Identical with the Gene Bank Ref. ID sequence except for the point mutation 493 A/G resulting in the amino acid Thr substitution by Ala.
Full length Clone DNA of Human coagulation factor XIII, B polypeptide.
M13-47 and RV-M
The plasmid is confirmed by full-length sequencing.
Antibiotic in E.coli
Storage & Shipping
Each tube contains lyophilized plasmid.
The lyophilized plasmid can be stored at ambient temperature for three months.
Factor XIII cDNA ORF Neucleotide Sequence and Amino Acid Sequence Information
**Sino Biological guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories.**
Factor XIII cDNA ORF Clone in Cloning Vector, Human: Alternative Names
Coagulation factor 13 cDNA ORF Clone, Human; Coagulation factor XIII cDNA ORF Clone, Human; FXIIIB cDNA ORF Clone, Human
Factor XIII Background Information
Coagulation factor XIII B chain, also known as Fibrin-stabilizing factor B subunit, Protein-glutamine gamma-glutamyltransferase B chain, Transglutaminase B chain and F13B, is a secreted protein which contains 1 Sushi ( CCP / SCR ) domains. 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 composed of just 2 A subunits, which are identical to those of plasma origin. 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. Factor XIII 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. Defects in F13B are the cause of factor XIII subunit B deficiency ( FA13BD ) which is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.
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