Disease relevance of PRH2

• PBMC were diluted, stimulated, and tested on EK cell targets infected with EIAV and recombinant vaccinia viruses expressing EIAV Env or Gag/Pr proteins [1].
• (His)(6)-YUH1, the HIV Pr mutant, and the (His)(6)-Ub-CTAPIII substrate were all expressed individually in Escherichia coli [2].
• The previously established close correlation between the Pa and Pr phenotypes and the genetic variants of salivary peroxidase (a powerful antibacterial system in the oral cavity) may provide an explanation for the relationship of certain proline-rich protein phenotypes to dental caries [3].
• Extensive proteolytic degradation of IgA1 is induced by a number of bacterial species often associated with periodontal diseases, including P. gingivalis, Pr. intermedia, and Pr. nigrescens [4].

High impact information on PRH2

• We have shown that genes for at least six human parotid proteins, parotid acidic protein (Pa), proline-rich protein (Pr), double-banded protein (Db), glycoprotein (Gl), parotid middle-band protein (Pm), and parotid-size variant (Ps) are linked [5].
• The 4-kb region of sequenced DNA from PRH1 differs by an average of 8.7% from the same region in PRH2, but the nucleotide sequences of the exon 3 of the two genes differ by only 0.2% [6].
• Distributions of the acidic proline-rich (Pr), parotid acidic (Pa), double band (Db), parotid size variant (Ps), parotid middle band (Pm), and parotid basic (Pb) protein phenotypes were similar in both caries-free and caries-active subjects [7].
• On PRH1, the proteins PIF-s, Db-s, and Pa are coded for, whereas PRP-1 and PRP-2 are coded for on the PRH2 locus [8].
• In 107 randomly collected samples from whites, PIF is strongly associated with Db (chi 2(1) = 20.02; P less than 0.0001) and Gl (chi 2(1) = 12.58; P = 0.0005) but not with Pr, Ps, Pm, and Pa proteins [9].

Biological context of PRH2

• In the present report, phenotypes of PRPs, the ratio of PRPs derived from the two loci (PRH1 and PRH2), and PRP concentration and output in parotid and submandibular saliva derived from the two loci are presented [8].
• The allelic products of Gl show evidence for linkage disequilibrium with the products of the Pr, Db, and Pa loci (P less than 0.0005) [10].
• Genetic polymorphism of the major parotid salivary glycoprotein (Gl) with linkage to the genes for Pr, Db, and Pa [10].

Anatomical context of PRH2

• The acidic proline-rich proteins (Pr) showing genetic polymorphism were purified from human parotid salivas by gel filtration and ion exchange chromatography [11].

Other interactions of PRH2

• A frequent mutation in the acidic proline-rich protein gene, PRH2, causing a Q147K change closely adjacent to the bacterial binding domain of the cognate salivary PRP (Pr1') in Afro-Americans. Mutations in brief no. 154. Online [12].
• Human salivary proline-rich (Pr) proteins: a posttranslational derivation of the phenotypes [11].

Analytical, diagnostic and therapeutic context of PRH2

• Cross-reactivity without spurring between all fractions containing major Pr proteins in both immunoelectrophoresis and double immunodiffusion suggests that these proteins are immunologically very similar or identical [13].

References