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Gene Review

Nprl3  -  nitrogen permease regulator-like 3

Mus musculus

Synonyms: -14 gene, Aag, Alpha-globin regulatory element-containing gene protein, CGTHBA, HS-26, ...
 
 
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Disease relevance of Mare

 

High impact information on Mare

  • Quantitative analysis shows that the relative amounts of V alpha 14 gene-mediated signal sequences in extrathymic tissues are higher than those in thymus [4].
  • These regulatory T cells express CD4 molecules and recognize a dominant peptide from the TCR variable framework region of V beta 8.2, in the context of the major histocompatibility complex class II molecule, I-Au, and predominantly use the TCR V beta 14 gene segment [5].
  • Positive selection determines T cell receptor V beta 14 gene usage by CD8+ T cells [6].
  • The loss of Aag renders cells significantly more sensitive to methyl methanesulfonate-induced chromosome damage, and to cell killing induced by two methylating agents, one of which produces almost exclusively 3MeAs [2].
  • Aag null embryonic stem cells become sensitive to two cancer chemotherapeutic alkylating agents, namely 1,3-bis(2-chloroethyl)-1-nitrosourea and mitomycin C, indicating that Aag status is an important determinant of cellular resistance to these agents [2].
 

Biological context of Mare

 

Anatomical context of Mare

  • To further test the importance of HS-26 at its natural locus, we have generated embryonic stem cells and chimeric animals in which 350 bp containing HS-26 have been replaced by a neomycin resistance gene by homologous recombination [12].
  • In clones from which HS-40 had been deleted, human alpha-globin gene expression was severely reduced, although basal levels of alpha 1 and alpha 2-globin mRNA expression representing less than 3% of the level in control cell lines were detected [1].
  • In contrast to the synergistic interaction between the DNase I hypersensitive sites of beta locus LCR, combination of HS-40 with these DNase I hypersensitive sites failed to display cooperativity in K562 cells and inhibited enhancer function in MEL cells [13].
  • Aag null cells have no detectable Aag transcripts or 3MeA DNA glycosylase activity [2].
 

Associations of Mare with chemical compounds

  • Weanling wild-type or 3-methyladenine glycosylase (Aag) null mice were maintained on a FA- diet or the same diet supplemented with folic acid (FA+) for 4 weeks [14].
  • The effect of dietary folic acid deficiency on the cytotoxic and mutagenic responses to methyl methanesulfonate in wild-type and in 3-methyladenine DNA glycosylase-deficient Aag null mice [14].
  • The heme-dependent expression of alpha-globin occurred at the transcriptional level since the expression of human alpha-globin gene promoter-reporter gene containing hypersensitive site-40 (HS-40) was decreased when K562 cells were cultured with SA [15].
  • Surprisingly, 7-methylguanine is removed equally efficiently in AAG:(+/+) and AAG:(-/-) cells, suggesting that another DNA glycosylase acts on lesions previously thought to be repaired by Aag [16].
  • In vivo repair of methylation damage in Aag 3-methyladenine DNA glycosylase null mouse cells [16].
 

Other interactions of Mare

  • Properties of the mouse alpha-globin HS-26: relationship to HS-40, the major enhancer of human alpha-globin gene expression [12].
  • Seven of the 16 Th-cell clones expressed beta-chain variable region (V beta) V beta 8 (8.2 or 8.3) genes and three expressed V beta 4, whereas two clones each used a V beta 1 or V beta 2 or V beta 14 gene, suggesting some restriction in TCR gene usage [17].

