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F13B Blocking Peptide (N-term)

Synthetic peptide

     
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Product Information
Primary Accession P05160
Other Accession NP_001985.2
Additional Information
Gene ID 2165
Other Names Coagulation factor XIII B chain, Fibrin-stabilizing factor B subunit, Protein-glutamine gamma-glutamyltransferase B chain, Transglutaminase B chain, F13B
Target/Specificity The synthetic peptide sequence is selected from aa 166-179 of HUMAN F13B
Format Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name F13B
Function The B chain of factor XIII is not catalytically active, but is thought to stabilize the A subunits and regulate the rate of transglutaminase formation by thrombin.
Cellular Location Secreted
Research Areas
Citations (0)
citation

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Background

This gene encodes coagulation factor XIII B subunit. Coagulation factor XIII is the last zymogen to become activated in the blood coagulation cascade. Plasma factor XIII is a heterotetramer composed of 2 A subunits and 2 B subunits. The A subunits have catalytic function, and the B subunits do not have enzymatic activity and may serve as a plasma carrier molecules. Platelet factor XIII is comprised only of 2 A subunits, which are identical to those of plasma origin. Upon activation by the cleavage of the activation peptide by thrombin and in the presence of calcium ion, the plasma factor XIII dissociates its B subunits and yields the same active enzyme, factor XIIIa, as platelet factor XIII. This enzyme acts as a transglutaminase to catalyze the formation of gamma-glutamyl-epsilon-lysine crosslinking between fibrin molecules, thus stabilizing the fibrin clot. Factor XIII deficiency is classified into two categories: type I deficiency, characterized by the lack of both the A and B subunits; and type II deficiency, characterized by the lack of the A subunit alone. These defects can result in a lifelong bleeding tendency, defective wound healing, and habitual abortion.

References

Silva, L.K., et al. Eur. J. Hum. Genet. 18(11):1221-1227(2010)
Romero, R., et al. Am. J. Obstet. Gynecol. 203 (4), 361 (2010) :
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Romero, R., et al. Am. J. Obstet. Gynecol. 202 (5), 431 (2010) :
Davila, S., et al. Genes Immun. 11(3):232-238(2010)

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$ 277.78
Cat# BP20162a
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