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Gene Review

Igh  -  immunoglobulin heavy chain complex

Mus musculus

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Disease relevance of Igh

  • Insertion of Myc into Igh accelerates peritoneal plasmacytomas in mice [1].
  • We conclude that Myc(His) insertion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse model for understanding the transformation-inducing consequences of the MYC/Myc-activating endemic Burkitt lymphoma t(8;14)/plasmacytoma T(12;15) translocation [2].
  • Thus, our characterization of the region 5' of the VH gene cluster demonstrated the presence of a single cluster of DNase I hypersensitive sites within the 5' flanking region, and identified a candidate Igh regulatory region defined by pro-B cell-specific hypersensitivity and interaction with factors implicated in regulating VDJ recombination [3].
  • T-cell responsiveness to LCMV segregates as a single locus in crosses between BALB/cA and C.B-17 mice. Evidence for regulation by a gene outside the Igh region [4].
  • The course of systemic infection with lymphocytic choriomeningitis virus (LCMV) was studied in BALB/cA and C.B-17 mouse strains differing in the immunoglobulin heavy chain region (Igh) [4].

Psychiatry related information on Igh

  • These data demonstrate a selective genetic linkage of discrete T15 Id determinants, AB1-2 and B36-82 with the Igh allotype [5].

High impact information on Igh


Chemical compound and disease context of Igh

  • Mesangial glomerulonephritis was induced in mice by intravenous injection of preformed soluble immune complexes of dextran sulfate and either IgA (J 558) or IgM (MOPC 104 E) anti-dextran MAb (passive model) or by immunization with DEAE dextran (active model) [9].
  • These studies examined the fate of Factor XIII (fibrin-stabilizing factor) in mice with plasmacytoma (MOPC-300, MOPC-384, MOPC-467, and J-558) [10].
  • Among the TGB5 Id+, GT+ antibodies, which dominate the neonatal response to (T,G)-A-L, two VH gene families were used: J558 (high frequency) and 36-60 (low frequency) [11].
  • Tumor cells treated in vitro with TSA showed delayed onset and rate of tumor growth in 70% of the J558 plasmacytoma and 100% of the B16 melanoma injected animals [12].
  • More mature lymphomas (BAL-17, CH12 and CH27) and fully differentiated myelomas (J558 and MOPC-315) are insensitive to PGE2 [13].

Biological context of Igh


Anatomical context of Igh

  • Thus, isotypes encoded by genes on the 3' end of the Igh-gamma gene complex, which in the absence of T cells have a low probability of being switched to, are the most influenced by T cell help [17].
  • C.B-20 ( Ighb ) mice challenged with BALB/c ( Igha ) spleen cells (or vice-versa) generate cytotoxic T lymphocytes (CTL) that recognize an antigen, H-40, controlled by an Igh-linked gene [18].
  • Prior to rearrangement, Igh moves from its default peripheral location near the nuclear envelope to an interior compartment, and after rearrangement it returns to the periphery [19].
  • Insertion of c-Myc into Igh induces B-cell and plasma-cell neoplasms in mice [2].
  • Influence of Igh-linked gene products on the generation of T helper cells in the response to sheep erythrocytes [20].

Associations of Igh with chemical compounds

  • To identify any sites in Igh responsible for its association with the periphery, we systematically analyzed the nuclear positions of the Igh locus in mouse non-B- and B-cell lines and, importantly, in primary splenic lipopolysaccharide-stimulated B cells and plasmablasts [19].
  • Immunogenetics of BCG-induced anergy in mice. Control by Igh- and H-2-linked genes [21].
  • After stopping anti-mu treatment of C.AL-20 mice, ABA-specific Ts repertoires undergo a defined expansion shown by their acquisition of an additional Ts network that displays Igh restrictions characteristic of normal C.AL-20 mice [22].
  • Regulation of T15 idiotype dominance. II. Genes unlinked to the Igh locus regulate T15 dominance of the secondary adoptive transfer response to phosphocholine [23].
  • Analysis of sera from AXC Igh recombinant mice maps the 91A3 marker to the left of Igh-Dex, consistent with the location of the VH genes controlling the arsonate CRI [24].

