Mouse Coagulation factor X III ELISA Kit

Name: Mouse Coagulation factor X III ELISA Kit
SKU: DEIA-BJ2452
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, cell culture supernatants, body fluid and tissue homogenate

Species Reactivity

Mouse

Detection Method

Competitive ELISA

Intended Use

Mouse Coagulation factor X III ELISA Kit kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Coagulation factor X III. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.

Contents of Kit

1. MICROTITER PLATE: 96 wells
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
4. SUBSTRATE A: 6 mL
5. SUBSTRATE B: 6 mL
6. STOP SOLUTION: 6 mL
7. WASH SOLUTION (100 x): 10 mL
8. BALANCE SOLUTION: 3 mL

Storage

All components of this kit are stable at 2-8°C until the kit's expiration date.

Detection Range

0.5-10 ng/mL

Sensitivity

0.1 ng/mL

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Genomic ancestry of a sample population from the state of Sao Paulo, Brazil

AMERICAN JOURNAL OF HUMAN BIOLOGY

Authors: Ferreira, Luzitano Brandao; Mendes-Junior, Celso Teixeira; Vieira Wiezel, Claudia Emilia; Luizon, Marcelo Rizzatti; Simoes, Aguinaldo Luiz

Abstract

Allelic frequencies of eight autosomal short-tandem repeat (STR) loci (TH01, TPOx, CSF1PO, vWA, FES/FPS, F13A1, F13B, and CD4) were determined in 400 individuals born in the State of Sao Paulo. No significant deviations from Hardy-Weinberg equilibrium were found in any loci analyzed. The Unweighted Pair-Group Method with Arithmetic Mean (UPGMA) tree constructed based on genetic distances revealed that the present population was grouped with Europeans, and separated from African and Amerindian populations. Estimates of admixture components based on the gene identity method revealed 79% European, 14% African, and 7% Amerindian contributions to this Brazilian population sample.

Homozygous intronic mutation leading to inefficient transcription combined with a novel frameshift mutation in F13A1 gene causes FXIII deficiency

JOURNAL OF HUMAN GENETICS

Authors: Wang, Wei; Huang, Lijun; Ma, Qiuling; Xiao, Deqian; Chen, Xiaodan; Yang, Zhigang; Wang, Xiaoying; Zhou, Keyuan; Li, Gang; Xiao, Man; Du, Guankui; Hao, Xinbao; Cai, Wangwei

Abstract

Two novel mutations, 602-605delAAAG in exon 5 and Int1(+12)C > A, of the F13A1 gene were identified in a Chinese factor XIII (FXIII)-deficient family. The 602-605delAAAG mutation results in the premature termination of translation. To determine the functional effect of the Int1(+12)A mutation, we transiently expressed luciferase reporters in U937 cells. We found that the first 951 bp of F13A1 intron 1 is involved in regulating the expression of the F13A1 gene and that Int1(+12)A results in its reduced expression. Electrophoretic mobility shift assay indicated that Int1(+12)A causes reduced protein binding. An Sp1 site was predicted in the sequence containing Int1(+12)C, which the Int1(+12)A mutation eliminates. Co-transfection of a plasmid expressing Sp1 revealed that Sp1 is involved in regulating the expression of FXIIIA and that Int1(+12) A leads to inefficient transcription. These results provide the first insight into a novel regulatory mechanism involving intron 1 in the F13A1 gene. Journal of Human Genetics (2011) 56, 460-463; doi:10.1038/jhg.2011.41; published online 21 April 2011