Disease relevance of H2-Q10

• Calculations based on Q10 values suggested that this hypothermia accounted, at most, for half the metabolic change measured [1].
• We also studied the possible immunomodulatory effects of two anti-radical substances known to have non-specific immunostimulant effects namely, L-carnitine (200 mg/kg body weight i.p.) and Q10 (200 mg/kg body weight, p.o.). Both drugs were given 1 h prior to each EMF exposure [2].
• Co Q10 showed a protective effect against a subacute toxicity in mice induced by two intraperitoneal administrations of ADM (15 mg/kg) [3].

High impact information on H2-Q10

• Our previous studies indicate that the Q10 gene is a potential donor gene for the generation of mutations at the H-2K locus by inter-gene transfer of genetic information [4].
• Thus the lack of polymorphism in class I genes at the Q10 locus implies either that they are not recipients for such exchanges or that selective pressure prevents the accumulation of mutations in genes at this locus [4].
• DNA sequence analysis of a class I gene (Q10), which maps to the Qa2,3 locus in the C57BL/10 (H-2b haplotype) mouse, reveals that it is almost identical to a cDNA clone (pH16) isolated from a SWR/J (H-2q haplotype) mouse liver cDNA library [4].
• In comparative studies, ubiquinone-8 had a clearly higher activity than ubiquinones-4, Q6, and Q10 [5].
• The DNA sequence of the Q10 genes appears to be highly conserved amongst strains of mice and has only been found to be transcribed in the liver [6].

Chemical compound and disease context of H2-Q10

• Anti-hyperlipemic agents such as MDS, nicomol, Ino-N and Co Q10 strongly protected against the ADM-induced toxicity, and the mice administered these drugs lived significantly longer than the control mice [7].

Biological context of H2-Q10

• Analysis with class I probes and other probes unique to the H-2D:Qa subregion indicates that the class I gene organization of t12 is: D1-D2-Q1-Q2-Q3-Qx-Q4-Q5-Q10, while that of tw5 is: D1-D2-Q1-Q2-Q4-Q5-Q10 [8].
• A comparison of the molecular maps of the t12 and tw5 chromosomes revealed an extremely mosaic pattern of diversity: The regions between D1 and D2, and between Q4 and Q10, are very similar in both chromosomes [8].
• The H-2 haplotypes rank according to their levels of Q10 as follows: z, s greater than k, b greater than d, q greater than f; and the actual values range from to 60 micrograms/ml to undetectable levels in serum [9].
• Our most striking observation is that one of these factors, which we named TA-f, binds in the TATA box region of Q10 and Kb and displays tissue-specific expression, in that we found the activity only in liver and kidney [10].
• Endoglycosidase F treatment of both the L cell and serum forms of the soluble molecule yielded two products with mol. wts. of approximately 32 000 and 35 000; this is consistent with the observation that the predicted Q10 protein sequence has two potential glycosylation sites [6].

Anatomical context of H2-Q10

• The histocompatibility class I molecule H2-Q10 (HA10_MOUSE) and proteasome activator PA28 alpha-subunit (PSME1_MOUSE) were found up-regulated in ANXB1 DNA immunized mice, which may contribute to the augmented activation of T lymphocytes [11].
• Nevertheless, these animals demonstrate cytotoxic T-lymphocyte (CTL) activity specific for Q10/L, although it is less than that obtained from non-TG littermates [12].
• Q10, which exhibits liver-specific expression, and H-2Kb, a transplantation antigen gene, were examined in liver, spleen, thymus, and cell-line DNAs [13].
• We examined the midgestation mouse embryo for transcripts related to the secreted transplantation antigen Q10 and show here that this gene is transcribed in the endoderm of the visceral yolk sac [14].
• Expression of Q10/L on hepatocytes renders mice functionally tolerant, although in vitro we observe that TG animals have normal numbers of CTL.Pf directed against this antigen [15].

Associations of H2-Q10 with chemical compounds

• The second construct, designated C2, is similar but has the human alpha 3 replaced by the Q10 alpha 3 domain [16].
• The Q10 class I gene, however, encodes a secreted glycoprotein that is highly homologous to the membrane-bound molecules [17].
• Since treatment of newborns with 5-azacytidine, which led to inhibition of methylation, resulted in the suppression of Q10, we conclude that hypermethylation in the 3'-flanking region is responsible, at least in part if not in full, for the activation of the Q10 gene in the liver [17].
• 8. A single saturable component (Km = 16 +/- 3 microM; V37 = 57 +/- 8 pmol/min/10(7) cells) was delineated, with the same temperature dependence (Q10 27-37 degrees = 3.2 +/- 0.4; Arrenhius constant = 11.1 +/- 3 kcal/mol) and same specificity for various folate compounds [18].
• This transport system is highly temperature-dependent (the Q10 falls between 3 and 4) and is inhibited by papaverine, theophylline, Persantin, Probenecid, phenethyl alcohol and p-chloromercuribenzoate, but not by 500 muM cyclic AMP, AMP, or adenosine [19].

Physical interactions of H2-Q10

• Peptides eluted from Q10 displayed a binding motif typical of H-2K, D, and L ligands [20].

Other interactions of H2-Q10

• Regulatory elements involved in the liver-specific expression of the mouse MHC class I Q10 gene: characterization of a new TATA-binding factor [10].
• Q10 is a Qa region gene, which was found to be expressed in liver and yolk sac, a regulatory pattern more evocative of the expression of a large set of serum proteins secreted by the liver than of a classical class I antigen [10].

Analytical, diagnostic and therapeutic context of H2-Q10

• There is a dramatic decrease after the injection of irritants or syngeneic tumor transplantation, but allostimulation has no effect on Q10 levels [9].
• To measure the amount of Q10 in various mouse sera, a quantitative Western blot assay was developed [9].
• Site-specific mutagenesis of the class I regulatory element the Q10 gene allows expression in non-liver tissues [21].
• Analysis of liver cells from these lines by flow cytometry and immunofluorescence demonstrated the presence of the Q10/L Ag solely on hepatocytes [22].
• Groups of tumors that received Q10 and radiotherapy had a significantly lower specific growth delay (SGD) than the radiotherapy-only groups [23].

References