, 2007). In fact, SK was suggested as spreading factor (Lahteenmaki et al., 2005) and the nephritis streptococci-associated protein (Johnston & Zabriskie, 1986). www.selleckchem.com/screening/stem-cell-compound-library.html SK (414 amino acid residues) contains three structural domains (α, β and γ) that exhibit synergistic effects on Plg activation (Kunamneni et al., 2007).
The SK-encoding genes (sk) from groups A (ska), C and G (skcg) represent different degrees of heterogeneity even in the same group of streptococci (Huang et al., 1989). The highest degree of variability in sk has been attributed to the β-domain by identification of two distinct variable regions – V1 and V2 – that comprise residues 147–218 and 244–264, respectively (Lizano & Johnston, 2005). The large number of nonconserved amino acids in the V1 region has been proposed to be the main source of sk allelic variation and responsible for differences in functional activities of different SK proteins and/or the severity of the streptococcal infections (Huang et al., 1989). In this context, the availability of a rapid and accessible assay to differentiate SK allelic variants to identify the potential pathogenic streptococci gained importance. To address this
concern, based on polymorphism of V1 region of SK β-domain (sk-V1) and using restriction enzymes MluI, PvuII, DraI and DdeI, a PCR–restriction fragment length polymorphism (PCR/RFLP) Ureohydrolase method was introduced (Johnston et al., 1991). Using this assay, a total of 125 GAS including APSGN- and non-APSGN-associated isolates were classified Afatinib in vivo into six sk allelic variants (sk1-sk6) in which certain variants (sk1, sk2 and sk6) were assigned as nephritogenic (SKN) (Johnston et al., 1991). Subsequently, nine ska variants (including three new sk alleles; sk7-sk9) among 53 Ethiopian GAS isolates from APSGN, tonsillitis
and healthy carriers were identified (Tewodros et al., 1993). Surprisingly, results of this prior study showed an even distribution of the SKN variants among APSGN and non-APSGN isolates, indicating no correlation between sk allelic variations and the disease manifestation (Tewodros et al., 1993). In parallel, studies on strains isolated from aboriginal communities in Australia indicated no association of SKN alleles with APSGN (Haase et al., 1994). Using the same PCR/RFLP method and strains collected from two geographically distinct locations (Ethiopia and Sweden), the lack of correlation between disease manifestation and sk allelic variations for GCS/GGS (besides GAS) was also shown (Tewodros et al., 1996). Results of this preceding study identified other new sk variants (sk10-sk14) that (together with sk5) were proposed as unique alleles belonging to GCS/GGS strains (Tewodros et al., 1996).