Physical interactions of Igh


Regulatory relationships of Igh

  • Identification of VH438, which shared VH hybridization pattern with 6% of a panel of 352 MRL/lpr hybridomas, suggests that the frequency of J558 use among spontaneously activated B cells in MRL/lpr mice is greater than previously reported [28].
  • Ezh2 controls B cell development through histone H3 methylation and Igh rearrangement [29].
  • Igh-linked genes that influence BCG-induced splenomegaly were located on the centrometric side of the Igh-1 locus [30].
  • The implication from replication timing studies in the B-cell line MPC11 was that early replication of the Igh locus was regulated by sequences downstream of the C alpha gene [31].
  • Subsequent activation of the V(H) locus happens in at least three differentially regulated domains: an interleukin-7-regulated domain consisting of the 5' J558 family, an intermediate domain and the 3' V(H) genes, which are hyperacetylated in response to DJ(H) recombination [32].

Other interactions of Igh

  • Genes coding for the determinants were shown to be accommodated somewhere in the right side of the Igh variable region gene (Igh-V) cluster, as the antibody activity was completely absorbed with BAB-14 thymocytes [14].
  • The gene maps to the Igh-C region end of the Igh complex, telomeric to Tsu in the region of Pre-1 [18].
  • The alloantiserum was raised in BALB/c (H-2d, Igh-1a) mice hyperimmunized with spleen cells of Igh allotype congenic mice, CB-20 (H-2d, Igh-1b) [14].
  • Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex [33].
  • The data are consistent with the interpretation that the latter 5 strains do not process Igh-Gte genes and the Igh haplotypes of these strains represent examples of crossing over within the Igh complex [34].

