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Ugt1a9  -  UDP glucuronosyltransferase 1 family,...

Mus musculus

Synonyms: A12, UDP-glucuronosyltransferase 1-7, UDP-glucuronosyltransferase 1-9, UDP-glucuronosyltransferase 1A9, UDPGT, ...
 
 
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Disease relevance of Ugt1a9

 

High impact information on Ugt1a9

  • Compared to mice immunized with thioredoxin alone, mice immunized with A12-thioredoxin had significantly reduced lung P. carinii burdens after CD4+ T-cell depletion and challenge with P. carinii [6].
  • A12 perikarya and median eminence but was not reduced in other DA areas, such as substantia nigra, at all ages; A12 fluorescence was virtually absent in Snell dwarf adults [7].
  • Thus, compared with normal mice of the same strain, the A12 deficit is more severe in Snell (dw/dw) than in Ames (df/df) dwarf hypothalamus (48% of DF/?), as previously reported, and develops as a decline from the population present at 7 d rather than first increasing [7].
  • The total A12 TH-positive cell number was reduced (P < 0.01) in all PRL-treated dwarfs (1826 +/- 58) compared with that in normal mice (3340 +/- 180), and was not different from that in untreated dwarfs (1953 +/- 304) regardless of the PRL regimen [8].
  • Total numbers of TH-immunostained cells in A12 and medial zona incerta (area A13) regions were counted, and the intensity of TH immunostaining was assessed by computerized image analysis [8].
 

Biological context of Ugt1a9

  • Within A12, both dorsal and ventral TH cell numbers were reduced in vehicle-treated dwarfs (P < 0.01); the reduction was greater in the ventral subpopulation (P < 0.01) [9].
  • This synthesis is modulated by a process associated with spontaneous muscle contractile activity since both total enzyme levels and the proportion of A12 AChE expressed on the cell surface are decreased when the cells are grown in the sodium channel blocker tetrodotoxin, which blocks muscle contraction [10].
  • Dwarfs and normal animals of both types also were treated with a drug regimen to deplete sequentially neuronal CA stores (reserpine), inhibit CA oxidation (nialamide) and load dopaminergic A12 cells with exogenous transmitter (norepinephrine), in order to test viability and axonal transport capacity of A12 neurons [11].
  • A 32 AA residue, in a tandem repeat configuration (32dimer), of sero/subtype A-12 Lp ab VP1 (AA 132-168) was highly immunogenic for its homologous subtype and partially protective for FMDV serotype A strain A24 [12].
  • A pI 5.6, 28-kd genetically variant brain polypeptide designated A12 maps to chromosome 1 and shows identity with the known mouse locus LTW-4 [13].
 

Anatomical context of Ugt1a9

  • A12 AChE has been the subject of much study because it is thought to be a major functional enzyme form normally found in the basal lamina at the neuromuscular junction [10].
  • In this paper, we show that muscle fibers derived from mouse embryos and neonates are also able to synthesize substantial percentages of their AChE as the A12 form when grown in vitro [10].
  • When grown in primary cell culture in the absence of neurons, muscle cells from a variety of species synthesize several forms of acetylcholinesterase (AChE), including the collagen-tailed A12 form [10].
  • In the arcuate nucleus (ARC) of colchicine-treated nursing mice which received peripheral injections of Fluoro-Gold (FG) to retrogradely label neuroendocrine cells, virtually all dorsal A12 TH-ir perikarya simultaneously expressed, with individual variations, NPY-, ENK- and NT-irs, and all contained FG [14].
 

Associations of Ugt1a9 with chemical compounds

  • Recent studies in this laboratory have revealed that this condition develops postnatally, in that A12 DA fails to increase and the number of TH-positive cells decreases after 21 days of age [9].
  • A novel feature of mouse muscle cultures, not seen in those from rat and chick, is the presence of a secreted enzyme form that sediments in the same position as the cellular A12 form (when separated on sucrose density gradients containing high salt) and is also collagenase sensitive [10].
  • Two genetic correlations are reported, one between an isoelectric point variant of A7 (a 71 kd, pI 5.4 abundant protein) and resistance to signs of ethanol withdrawal and the other between A12 (a 28 kd, pI 5.6 protein) and ethanol intake [15].
  • 1. Pyridostigmine bromide was administered subcutaneously in mice, in a dose of 4.0 or 2.0 mu moles/kg, and the activity of the predominant (G1, G4 and A12) molecular forms of acetylcholinesterase were examined in diaphragm, extensor digitorum longus (EDL), and soleus muscles at 3 h, 6 h, 24 h and 5 days [16].
 

