Disease relevance of Mup1

• In an ischemic control group, M1 receptor binding decreased in the frontal cortex and M1 receptor mRNA increased in the hippocampus 2 weeks after the ischemia [1].
• DMAV and trimethylarsine oxide (TMAO) were converted to M-2 and M-3 and M-1 by Escherichia coli strain A3-6 isolated from the ceca of DMAV-administered rats, respectively [2].
• Anticonvulsant and proconvulsant effects of tramadol, its enantiomers and its M1 metabolite in the rat kindling model of epilepsy [3].
• Seizures were also observed after the (+)-enantiomer and the (+)-enantiomer of the M1 metabolite, but experiments with higher doses of these compounds were limited by marked respiratory depression [3].
• However, we did not detect ubiquitinated M1 protein fragments in the cytoplasm of Morris hepatoma 5123tc [4].

Psychiatry related information on Mup1

• The M1 mRNA levels remained at this reduced degree of expression even after withdrawal symptoms had subsided [5].

High impact information on Mup1

• Circular dichroism studies of renal ligandin revealed percent helical structure similar to hepatic ligandin and primary association contrasts were derived for BSP (10-6 M-1) and PAH, probenecid, and penicillin (10-3 M-1) [6].
• Major urinary metabolites in hamsters and rats treated with N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine [7].
• A reverse-phase high performance liquid chromatography assay was developed for jeasuring FT, M1, M2, and 5-fluorouracil (FU) plasma levels [8].
• Two hydroxylated metabolies (M1 and M2) have been isolated from rabbit urine after administration of Ftorafur (FT) [8].
• A horse liver thymidine phosphorylase ,reparation capable of catalyzing the conversion of beta-ribo-2'-deoxy-5-fluorouracil to FU was inactive against FT and M1 [8].

Chemical compound and disease context of Mup1

• Escherichia coli A3-6 isolated from a rat yielded two unknown arsenic compounds (M-2 and M-3) from dimethylarsinic acid and M-1 from trimethylarsine oxide (TMAO) in the presence of cysteine (Cys) [9].

Biological context of Mup1

• The cloned region of the M2-type mRNA showed a high degree of sequence homology with the M1-type mRNA and some homology with the L-type mRNA as determined by dot blot hybridization [10].
• [3H]Telenzepine has been shown to bind with high affinity (3 x 10(9) M-1) to a subpopulation of muscarinic binding sites in rat cerebral cortex, which have a high affinity for pirenzepine [11].
• It revealed that the first exon (exon M1) encodes the 5' non-coding sequence of mRNA I, while the second exon (exon AH1) encodes those of mRNAs II and III and the following eight exons (exons 2 to 9) are shared commonly by all the mRNA species [12].
• We discovered that valproate regulates expression of 28 genes, including three isoenzymes (M1, A3 and A4) of glutathione S-transferase (GST), an important protective factor against oxidative stress [13].
• PP (x10(3) M-1), Eh(NAD+/NADH) (x - 1 mV), and deltaG(ATP hydrolysis) (x - 1 kcal/mol) were 1.9 +/- 0.4, 266 +/- 4, and 9.7 +/- 0.2, respectively, in the control group and 4.0 +/- 0.9, 274 +/- 5 and 13.0 +/- 0.2, respectively, in the UTI group after transfusion (p <.001, p <.001, and p <.001, respectively) [14].

Anatomical context of Mup1

• In rat eye the highest levels of Mup1 reactivity were found in retinal photoreceptors [15].
• Two cDNAs, M1 and M2, recently isolated by the differential display method from embryonic rat cerebral hemisphere were characterized and their patterns of spatiotemporal expression analysed in developing rat forebrain by in situ hybridization histochemistry and correlative immunocytochemistry [16].
• These findings suggest M1 and/or M2 genes are involved in early regional specification of the hippocampus and related structures in paramedian regions of the forebrain, and that cell populations expressing these genes in advance of developing axonal pathways may be involved in the early specification of tract location [16].
• Its location corresponds to the fimbrial anlage, and immunocytochemical localization of M1 protein indicates its expression in radial glial cells [16].
• As a consequence, the stereoselectivity of the enantiomers varied from 500 (M1 receptors in cerebral cortex) to 75 (cardiac receptors) [11].

Associations of Mup1 with chemical compounds

• Male-specific development of P-450g and P-450 M-1 (IIC11) mRNA were imprinted similarly by testosterone [17].
• M1 muscarinic receptor-mediated facilitation of acetylcholine release in the rat urinary bladder [18].
• The level of GST M1 protein and GST activity were also increased by chronic valproate treatment [13].
• 4. The facilitation of transmitter release was antagonized completely by the administration of atropine (1 microM) or pirenzepine (0.05 microM), a selective M1 antagonist [18].
• In addition, chronic treatment with lithium, another commonly prescribed mood stabilizer, also increased levels of GST M1 mRNA and protein [13].

Other interactions of Mup1

• The loci Lap=1, Mup-1, and Svp-2 are linked neither to one another nor to the previously described Svp-1 and Es-4 loci [19].

Analytical, diagnostic and therapeutic context of Mup1

• Hypophysectomy of male rats decreased hepatic content of P-450 M-1 mRNA by approximately 50%, and intermittent injections of growth hormone completely restored this mRNA [17].
• Receptor affinity was not statistically different in intact young or old animals (4.51 +/- 0.41 X 10(9) and 4.51 +/- 1.23 X 10(9) M1, respectively), and receptor affinity increased in both groups in response to castration [20].
• Regulation of GST M1, GST A3 and GST A4 was verified using northern blotting hybridization [13].
• Our long-term oral administration of dimethylarsinic acid (DMAV) in rats revealed that three unidentified metabolites, M-1, M-2, and M-3, were detected in urine and feces [2].
• Major urinary metabolites identified by LC-MS/MS and quantified by HPLC radioassay were N-phenylacetyl-L-glycine (64.9% of dose) and N-benzyl-L-glycine (9.9% of dose) [21].

References