Analytical, diagnostic and therapeutic context of Igh


  1. Insertion of Myc into Igh accelerates peritoneal plasmacytomas in mice. Park, S.S., Shaffer, A.L., Kim, J.S., duBois, W., Potter, M., Staudt, L.M., Janz, S. Cancer Res. (2005) [Pubmed]
  2. Insertion of c-Myc into Igh induces B-cell and plasma-cell neoplasms in mice. Park, S.S., Kim, J.S., Tessarollo, L., Owens, J.D., Peng, L., Han, S.S., Tae Chung, S., Torrey, T.A., Cheung, W.C., Polakiewicz, R.D., McNeil, N., Ried, T., Mushinski, J.F., Morse, H.C., Janz, S. Cancer Res. (2005) [Pubmed]
  3. Identification of a candidate regulatory element within the 5' flanking region of the mouse Igh locus defined by pro-B cell-specific hypersensitivity associated with binding of PU.1, Pax5, and E2A. Pawlitzky, I., Angeles, C.V., Siegel, A.M., Stanton, M.L., Riblet, R., Brodeur, P.H. J. Immunol. (2006) [Pubmed]
  4. T-cell responsiveness to LCMV segregates as a single locus in crosses between BALB/cA and C.B-17 mice. Evidence for regulation by a gene outside the Igh region. Christensen, J.P., Marker, O., Thomsen, A.R. Scand. J. Immunol. (1993) [Pubmed]
  5. Regulation of idiotope expression. IV. Genetic linkage of two D region-dependent T15 idiotopes to the IgH allotype. Cronkhite, R., Schulze, D., Cerny, J. J. Immunol. (1989) [Pubmed]
  6. One heavy chain variable region gene segment subfamily in the BALB/c mouse contains 500-1000 or more members. Livant, D., Blatt, C., Hood, L. Cell (1986) [Pubmed]
  7. AID is required to initiate Nbs1/gamma-H2AX focus formation and mutations at sites of class switching. Petersen, S., Casellas, R., Reina-San-Martin, B., Chen, H.T., Difilippantonio, M.J., Wilson, P.C., Hanitsch, L., Celeste, A., Muramatsu, M., Pilch, D.R., Redon, C., Ried, T., Bonner, W.M., Honjo, T., Nussenzweig, M.C., Nussenzweig, A. Nature (2001) [Pubmed]
  8. Novel primitive lymphoid tumours induced in transgenic mice by cooperation between myc and bcl-2. Strasser, A., Harris, A.W., Bath, M.L., Cory, S. Nature (1990) [Pubmed]
  9. Enzymolysis of glomerular immune deposits in vivo with dextranase/protease ameliorates proteinuria, hematuria, and mesangial proliferation in murine experimental IgA nephropathy. Gesualdo, L., Ricanati, S., Hassan, M.O., Emancipator, S.N., Lamm, M.E. J. Clin. Invest. (1990) [Pubmed]
  10. Factor XIII deficiency in BALB/c mice with plasmacytoma. Eipe, J., Yakulis, V., Costea, N. Cancer Res. (1977) [Pubmed]
  11. Neonatal and adult primary B cells use the same germ-line VH and V kappa genes in their (T,G)-A-L-specific repertoire. Borriero, L., Giorgetti, C., Smith, G., Landry, D., Selsing, E., Zhukovsky, E., Press, J.L. J. Immunol. (1990) [Pubmed]
  12. An epigenetically altered tumor cell vaccine. Khan, A.N., Magner, W.J., Tomasi, T.B. Cancer Immunol. Immunother. (2004) [Pubmed]
  13. A molecular analysis of PGE receptor (EP) expression on normal and transformed B lymphocytes: coexpression of EP1, EP2, EP3beta and EP4. Fedyk, E.R., Ripper, J.M., Brown, D.M., Phipps, R.P. Mol. Immunol. (1996) [Pubmed]
  14. Two distinct allotypic determinants on the antigen-specific suppressor and enhancing T cell factors that are encoded by genes linked to the immunoglobulin heavy chain locus. Tokuhisa, T., Taniguchi, M. J. Exp. Med. (1982) [Pubmed]
  15. The T suppressor cell alloantigen Tsud maps near immunoglobulin allotype genes and may be an heavy chain constant-region marker on a T cell receptor. Owen, F.L., Riblet, R., Taylor, B.A. J. Exp. Med. (1981) [Pubmed]
  16. Deletional mapping of fifteen mouse VH gene families reveals a common organization for three Igh haplotypes. Mainville, C.A., Sheehan, K.M., Klaman, L.D., Giorgetti, C.A., Press, J.L., Brodeur, P.H. J. Immunol. (1996) [Pubmed]
  17. T cell regulation of immunoglobulin class expression in the antibody response to trinitrophenyl-ficoll. Evidence for T cell enhancement of the immunoglobulin class switch. Mongini, P.K., Paul, W.E., Metcalf, E.S. J. Exp. Med. (1982) [Pubmed]
