Rabbit Fibrinogen Matched Antibody Pair (ABPR-L002)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
Sufficient reagent for 4 x 96 well plates
Sample
Plasma
Species Reactivity
Rabbit
Intended Use
This antibody pair set comes with matched antibody pair to detect and quantify protein level of Human FGA
Contents of Kit
1. Capture Antibody (yellow): 0.4 ml of affinity-purified polyclonal anti-rabbit fibrinogen antibody for coating plates.
2. Detecting Antibody (red): 0.4 ml of peroxidase conjugated polyclonal anti-rabbit fibrinogen antibody for detection of captured fibrinogen.
Note: Reagents are sufficient for at least 4×96 well plates using recommended protocols. Antibodies are supplied in a 50% (v/v) glycerol solution for storage at –10 to -20°C. Keep vials tightly capped. Do not store in frost-free freezers.
Storage
-10 to -20°C
General Description
Fibrinogen is an abundant plasma protein (5-10 uM) produced in the liver. The intact protein has a molecular weight of 340 kDa and is composed of 3 pairs of disulphide-bound polypeptide chains named Aα, Bβ and γ. Fibrinogen is a triglobular protein consisting of a central E domain and terminal D domains. Proteolysis by thrombin results in release of Fibrinopeptide A (FPA, Aα1-16) followed by Fibrinopeptide B (FPB, Bβ1-14) and the fibrin monomers that result polymerize in a half-overlap fashion to form insoluble fibrin fibrils. The chains of fibrin are referred to as α, β and γ, due to the removal of FPA and FPB. The polymerised fibrin is subsequently stabilized by the transglutaminase activated Factor XIII that forms amide linkages between γ chains and, to a lesser extent, α chains of the fibrin molecules. Proteolysis of fibrinogen by plasmin initially liberates C-terminal residues from the Aα chain to produce fragment X (intact D-E-D, which is still clottable). Fragment X is further degraded to non-clottable fragments Y (D-E) and D. Fragment Y can be digested into its constituent D and E fragments. Digestion of non-crosslinked fibrin with plasmin is very similar to the digestion of fibrinogen, which results in production of fragments D and E. Degradation of crosslinked fibrin by plasmin results in fragment DD (D-Dimer consisting of the D domains of 2 fibrin molecules crosslinked via the γ chains), fragment E (central E domain) as well as DDE in which fragment E is non-covalently associated with DD. For human crosslinked fibrin, the relative weights of the cleavage fragments produced are: 184 kDa for fragment DD, 92 kDa for D, 50 kDa for E, 1.54 kDa for FPA and 1.57 kDa for FPB.

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References


Estrous synchronization in ewes: The use of progestogens and prostaglandins

ACTA AGRICULTURAE SCANDINAVICA SECTION A-ANIMAL SCIENCE

Authors: Yu, X. J.; Wang, J.; Bai, Y. Y.

This review summarizes the first principles, hormone types, and applied research related to the synchronization of estrus in ewes. The hormones used to induce synchronization include progestogens, such as medroxyprogesterone acetate (MAP), fluorogestone acetate (FGA), a controlled internal drug-releasing (CIDR) device, progesterone (P-4), norgestomet, and prostaglandins. These are usually combined with gonadotropins. Research on these hormones indicates that CIDR, MAP, and FGA can be regarded as equally effective for induction of estrus in ewes. Prostaglandins are a suitable alternative for estrous synchronization especially considering that progestogens may have negative effects on the functionality of ovulatory follicles. Artificial insemination, embryo transfer, and the acceleration of herd genetic trait improvement are among the potential practical applications of synchronous estrus in ewes.

Genetic and chromosomal variation-caused inconsistencies in two parental tests

FORENSIC SCIENCE INTERNATIONAL GENETICS SUPPLEMENT SERIES

Authors: Li, Chen; Li, Yifan; Jia, Li; Chen, Chong; Yan, Shi; Chen, Chuguang; Liu, Yacheng; Ren, He

Two special cases were reported where inconsistency between children and the fathers were observed at FGA locus. Regular additional STR tests were performed and no more inconsistency was observed in the first case. Through the following TA cloning and sequencing, the first case turned to be a two-step mutation between child and father. In the second case, however, one more inconsistency was found in the additional WA at D4S2366, which was on Chr. 4 as well. Then, seven randomly selected STR-loci on Chromosome 4 were analyzed, indicating a possible maternal uniparental disomy (UPD) in the child with normal phenotype. This study emphasizes gene or chromosomal variations may mislead parentage test, especially variations like UPD that are relatively unfamiliar to investigators. If all the inconsistent loci are on the same chromosome, investigators should take UPD into consideration, and further tests, like chromosomal-specific STR-typing, should be applied to prevent pseudo-exclusions.

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