mar;113(3):567-76. doi: 10.1160/TH14-07-0629. Epub 2014 Nov , 27. PMID:25427968 doi:https://dx.doi.org/10.1160/TH14-07-0629
- ↑ de Moerloose P, Neerman-Arbez M. Congenital fibrinogen disorders. Semin Thromb Hemost. 2009 Jun;35(4):356-66. doi: 10.1055/s-0029-1225758. Epub, 2009 Jul 13. PMID:19598064 doi:https://dx.doi.org/10.1055/s-0029-1225758
- ↑ Baker KR, Rice L. The amyloidoses: clinical features, diagnosis and treatment. Methodist Debakey Cardiovasc J. 2012 Jul-Sep;8(3):3-7. doi: 10.14797/mdcj-8-3-3. PMID:23227278 doi:https://dx.doi.org/10.14797/mdcj-8-3-3
