Anti-GP9 monoclonal antibody, clone GRP-P [FITC]

Bacteriophage T4 gene product 9 (gp9) is a structural protein of baseplate that plays a key role at the beginning of the infection process. Biologically active gp9 is a trimer that consists of three domains. It is a convenient model to study folding and oligomerization mechanisms of complex multidomain proteins. The influence of deletions and mutations of several amino acid residues in the C-terminal part of molecule on protein folding, oligomerization, and functional activity has been studied. It was determined that gp9 trimerization occurs post-translationally. It was shown that Gln282 and Ile284 are essential for gp9 trimer stabilization. The disruption of hydrogen bonds formed by Gln282 with Leu203 and Thr205 of neighboring chain has effect not only on interaction between monomers within trimer but also on folding of the polypeptide chain. Tsf (temperature sensitive for folding) and su (suppressor) mutations in the C-terminal region of the polypeptide chain affecting protein folding have been found.

Background: P. aeruginosa is one of the top three causes of opportunistic human bacterial infections. The remarkable variability in the clinical outcomes of this infection is thought to be associated with genetic predisposition. However, the genes underlying host susceptibility to P. aeruginosa infection are still largely unknown. Results: As a step towards mapping these genes, we applied a genome wide linkage analysis approach to a mouse model. A large F2 intercross population, obtained by mating P. aeruginosa-resistant C3H/HeOuJ, and susceptible A/J mice, was used for quantitative trait locus (QTL) mapping. The F2 progenies were challenged with a P. aeruginosa clinical strain and monitored for the survival time up to 7 days post-infection, as a disease phenotype associated trait. Selected phenotypic extremes of the F2 distribution were genotyped with high-density single nucleotide polymorphic (SNP) markers, and subsequently QTL analysis was performed. A significant locus was mapped on chromosome 6 and was named P. aeruginosa infection resistance locus 1 (Pairl1). The most promising candidate genes, including Dok1, Tacr1, Cd207, Clec4f, Gp9, Gata2, Foxp1, are related to pathogen sensing, neutrophils and macrophages recruitment and inflammatory processes. Conclusions: We propose a set of genes involved in the pathogenesis of P. aeruginosa infection that may be explored to complement human studies.