High impact information on PSMA2

• It was found that two anti-atherogenic compounds, BO-653 and probucol, inhibited the expression of three alpha-type proteasome subunits, PMSA2, PMSA3, and PMSA4 in human umbilical vein endothelial cells [1].
• Isolation and characterization of alpha-type HC3 and beta-type HC5 subunit genes of human proteasomes [2].
• Interestingly, the HC3 gene possesses an additional silencer element in the 5'-upstream region near the first exon [2].
• HC3 was less likely than HC2 to test positive for specimens that tested positive by PCR for any untargeted types (P < 0.001) [3].
• On the other hand, genes of three subunits of proteasome (PSMA2, PSMA3, PSMA4) were down-regulated by these antioxidants [4].

Biological context of PSMA2

• The genes for the alpha-type HC3 (PMSA2) and beta-type HC5 (PMSB1) subunits of human proteasomes map to chromosomes 6q27 and 7p12-p13 by fluorescence in situ hybridization [5].
• These results show that the human proteasomal HC3 and HC5 genes differ not only in their genomic structures, such as their numbers of exons and their exon-intron organizations, but also in the mechanisms regulating their transcription, suggesting that they diverged at an early stage of evolution [2].

Other interactions of PSMA2

• HC3 was less likely than HC2 to test positive for untargeted PCR-detected single infections with HPV53 (P = 0.001) and HPV66 (P = 0.01) [3].

Analytical, diagnostic and therapeutic context of PSMA2

• There was good agreement between test positivity by PCR and by single type-specific HC3 probes for HPV16 (kappa = 0.76; 95% confidence interval [CI] = 0.71 to 0.82) and for HPV18 (kappa = 0.73; 95% CI = 0.68 to 0.79) [3].

References