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Gene Review

Igh-V7183  -  immunoglobulin heavy chain (V7183 family)

Mus musculus

Synonyms: B9-scFv, IgG, IgH, IgVH1(VSG), VH7183, ...
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Disease relevance of Igh-V7183


High impact information on Igh-V7183

  • We have employed a method based on the Cre-loxP recombination system of bacteriophage P1 to generate a mouse strain in which the JH segments and the intron enhancer in the IgH locus are deleted [6].
  • We propose, therefore, that the T cell-negative regulator responsible for IgH gene extinction does not simply prevent IgH enhancer activation but interferes with gene expression more directly, perhaps by disrupting the transcription complex established as a result of tissue-specific enhancer activation [1].
  • This is probably an oversimplification: there are cell lines that transcribe IgH genes despite the deletion of the intron-enhancer [2].
  • Furthermore, unlike the intron-enhancer, the IgH 3' enhancer would become linked to a c-myc that rearranges into an IgH switch region [2].
  • Here we show that a strong B-cell-specific enhancer is indeed located at the 3'-end of the rat IgH locus, 25 kilobases downstream of C alpha [2].

Biological context of Igh-V7183

  • We find that AID targets cytosines in both donor and acceptor switch regions (S regions) with the deamination domains initiating approximately 150 nucleotides 3' of the I exon start sites and extending over several kilobases (the IgH intronic enhancer is spared) [7].
  • The ability of the mouse immunoglobulin heavy chain gene (IgH) enhancer to stimulate in vitro transcription from the adenovirus-2 major late promoter (Ad2MLP) has been investigated [8].
  • We report the nucleotide sequence of two cloned rheumatoid factor VH genes, Y19-10 (VH J558) and 129-48 (VH 7183) in which no major differences are observed between VH genes encoding the heavy chain of autoantibodies and antibodies against foreign antigens [9].
  • Unequal VH gene rearrangement frequency within the large VH7183 gene family is not due to recombination signal sequence variation, and mapping of the genes shows a bias of rearrangement based on chromosomal location [10].
  • Southern blot analysis using VH probes indicates that these recombinations may be accompanied by the deletion of germline VH genes belonging to both the VHQ52 and VH7183 families, suggesting that these gene families are interspersed in the NFS/N mouse [11].

Anatomical context of Igh-V7183


Associations of Igh-V7183 with chemical compounds


Physical interactions of Igh-V7183


Regulatory relationships of Igh-V7183

  • Reconstitution of Pax5 expression in Pax5-/- pro-B cells induced large-scale contraction and distal VH-DJH rearrangements of the IgH locus [23].
  • These results suggest that Id may play a role early in B-lymphoid-cell development to regulate transcription of the IgH locus [24].
  • The IgH 3'-enhancers induced the up-regulation of c-myc expression specifically in B cells of IgH-3'-E-myc mice [25].
  • We present strong evidence that ELF-1 is highly expressed in B-cells and is one of two major factors specifically interacting with the murine IgH enhancer pi site in B-cell nuclear extracts [22].

Other interactions of Igh-V7183

  • Pax5 is required for recombination of transcribed, acetylated, 5' IgH V gene segments [26].
  • Using sterile I(mu) transcription as an indicator of IgH enhancer activity, we see a direct correlation between E2A DNA binding activity and I(mu) transcription in stable BxT hybrids [27].
  • By contrast, none of the other IgH enhancer-binding proteins tested (E2-2, Pu.1, Oct-2, OCA-B, TFE3 and USF) were able to activate I(mu) transcription [27].
  • Our studies demonstrate that the IgH 3'-enhancers play an important role in c-myc deregulation and B cell lymphomagenesis in vivo [25].
  • These results support the notion that the control of anti-Sm production in MRL/lpr mice operates through the IgH locus [28].

