Human Protein C Inhibitor (PCI) Matched Antibody Pair

Name: Human Protein C Inhibitor (PCI) Matched Antibody Pair
SKU: ABPR-L024
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Plasma

Species Reactivity

Human

Detection Method

Sandwich ELISA

Intended Use

This antibody pair set comes with matched antibody pair to detect and quantify protein level of Human SERPINA5

Contents of Kit

1. Capture Antibody (yellow): 0.5 ml of polyclonal affinity purified anti-PCI antibody for coating plates.
2. Detecting Antibody (red): 0.5 ml of peroxidase conjugated polyclonal anti-PCI antibody for detection of captured PCI.
Note: Reagents are sufficient for at least 5×96 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

Protein C Inhibitor (PCI), also known as Plasminogen Activator Inhibitor 3 (PAI3), is a member of the SERPIN family of proteinase inhibitors. It is produced in the liver as a single chain glycoprotein (mass of 57 kDa) and circulates in plasma at a concentration of 5 μg/ml (~90 nM). PCI is also found in urine in lower concentrations of 250 ng/mL (~0.4 nM). PCI is the primary inhibitor of activated Protein C (APC) in plasma but demonstrates a relatively broad specificity, also inhibiting thrombin, FXa, F.XIa, kallikrein, tPA, urokinase, prostate specific antigen, acrosin, chymotrypsin and trypsin. The preferred enzyme target for PCI appears to be thrombin and this interaction is increased by more than 100 fold in the presence of thrombomodulin. Like ATIII and HCII, the inhibitory activity of PCI towards some of these enzymes is stimulated by high concentrations of heparin (5 U/ml) which can accelerate the rate of inactivation as much as 50 fold. Enzyme inhibition by PCI occurs through proteolytic cleavage at Arg354-Ser355 and subsequent rapid formation of a stable, inactive 1:1 enzyme-PCI complex. Interaction with APC results in an SDS-stable APC-PCI complex of 102 kDa.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Proteome analysis of testis from infertile protein C inhibitor-deficient mice reveals novel changes in serpin processing and prostaglandin metabolism

ELECTROPHORESIS

Authors: Yang, Hanjiang; Wahlmueller, Felix Christof; Uhrin, Pavel; Baumgartner, Roland; Mitulovic, Goran; Sarg, Bettina; Geiger, Margarethe; Zellner, Maria

Abstract

Serine protease inhibitors (serpin) have therapeutic potential in a variety of pathogenic processes, ranging from thrombosis and altered immune response to liver cirrhosis. To investigate the physiological effects of protein C inhibitor (PCI, serpinA5), its gene was inactivated in a mouse model, resulting in male infertility. In the present report, 2D differential gel electrophoresis was utilized to investigate the molecular mechanisms for PCI involvement in male reproduction. Comparing the testes proteomes of three PCI-knockout mice with three wild types demonstrated similar patterns with the exception of amassive upregulation of prostaglandin reductase 1 (tenfold; p < 0.002) and the complete shifts in the molecular weights of serpinA1C and serpinA3K. All these PCI-dependent proteome changes were immunologically verified. Unbiased proteome analysis indicated that inactivation of serpinA5 strongly influenced both the protein species pattern of other A-clade serpins as well as prostaglandin metabolism in the testes.

Genetic variants in SERPINA4 and SERPINA5, but not BCL2 and SIK3 are associated with acute kidney injury in critically ill patients with septic shock

CRITICAL CARE

Authors: Vilander, Laura M.; Kaunisto, Mari A.; Vaara, Suvi T.; Pettila, Ville

Abstract

Background: Acute kidney injury (AKI) is a multifactorial syndrome, but knowledge about its pathophysiology and possible genetic background is limited. Recently the first hypothesis-free genetic association studies have been published to explore individual susceptibility to AKI. We aimed to replicate the previously identified associations between five candidate single nucleotide polymorphisms (SNP) in apoptosis-related genes BCL2, SERPINA4, SERPINA5, and SIK3 and the development of AKI, using a prospective cohort of critically ill patients with sepsis/ septic shock, in Finland. Methods: This is a prospective, observational multicenter study. Of 2567 patients without chronic kidney disease and with genetic samples included in the Finnish Acute Kidney Injury (FINNAKI) study, 837 patients had sepsis and 627 patients had septic shock. AKI was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, considering stages 2 and 3 affected (severe AKI), stage 0 unaffected, and stage 1 indecisive. Genotyping was done using iPLEX (TM) Assay (Agena Bioscience). The genotyped SNPs were rs8094315 and rs12457893 in the intron of the BCL2 gene, rs2093266 in the SERPINA4 gene, rs1955656 in the SERPINA5 gene and rs625145 in the SIK3 gene. Association analyses were performed using logistic regression with PLINK software. Results: We found no significant associations between the SNPs and severe AKI in patients with sepsis/ septic shock, even after adjustment for confounders. Among patients with septic shock (252 with severe AKI and 226 without AKI (149 with KDIGO stage 1 excluded)), the SNPs rs2093266 and rs1955656 were significantly (odds ratio 0.63, p = 0.04276) associated with stage 2-3 AKI after adjusting for clinical and demographic variables. Conclusions: The SNPs rs2093266 in the SERPINA4 and rs1955656 in the SERPINA5 were associated with the development of severe AKI (KDIGO stage 2-3) in critically ill patients with septic shock. For the other SNPs, we did not confirm the previously reported associations.