  18. H-40, an antigen controlled by an Igh linked gene and recognized by cytotoxic T lymphocytes. I. Genetic analysis of H-40 and distribution of its product on B cell tumors. Forman, J., Riblet, R., Brooks, K., Vitetta, E.S., Henderson, L.A. J. Exp. Med. (1984) [Pubmed]
  19. Sites that direct nuclear compartmentalization are near the 5' end of the mouse immunoglobulin heavy-chain locus. Yang, Q., Riblet, R., Schildkraut, C.L. Mol. Cell. Biol. (2005) [Pubmed]
  20. Influence of Igh-linked gene products on the generation of T helper cells in the response to sheep erythrocytes. Nutt, N., Haber, J., Wortis, H.H. J. Exp. Med. (1981) [Pubmed]
  21. Immunogenetics of BCG-induced anergy in mice. Control by Igh- and H-2-linked genes. Callis, A.H., Schrier, D.J., David, C.S., Moore, V.L. Immunology (1983) [Pubmed]
  22. T cell development in B cell-deficient mice. V. Stopping anti-mu treatment results in Igh-restricted expansion of the T suppressor cell repertoire concomitant with the development of normal immunoglobulin levels. Hayglass, K.T., Benacerraf, B., Sy, M.S. J. Exp. Med. (1986) [Pubmed]
  23. Regulation of T15 idiotype dominance. II. Genes unlinked to the Igh locus regulate T15 dominance of the secondary adoptive transfer response to phosphocholine. Wicker, L.S., Guelde, G., Scher, I., Kenny, J.J. J. Immunol. (1985) [Pubmed]
  24. VH families in the antibody response to p-azophenylarsonate: correlation between serology and amino acid sequence. Milner, E.C., Capra, J.D. J. Immunol. (1982) [Pubmed]
  25. Genetic linkage of the cytolytic T lymphocyte repertoire and immunoglobulin heavy chain genes. Sherman, L.A. J. Exp. Med. (1982) [Pubmed]
  26. Genetics of the alpha 1,6-dextran response: expression of the QUPC52 idiotype in different inbred and congenic strains of mice. D'Hoostelaere, L., Potter, M. J. Immunol. (1982) [Pubmed]
  27. Comparative analysis of human and mouse 3' Igh regulatory regions identifies distinctive structural features. Sepulveda, M.A., Garrett, F.E., Price-Whelan, A., Birshtein, B.K. Mol. Immunol. (2005) [Pubmed]
  28. Variable region sequence analysis of anti-DNA antibodies: evidence for a family of closely related germ-line VH genes encoding lupus autoantibodies. Foster, M.H., Madaio, M.P., Barrett, K.J. DNA Cell Biol. (1992) [Pubmed]
  29. Ezh2 controls B cell development through histone H3 methylation and Igh rearrangement. Su, I.H., Basavaraj, A., Krutchinsky, A.N., Hobert, O., Ullrich, A., Chait, B.T., Tarakhovsky, A. Nat. Immunol. (2003) [Pubmed]
  30. Genetic control of BCG-induced granulomatous inflammation in mice. Sternick, J.L., Schrier, D.J., Moore, V.L. Exp. Lung Res. (1983) [Pubmed]
  31. Regulation of the replication of the murine immunoglobulin heavy chain gene locus: evaluation of the role of the 3' regulatory region. Michaelson, J.S., Ermakova, O., Birshtein, B.K., Ashouian, N., Chevillard, C., Riblet, R., Schildkraut, C.L. Mol. Cell. Biol. (1997) [Pubmed]
  32. Stepwise activation of the immunoglobulin mu heavy chain gene locus. Chowdhury, D., Sen, R. EMBO J. (2001) [Pubmed]
  33. Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex. Schrier, D.J., Sternick, J.L., Allen, E.M., Moore, V.L. J. Immunol. (1982) [Pubmed]
  34. Idiotypic analysis of anti-GAT antibodies. IX. Genetic mapping of the Gte idiotypic marker within the Igh-V locus. Ju, S.T., Dorf, M.E. J. Immunol. (1981) [Pubmed]
  35. Location of Myc, Igh, and Igk on Robertsonian fusion chromosomes is inconsequential for Myc translocations and plasmacytoma development in mice, but Rb(6.15)-carrying tumors prefer Igk-Myc inversions over translocations. Silva, S., Wiener, F., Klein, G., Janz, S. Genes Chromosomes Cancer (2005) [Pubmed]
  36. Similarities between transplantation antigens on methylcholanthrene-induced sarcomas and T-cell regulatory molecules. Flood, P.M., Deleo, A.B., Old, L.J., Gershon, R.K. Ann. N. Y. Acad. Sci. (1983) [Pubmed]
  37. Molecular analysis of spontaneous nephrotropic anti-laminin antibodies in an autoimmune MRL-lpr/lpr mouse. Foster, M.H., Sabbaga, J., Line, S.R., Thompson, K.S., Barrett, K.J., Madaio, M.P. J. Immunol. (1993) [Pubmed]
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