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Large  -  like-glycosyltransferase

Mus musculus

Synonyms: Acetylglucosaminyltransferase-like 1A, BPFD#36, Glycosyltransferase-like protein LARGE1, Gyltl1a, Kiaa0609, ...
 
 
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Disease relevance of Large

  • Finally, the causative gene in the myodystrophy (myd) mouse is a putative bifunctional glycosyltransferase (Large) [1].
  • The Large mutants are excellent models for addressing the importance of glycosylation in neuromuscular disease [2].
  • A new recessive mutation, myd, causing a diffuse and progressive myopathy in the mouse is described [3].
  • Suppression of Gastric Acid Production by Proton Pump Inhibitor Treatment Facilitates Colonization of the Large Intestine by Vancomycin-Resistant Enterococcus spp. and Klebsiella pneumoniae in Clindamycin-Treated Mice [4].
  • The Expression of CD30 in Anaplastic Large Cell Lymphoma Is Regulated by Nucleophosmin-Anaplastic Lymphoma Kinase-Mediated JunB Level in a Cell Type-Specific Manner [5].
 

High impact information on Large

  • Here we show that the gene mutated in myd encodes a glycosyltransferase, Large. The human homolog of this gene (LARGE) maps to chromosome 22q [6].
  • Myogenin and MyoD thus form part of a gene family regulating myogenesis, and together with myd may constitute a set of factors that interact to regulate the determination and differentiation of muscle cells [7].
  • We conclude that there is a simple genetic basis for myogenic determination and that a single gene, myd, converts 10T1/2 cells to a myoblast lineage [8].
  • Allorestricted cytotoxic T cells. Large numbers of allo-H-2Kb-restricted antihapten and antiviral cytotoxic T cell populations clonally develop in vitro from murine splenic precursor T cells [9].
  • RESULTS: Large (1.0-cm diameter) tumors had approximately 10-fold more survivin than small (0.2-cm diameter) tumors [10].
 

Chemical compound and disease context of Large

 

Biological context of Large

 

Anatomical context of Large

 

Associations of Large with chemical compounds

  • Activation of NFATc3 Down-regulates the beta1 Subunit of Large Conductance, Calcium-activated K+ Channels in Arterial Smooth Muscle and Contributes to Hypertension [19].
  • 3. Large m.e.p.p.s appear to be due to an increase in muscle fibre input resistance and to the quantal release of abnormally large amounts of acetylcholine from motor nerve terminals [20].
  • 4 Large doses of (-)-amphetamine were without effect, demonstrating that the long-lasting impairment of transmitter uptake-storage mechanism in striatal dopamine nerve terminals is selective for (+)-amphetamine [21].
  • (d) Large N-terminal alkane substituents added to 3,4,3-LICAM(C) increased ligand lipophilicity, hindered Pu chelation, and delayed excretion [22].
  • CONCLUSIONS: Large tumour volume and corresponding delay in castration reduced the time to androgen-independent tumour recurrence and survival [23].
 

Regulatory relationships of Large

 

Other interactions of Large

  • These results demonstrate that the Large glycosyltransferase but not dystrophin is required for normal basilar pontine development [24].
  • Shiverer oligodendrocytes that carry two doses of the Mbp1 transgene contain two types of membrane sheet regions, i.e. regions filled with aberrant punctate foci of MBP, and regions with normal domains of MBP [14].
  • CONCLUSIONS: Large variations in hepatic bile salt flux have minor effects on expression of murine Ntcp and Bsep in vivo, suggesting that these transporters are abundantly expressed and able to accommodate a wide range of 'physiological' bile salt fluxes [25].
  • Heritabilities for the three traits were estimated to be 0.47 for leptin, 0.46 for HDL-TG, and 0.46 for Large HDL-apo A-I [26].
  • We have developed four new mammary adenocarcinoma cell lines from the C3(1)/SV40 Large T-antigen (Tag) transgenic mouse model: M28N2 and M27H4 (weakly tumorigenic), M6 (carcinoma), and M6C (metastatic) [27].
 

