Rat Thrombin Activatable Fibrinolysis Inhibitor ELISA Kit

Name: Rat Thrombin Activatable Fibrinolysis Inhibitor ELISA Kit
SKU: DEIA-BJ2293
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

Rat

Detection Method

Sandwich ELISA

Intended Use

Rat Thrombin Activatable Fibrinolysis Inhibitor ELISA Kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Thrombin Activatable Fibrinolysis Inhibitor. 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

5-100 ng/mL

Sensitivity

1.0 ng/mL

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Clostridium perfringens in retail chicken

ANAEROBE

Authors: Nowell, Victoria J.; Poppe, Cornelis; Parreira, Valeria R.; Jiang, Yan-Fen; Reid-Smith, Richard; Prescott, John F.

Abstract

Clostridium perfringens isolates were recovered by enrichment from retail grocery chicken samples (n = 88) in Ontario, Canada, with one sample per site. The gene associated with necrotic enteritis in chickens, netB, was found in 21% of the isolates. The tpeL gene was found in 2% and the cpb2 gene in 68% (95% "atypical" genes) of isolates. This study suggests that netB-positive C. perfringens can reach people through retail chicken. (C) 2009 Elsevier Ltd. All rights reserved.

Pro-inflammatory cytokines reduce human TAFI expression via tristetraprolin-mediated mRNA destabilisation and decreased binding of HuR

THROMBOSIS AND HAEMOSTASIS

Authors: Komnenov, Dragana; Scipione, Corey A.; Bazzi, Zainab A.; Garabon, Justin J. W.; Koschinsky, Marlys L.; Boffa, Michael B.

Abstract

Thrombin activatable fibrinolysis inhibitor (TAFI) is the zymogen form of a basic carboxypeptidase (TAFIa) with both anti-fibrinolytic and anti-inflammatory properties. The role of TAFI in inflammatory disease is multifaceted and involves modulation both of specific inflammatory mediators as well as of the behaviour of inflammatory cells. Moreover, as suggested by in vitro studies, inflammatory mediators are capable of regulating the expression of CPB2, the gene encoding TAFI. In this study we addressed the hypothesis that decreased TAFI levels observed in inflammation are due to post-transcriptional mechanisms. Treatment of human HepG2 cells with pro-inflammatory cytokines TNF alpha, IL-6 in combination with IL-1 beta, or with bacterial lipopolysaccharide (LPS) decreased TAFI protein levels by approximately two-fold over 24 to 48 hours of treatment. Conversely, treatment of HepG2 cells with the anti-inflammatory cytokine IL-10 increased TAFI protein levels by two-fold at both time points. We found that the mechanistic basis for this modulation of TAFI levels involves binding of tristetraprolin (TTP) to the CPB2 3'-UTR, which mediates CPB2 mRNA destabilisation. In this report we also identified that HuR, another ARE-binding protein but one that stabilises transcripts, is capable of binding the CBP2 3'UTR. We found that pro-inflammatory mediators reduce the occupancy of HuR on the CPB2 3'-UTR and that the mutation of the UP binding site in this context abolishes this effect, although UP and HuR appear to contact discrete binding sites. Interestingly, all of the mediators tested appear to increase TAFI protein expression in THP-1 macrophages, likewise through effects on CPB2 mRNA stability.