References

  1. Targeted inactivation of the major positive regulatory element (HS-40) of the human alpha-globin gene locus. Bernet, A., Sabatier, S., Picketts, D.J., Ouazana, R., Morlé, F., Higgs, D.R., Godet, J. Blood (1995) [Pubmed]
  2. Repair-deficient 3-methyladenine DNA glycosylase homozygous mutant mouse cells have increased sensitivity to alkylation-induced chromosome damage and cell killing. Engelward, B.P., Dreslin, A., Christensen, J., Huszar, D., Kurahara, C., Samson, L. EMBO J. (1996) [Pubmed]
  3. mig-14 is a horizontally acquired, host-induced gene required for salmonella enterica lethal infection in the murine model of typhoid fever. Valdivia, R.H., Cirillo, D.M., Lee, A.K., Bouley, D.M., Falkow, S. Infect. Immun. (2000) [Pubmed]
  4. Extrathymic development of V alpha 14-positive T cells. Makino, Y., Yamagata, N., Sasho, T., Adachi, Y., Kanno, R., Koseki, H., Kanno, M., Taniguchi, M. J. Exp. Med. (1993) [Pubmed]
  5. The involvement of T cell receptor peptide-specific regulatory CD4+ T cells in recovery from antigen-induced autoimmune disease. Kumar, V., Sercarz, E.E. J. Exp. Med. (1993) [Pubmed]
  6. Positive selection determines T cell receptor V beta 14 gene usage by CD8+ T cells. Liao, N.S., Maltzman, J., Raulet, D.H. J. Exp. Med. (1989) [Pubmed]
  7. Erythroid gene suppression by NF-kappa B. Liu, J.J., Hou, S.C., Shen, C.K. J. Biol. Chem. (2003) [Pubmed]
  8. Analysis of the human alpha globin upstream regulatory element (HS-40) in transgenic mice. Sharpe, J.A., Chan-Thomas, P.S., Lida, J., Ayyub, H., Wood, W.G., Higgs, D.R. EMBO J. (1992) [Pubmed]
  9. Derepression of human embryonic zeta-globin promoter by a locus-control region sequence. Huang, B.L., Fan-Chiang, I.R., Wen, S.C., Koo, H.C., Kao, W.Y., Gavva, N.R., Shen, C.K. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  10. Non-erythroid genes inserted on either side of human HS-40 impair the activation of its natural alpha -globin gene targets without being themselves preferentially activated. Espéret, C., Sabatier, S., Deville, M.A., Ouazana, R., Bouhassira, E.E., Godet, J., Morlé, F., Bernet, A. J. Biol. Chem. (2000) [Pubmed]
  11. Proximal promoter elements of the human zeta-globin gene confer embryonic-specific expression on a linked reporter gene in transgenic mice. Pondel, M.D., Sharpe, J.A., Clark, S., Pearson, L., Wood, W.G., Proudfoot, N.J. Nucleic Acids Res. (1996) [Pubmed]
  12. Properties of the mouse alpha-globin HS-26: relationship to HS-40, the major enhancer of human alpha-globin gene expression. Bouhassira, E.E., Kielman, M.F., Gilman, J., Fabry, M.F., Suzuka, S., Leone, O., Gikas, E., Bernini, L.F., Nagel, R.L. Am. J. Hematol. (1997) [Pubmed]
  13. Analysis of enhancer function of the HS-40 core sequence of the human alpha-globin cluster. Chen, H., Lowrey, C.H., Stamatoyannopoulos, G. Nucleic Acids Res. (1997) [Pubmed]
  14. The effect of dietary folic acid deficiency on the cytotoxic and mutagenic responses to methyl methanesulfonate in wild-type and in 3-methyladenine DNA glycosylase-deficient Aag null mice. Branda, R.F., O'Neill, J.P., Brooks, E.M., Powden, C., Naud, S.J., Nicklas, J.A. Mutat. Res. (2007) [Pubmed]
  15. Heme-dependent up-regulation of the alpha-globin gene expression by transcriptional repressor Bach1 in erythroid cells. Tahara, T., Sun, J., Igarashi, K., Taketani, S. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  16. In vivo repair of methylation damage in Aag 3-methyladenine DNA glycosylase null mouse cells. Smith, S.A., Engelward, B.P. Nucleic Acids Res. (2000) [Pubmed]
  17. Junctional region sequences of T-cell receptor beta-chain genes expressed by pathogenic anti-DNA autoantibody-inducing helper T cells from lupus mice: possible selection by cationic autoantigens. Adams, S., Leblanc, P., Datta, S.K. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
 
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