Analytical, diagnostic and therapeutic context of Large

References

  1. Glycosylation defects: a new mechanism for muscular dystrophy? Grewal, P.K., Hewitt, J.E. Hum. Mol. Genet. (2003) [Pubmed]
  2. Rewiring enervated: thinking LARGEr than myodystrophy. Levedakou, E.N., Popko, B. J. Neurosci. Res. (2006) [Pubmed]
  3. Myodystrophy, a new myopathy on chromosome 8 of the mouse. Lane, P.W., Beamer, T.C., Myers, D.D. J. Hered. (1976) [Pubmed]
  4. Suppression of Gastric Acid Production by Proton Pump Inhibitor Treatment Facilitates Colonization of the Large Intestine by Vancomycin-Resistant Enterococcus spp. and Klebsiella pneumoniae in Clindamycin-Treated Mice. Stiefel, U., Rao, A., Pultz, M.J., Jump, R.L., Aron, D.C., Donskey, C.J. Antimicrob. Agents Chemother. (2006) [Pubmed]
  5. The Expression of CD30 in Anaplastic Large Cell Lymphoma Is Regulated by Nucleophosmin-Anaplastic Lymphoma Kinase-Mediated JunB Level in a Cell Type-Specific Manner. Hsu, F.Y., Johnston, P.B., Burke, K.A., Zhao, Y. Cancer Res. (2006) [Pubmed]
  6. Mutant glycosyltransferase and altered glycosylation of alpha-dystroglycan in the myodystrophy mouse. Grewal, P.K., Holzfeind, P.J., Bittner, R.E., Hewitt, J.E. Nat. Genet. (2001) [Pubmed]
  7. Myogenin, a factor regulating myogenesis, has a domain homologous to MyoD. Wright, W.E., Sassoon, D.A., Lin, V.K. Cell (1989) [Pubmed]
  8. Myogenic lineage determination and differentiation: evidence for a regulatory gene pathway. Pinney, D.F., Pearson-White, S.H., Konieczny, S.F., Latham, K.E., Emerson, C.P. Cell (1988) [Pubmed]
  9. Allorestricted cytotoxic T cells. Large numbers of allo-H-2Kb-restricted antihapten and antiviral cytotoxic T cell populations clonally develop in vitro from murine splenic precursor T cells. Reimann, J., Kabelitz, D., Heeg, K., Wagner, H. J. Exp. Med. (1985) [Pubmed]
  10. Effects of survivin antagonists on growth of established tumors and B7-1 immunogene therapy. Kanwar, J.R., Shen, W.P., Kanwar, R.K., Berg, R.W., Krissansen, G.W. J. Natl. Cancer Inst. (2001) [Pubmed]
  11. General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 2nd communication: effect on the peripheral nervous system and peripheral organs. Hirotsu, I., Kihara, T., Hattori, Y., Hatta, M., Hirose, N., Ishihara, T., Satoh, F. Arzneimittel-Forschung. (1988) [Pubmed]
  12. Mouse large can modify complex N- and mucin O-glycans on alpha-dystroglycan to induce laminin binding. Patnaik, S.K., Stanley, P. J. Biol. Chem. (2005) [Pubmed]
  13. Mutation of Large, which encodes a putative glycosyltransferase, in an animal model of muscular dystrophy. Grewal, P.K., Hewitt, J.E. Biochim. Biophys. Acta (2002) [Pubmed]
  14. Regulation of cytoskeleton by myelin components: studies on shiverer oligodendrocytes carrying an Mbp transgene. Dyer, C.A., Phillbotte, T., Wolf, M.K., Billings-Gagliardi, S. Dev. Neurosci. (1997) [Pubmed]
  15. Genetic and Structural Analysis of the Basolateral Amygdala Complex in BXD Recombinant Inbred Mice. Mozhui, K., Hamre, K.M., Holmes, A., Lu, L., Williams, R.W. Behav. Genet. (2007) [Pubmed]
  16. Disruption of the mouse Large gene in the enr and myd mutants results in nerve, muscle, and neuromuscular junction defects. Levedakou, E.N., Chen, X.J., Soliven, B., Popko, B. Mol. Cell. Neurosci. (2005) [Pubmed]
  17. Characterization of ATPase in sarcoplasmic reticulum from two strains of dystrophic mice. Neymark, M.A., Kopacz, S.J., Lee, C.P. Muscle Nerve (1980) [Pubmed]