Analytical, diagnostic and therapeutic context of Ugt1a9

  • Specific molecular forms of AChE were resolved by high-performance liquid chromatography such that slow anterograde (G1 + G2), fast anterograde and fast retrograde (G4 and A12) flows could be simultaneously studied [17].
  • Parasites used for vaccination have been promastigotes of the cloned parasite lines A12 and A52 derived from Leishmania major isolate L137, or long-term cultured promastigotes of the leishmaniasis recidiva isolate, L32 (L.t.tropica) [18].

References

  1. Plasmid DNA encoding replicating foot-and-mouth disease virus genomes induces antiviral immune responses in swine. Ward, G., Rieder, E., Mason, P.W. J. Virol. (1997) [Pubmed]
  2. Characterization of anti-idiotypic antibodies generated against foot-and-mouth disease virus neutralizing monoclonal antibodies. Baxt, B., Garmendia, A.E., Morgan, D.O. Viral Immunol. (1989) [Pubmed]
  3. Competition for cellular receptor sites among selected aphthoviruses. Sekiguchi, K., Franke, A.J., Baxt, B. Arch. Virol. (1982) [Pubmed]
  4. Ribosomal vaccines: immunological study. Dussourd d'Hinterland, L., Pinel, A.M., Rey, G. Arzneimittel-Forschung. (1980) [Pubmed]
  5. Study of the teratogenic activity of ribosomal vaccine. Labie, C. Arzneimittel-Forschung. (1980) [Pubmed]
  6. Active immunization against Pneumocystis carinii with a recombinant P. carinii antigen. Wells, J., Haidaris, C.G., Wright, T.W., Gigliotti, F. Infect. Immun. (2006) [Pubmed]
  7. Postnatal regression of hypothalamic dopaminergic neurons in prolactin-deficient Snell dwarf mice. Phelps, C.J. Endocrinology (2004) [Pubmed]
  8. Prolactin replacement in adult dwarf mice does not reverse the deficit in tuberoinfundibular dopaminergic neuron number. Romero, M.I., Phelps, C.J. Endocrinology (1995) [Pubmed]
  9. Prolactin replacement during development prevents the dopaminergic deficit in hypothalamic arcuate nucleus in prolactin-deficient Ames dwarf mice. Romero, M.I., Phelps, C.J. Endocrinology (1993) [Pubmed]
  10. Cellular and secreted forms of acetylcholinesterase in mouse muscle cultures. Rubin, L.L., Chalfin, N.A., Adamo, A., Klymkowsky, M.W. J. Neurochem. (1985) [Pubmed]
  11. Hypothalamic catecholamine histofluorescence in dwarf mice. Phelps, C.J., Sladek, J.R., Morgan, W.W., Bartke, A. Cell Tissue Res. (1985) [Pubmed]
  12. Antibodies elicited by a biosynthetic peptide related to a major immunogenic area of FMDV A12. Borca, M.V., Moore, D.M., Srikumaran, S., Morgan, D.O. Viral Immunol. (1990) [Pubmed]
  13. Fourteen genetically variant proteins of mouse brain: discovery of two new variants and chromosomal mapping of four loci. Goldman, D., Pikus, H.J. Biochem. Genet. (1986) [Pubmed]
  14. Plasticity in expression of immunoreactivity for neuropeptide Y, enkephalins and neurotensin in the hypothalamic tubero-infundibular dopaminergic system during lactation in mice. Ciofi, P., Crowley, W.R., Pillez, A., Schmued, L.L., Tramu, G., Mazzuca, M. J. Neuroendocrinol. (1993) [Pubmed]
  15. Use of chromosomally mapped and identified mouse brain proteins for behavioral genetic analysis of alcoholism. Goldman, D., Crabbe, J. Prog. Neuropsychopharmacol. Biol. Psychiatry (1986) [Pubmed]
  16. Effects of pyridostigmine on acetylcholinesterase in different muscles of the mouse. Lintern, M.C., Smith, M.E., Ferry, C.B. Human & experimental toxicology. (1997) [Pubmed]
  17. Axonal transport in mdx mouse sciatic nerve. Yamashita, S., Takenaka, H., Sugimoto, S., Chihara, E., Sawada, A., Matsukura, S., Hamada, M. J. Neurol. Sci. (1989) [Pubmed]
  18. Vaccination against cutaneous leishmaniasis in mice using nonpathogenic cloned promastigotes of Leishmania major and importance of route of injection. Mitchell, G.F., Handman, E., Spithill, T.W. The Australian journal of experimental biology and medical science. (1984) [Pubmed]
 
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