Analytical, diagnostic and therapeutic context of Igh-V7183


  1. Role of the octamer motif in hybrid cell extinction of immunoglobulin gene expression: extinction is dominant in a two enhancer system. Yu, H., Porton, B., Shen, L.Y., Eckhardt, L.A. Cell (1989) [Pubmed]
  2. A second B cell-specific enhancer 3' of the immunoglobulin heavy-chain locus. Pettersson, S., Cook, G.P., Brüggemann, M., Williams, G.T., Neuberger, M.S. Nature (1990) [Pubmed]
  3. T-cell-receptor beta- and I-A beta-chain genes of normal SWR mice are linked with the development of lupus nephritis in NZB x SWR crosses. Ghatak, S., Sainis, K., Owen, F.L., Datta, S.K. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  4. Lack of t(14;18) polymerase chain reaction-positive cells in highly purified CD34+ cells and their CD19 subsets in patients with follicular lymphoma. Voso, M.T., Hohaus, S., Moos, M., Haas, R. Blood (1997) [Pubmed]
  5. Bcl10 can promote survival of antigen-stimulated B lymphocytes. Tian, M.T., Gonzalez, G., Scheer, B., DeFranco, A.L. Blood (2005) [Pubmed]
  6. Independent control of immunoglobulin switch recombination at individual switch regions evidenced through Cre-loxP-mediated gene targeting. Gu, H., Zou, Y.R., Rajewsky, K. Cell (1993) [Pubmed]
  7. The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2-/- ung-/- mice. Xue, K., Rada, C., Neuberger, M.S. J. Exp. Med. (2006) [Pubmed]
  8. The mouse immunoglobulin heavy-chain enhancer: effect on transcription in vitro and binding of proteins present in HeLa and lymphoid B cell extracts. Augereau, P., Chambon, P. EMBO J. (1986) [Pubmed]
  9. Fine specificity, idiotypy, and nature of cloned heavy-chain variable region genes of murine monoclonal rheumatoid factor antibodies. Manheimer-Lory, A.J., Monestier, M., Bellon, B., Alt, F.W., Bona, C.A. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  10. Unequal VH gene rearrangement frequency within the large VH7183 gene family is not due to recombination signal sequence variation, and mapping of the genes shows a bias of rearrangement based on chromosomal location. Williams, G.S., Martinez, A., Montalbano, A., Tang, A., Mauhar, A., Ogwaro, K.M., Merz, D., Chevillard, C., Riblet, R., Feeney, A.J. J. Immunol. (2001) [Pubmed]
  11. Analysis of VH gene replacement events in a B cell lymphoma. Kleinfield, R.W., Weigert, M.G. J. Immunol. (1989) [Pubmed]
  12. Ordered rearrangement of immunoglobulin heavy chain variable region segments. Alt, F.W., Yancopoulos, G.D., Blackwell, T.K., Wood, C., Thomas, E., Boss, M., Coffman, R., Rosenberg, N., Tonegawa, S., Baltimore, D. EMBO J. (1984) [Pubmed]
  13. Immunoglobulin heavy chain binding protein. Haas, I.G., Wabl, M. Nature (1983) [Pubmed]
  14. The half-life of immunoglobulin mRNA increases during B-cell differentiation: a possible role for targeting to membrane-bound polysomes. Mason, J.O., Williams, G.T., Neuberger, M.S. Genes Dev. (1988) [Pubmed]
  15. Correlation between the amino acid position of arginine in VH-CDR3 and specificity for native DNA among autoimmune antibodies. Krishnan, M.R., Jou, N.T., Marion, T.N. J. Immunol. (1996) [Pubmed]
  16. Mutational analysis of the immunoglobulin heavy chain promoter region. Ballard, D.W., Bothwell, A. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  17. Positive and negative transcriptional states of a variegating immunoglobulin heavy chain (IgH) locus are maintained by a cis-acting epigenetic mechanism. Ronai, D., Berru, M., Shulman, M.J. J. Immunol. (2002) [Pubmed]
  18. Anti-IgM antibodies down modulate mu-enhancer activity and OTF2 levels in LPS-stimulated mouse splenic B-cells. Chen, U., Scheuermann, R.H., Wirth, T., Gerster, T., Roeder, R.G., Harshman, K., Berger, C. Nucleic Acids Res. (1991) [Pubmed]
  19. Expression of genes containing the IgH enhancer in non-lymphoid cells. Klein, B.Y., Morrison, S.L. Mol. Immunol. (1990) [Pubmed]
  20. Transcriptional regulation of the murine 3' IgH enhancer by OCT-2. Tang, H., Sharp, P.A. Immunity (1999) [Pubmed]
  21. Homologies between cell interaction molecular controlled by major histocompatibility complex- and Igh-V-linked genes that T cells use for communication. Tandem "adaptive" differentiation of producer and acceptor cells. Flood, P., Yamauchi, K., Singer, A., Gershon, R.K. J. Exp. Med. (1982) [Pubmed]
  22. ELF-1 interacts with and transactivates the IgH enhancer pi site. Akbarali, Y., Oettgen, P., Boltax, J., Libermann, T.A. J. Biol. Chem. (1996) [Pubmed]
  23. Pax5 induces V-to-DJ rearrangements and locus contraction of the immunoglobulin heavy-chain gene. Fuxa, M., Skok, J., Souabni, A., Salvagiotto, G., Roldan, E., Busslinger, M. Genes Dev. (2004) [Pubmed]
  24. Repression of immunoglobulin enhancers by the helix-loop-helix protein Id: implications for B-lymphoid-cell development. Wilson, R.B., Kiledjian, M., Shen, C.P., Benezra, R., Zwollo, P., Dymecki, S.M., Desiderio, S.V., Kadesch, T. Mol. Cell. Biol. (1991) [Pubmed]
  25. Regulatory elements in the immunoglobulin heavy chain gene 3'-enhancers induce c-myc deregulation and lymphomagenesis in murine B cells. Wang, J., Boxer, L.M. J. Biol. Chem. (2005) [Pubmed]
  26. Pax5 is required for recombination of transcribed, acetylated, 5' IgH V gene segments. Hesslein, D.G., Pflugh, D.L., Chowdhury, D., Bothwell, A.L., Sen, R., Schatz, D.G. Genes Dev. (2003) [Pubmed]
  27. E47 activates the Ig-heavy chain and TdT loci in non-B cells. Choi, J.K., Shen, C.P., Radomska, H.S., Eckhardt, L.A., Kadesch, T. EMBO J. (1996) [Pubmed]
  28. Regulation of anti-Sm autoantibodies by the immunoglobulin heavy chain locus. Halpern, M.D., Craven, S.Y., Cohen, P.L., Eisenberg, R.A. J. Immunol. (1993) [Pubmed]
  29. Visualization of looping involving the immunoglobulin heavy-chain locus in developing B cells. Sayegh, C., Jhunjhunwala, S., Riblet, R., Murre, C. Genes Dev. (2005) [Pubmed]
  30. High frequency of autoantibodies bearing cross-reactive idiotopes among hybridomas using VH7183 genes prepared from normal and autoimmune murine strains. Bellon, B., Manheimer-Lory, A., Monestier, M., Moran, T., Dimitriu-Bona, A., Alt, F., Bona, C. J. Clin. Invest. (1987) [Pubmed]
  31. Binding in vitro of multiple cellular proteins to immunoglobulin heavy-chain enhancer DNA. Peterson, C.L., Orth, K., Calame, K.L. Mol. Cell. Biol. (1986) [Pubmed]
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