Disease relevance of PSMD11

• These proteins are homologs to Escherichia coli S9 and S5 proteins [1].
• Small, round-structured viruses (SRSVs) detected from nonbacterial gastroenteritis outbreaks in Tokyo and Saitama Prefecture, Japan, during the period from 1977 to 1988 were tentatively classified into nine antigenic patterns from SRSV-1 (S-1) to SRSV-9 (S-9) by cross-immune electron microscopy (IEM) [2].
• A molecular model of the HTLV-1 PR in complex with this substrate was built, based on the crystal structure of the S9 mutant of Rous sarcoma virus PR, in order to understand the molecular basis of the enzyme specificity [3].
• In this study, we looked at whether capsaicin showed anti-mutagenic effects toward HCA-induced mutagenesis in Salmonella typhimurium TA98 when incubated with 0.5 mg liver S9 protein from rat, hamster and human [4].

High impact information on PSMD11

• Moreover, rapamycin treatment downregulated the mRNA and protein levels of the 26S p44.5 proteasome subunit, suggesting the involvement of the proteasome complex in the mechanisms of rapamycin-induced apoptosis [5].
• cDNA cloning and functional analysis of p44.5 and p55, two regulatory subunits of the 26S proteasome [6].
• S9-expressing secondary mesenchyme cells (SMCs) migrate from the vegetal plate into the blastocoel early in gastrulation and later populate the dorsal ectoderm [7].
• Addition of emodin to CL5 cell microM S9 inhibited its 7-ethoxycoumarin O-deethylation activity [8].
• Immunoblot analysis of CL5 S9 proteins revealed that emodin induced proteins immunorelated to P450s 1A1 and 1B1 [8].

Chemical compound and disease context of PSMD11

• Urine samples were collected at the end of the study work shifts and were analyzed for markers of cigarette smoking (nicotine, cotinine) and for mutagenicity, using a sensitive microsuspension assay (micro preincubation assay; Salmonella strain TA98 with or without S9 enzyme) [9].

Biological context of PSMD11

• Ethyl carbamate (EC, urethane) at 10(-2) M concentration induced more sister chromatid exchanges (SCEs) in cultured human peripheral blood lymphocytes in the absence of S9 mix than did 10(-2) M vinyl carbamate (VC), a possible proximate carcinogenic metabolite (Dahl et al., 1978) of EC [10].
• Treatment of CL5 cells with 100 microM emodin for 24 h induced benzo[a]pyrene hydroxylation, 7-ethoxyresorufin O-deethylation, and 7-ethoxycoumarin O-deethylation activities of S9 fractions [8].
• The present study examines the mutagenic activation of 2-aminofluorene (AF) with hepatic post-mitochondrial (S9) preparations derived from homozygous rapid (Patr/Patr) acetylator and homozygous slow (Pats/Pats) acetylator Syrian inbred hamsters and its relationship to acetylator genotype [11].
• Cdna cloning and gene expression of ribosomal S9 protein gene in the mollusk Corbicula fluminea: a new potential biomarker of metal contamination up-regulated by cadmium and repressed by zinc [12].
• The metabolic activation of AF utilizing standard hepatic S9 preparations exhibited typical saturation kinetics that did not differ between acetylator genotypes [11].

Anatomical context of PSMD11

• The S9 fraction of the established cell line metabolizes tolbutamide to hydroxytolbutamide [13].

Associations of PSMD11 with chemical compounds

• Treatment with 200 microg/ml beef, fish or pork FMEP extract for 6 h increased benzo[a]pyrene hydroxylase, 7-ethoxyresorufin and methoxyresorufin O-dealkylases activities in S9 [14].
• In contrast, capsaicin enhanced the mutagenicity of Trp-P-2 in TA98 when incubated with human liver S9 [4].
• The enzyme activity of CHL-UGT1A9 towards propranolol in S9 protein of the cell was determined by HPLC [15].
• In dose-response studies in which the concentrations of AF, AcCoA or S9 protein were varied, higher numbers of revertants were consistently generated with hepatic S9 derived from the slow acetylator compared to the rapid acetylator hamsters [11].
• However, the addition of AcCoA to the standard S9 mix resulted in a dose-dependent reduction in the number of histidine revertants [11].

Analytical, diagnostic and therapeutic context of PSMD11

• Western blot analysis showed that the S9-specific antibodies bound the 26S proteasome and its regulatory complex separated on non-denaturing gels [16].
• In SDS-PAGE samples of the two complexes, the S9-specific antibodies bound a single 46 kDa subunit [16].
• We have used whole amount in situ hybridization to analyze the patterns of expression of two genes, S9 and actin CyIIa, during the development of the sea urchin, Strongylocentrotus purpuratus [7].

References