  18. Killing of Normal Melanocytes, Combined with Heat Shock Protein 70 and CD40L Expression, Cures Large Established Melanomas. Sanchez-Perez, L., Kottke, T., Daniels, G.A., Diaz, R.M., Thompson, J., Pulido, J., Melcher, A., Vile, R.G. J. Immunol. (2006) [Pubmed]
  19. Activation of NFATc3 Down-regulates the beta1 Subunit of Large Conductance, Calcium-activated K+ Channels in Arterial Smooth Muscle and Contributes to Hypertension. Nieves-Cintrón, M., Amberg, G.C., Nichols, C.B., Molkentin, J.D., Santana, L.F. J. Biol. Chem. (2007) [Pubmed]
  20. A comparative electrophysiological study of motor end-plate diseased skeletal muscle in the mouse. Weinstein, S.P. J. Physiol. (Lond.) (1980) [Pubmed]
  21. Selective (+)-amphetamine neurotoxicity on striatal dopamine nerve terminals in the mouse. Jonsson, G., Nwanze, E. Br. J. Pharmacol. (1982) [Pubmed]
  22. Specific sequestering agents for the actinides: 10. Enhancement of 238Pu elimination from mice by poly(catechoylamide) ligands. Durbin, P.W., Jeung, N., Jones, E.S., Weitl, F.L., Raymond, K.N. Radiat. Res. (1984) [Pubmed]
  23. Effect of time of castration and tumour volume on time to androgen-independent recurrence in Shionogi tumours. So, A.I., Bowden, M., Gleave, M. BJU international. (2004) [Pubmed]
  24. Absence of the basilar pons in mice lacking a functional Large glycosyltransferase gene suggests a defect in pontine neuron migration. Litwack, E.D., Lee, Y., Mallott, J.M. Brain Res. (2006) [Pubmed]
  25. Effects of bile salt flux variations on the expression of hepatic bile salt transporters in vivo in mice. Wolters, H., Elzinga, B.M., Baller, J.F., Boverhof, R., Schwarz, M., Stieger, B., Verkade, H.J., Kuipers, F. J. Hepatol. (2002) [Pubmed]
  26. Serum leptin levels are independently correlated with two measures of HDL. Rainwater, D.L., Comuzzie, A.G., VandeBerg, J.L., Mahaney, M.C., Blangero, J. Atherosclerosis (1997) [Pubmed]
  27. Development and characterization of a progressive series of mammary adenocarcinoma cell lines derived from the C3(1)/SV40 Large T-antigen transgenic mouse model. Holzer, R.G., MacDougall, C., Cortright, G., Atwood, K., Green, J.E., Jorcyk, C.L. Breast Cancer Res. Treat. (2003) [Pubmed]
  28. Clearance pathways of soluble immune complexes in the pig. Insights into the adaptive nature of antigen clearance in humans. Davies, K.A., Chapman, P.T., Norsworthy, P.J., Jamar, F., Athanassiou, P., Keelan, E.T., Harrison, A.A., Binns, R.M., Haskard, D.O., Walport, M.J. J. Immunol. (1995) [Pubmed]
  29. CASK and Dlg form a PDZ protein complex at the mammalian neuromuscular junction. Sanford, J.L., Mays, T.A., Rafael-Fortney, J.A. Muscle Nerve (2004) [Pubmed]
  30. Quantitative analysis of striped coat-color patterns in Large White-->Duroc chimeric pigs with special reference to the genetic control mechanisms of the dominant black-eyed white phenotype. Inoué, K., Tanaka, S., Kashiwazaki, N., Nakao, H., Nakatsuji, N., Sakaki, N., Tojo, H., Tachi, C. Pigment Cell Res. (1996) [Pubmed]
  31. Polymerase chain reaction and restriction endonuclease digestion for selected members of the "Mycoplasma mycoides cluster" and Mycoplasma putrefaciens. Rodriguez, J.L., Ermel, R.W., Kenny, T.P., Brooks, D.L., DaMassa, A.J. J. Vet. Diagn. Invest. (1997) [Pubmed]
 
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