The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

H2-L  -  histocompatibility 2, D region locus L

Mus musculus

Synonyms: H-2 class I histocompatibility antigen, L-D alpha chain, H-2L
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of H2-L

  • Thus, the lack of H-2L antigenic specificities does not produce a general loss of responsiveness for other viruses even when a highly cross-reactive pox virus (vaccinia) was studied [1].
  • It was found that BALB/c-H-2db mice, which lack detectable cell-surface H-2L gene products, were able to generate influenza- and vaccinia-immune cytotoxic T cells which lyse D region-compatible target cells, although they have been reported to be incapable of making a similar response to ectromelia virus (7) [1].
  • H-2L-restricted recognition of viral antigens In the H-2d haplotype, anti-vesicular stomatitis virus cytotoxic T cells are restricted solely by H-2L [2].
  • One was the survival ratio at an early stage after an intravenous (iv) inoculation of radiolabeled B16 H-2L cells, the other was the formation of pulmonary metastases after iv injection with the tumor cells [3].
  • We have investigated the effects of administration of C. parvum on host anti-metastatic activity against B16 melanoma H-2L, a natural killer (NK) sensitive clone with a low expression of H-2b [3].
 

High impact information on H2-L

  • Consistent with this function is the finding that these transplantation antigens (encoded by the H-2K, H-2D and H-2L genes in mice) are cell-surface glycoproteins with their amino-termini protruding extracellularly and their carboxy-termini located inside the cell [4].
  • Molecular evidence that the H-2D and H-2L genes arose by duplication. Differences between the evolution of the class I genes in mice and humans [5].
  • The above procedures clearly implicated the H-2L region in the thymocyte rosetting of d and k haplotypes [6].
  • Finally, the critical role played by the H-2L region in this rosetting phenomenon was demonstrated by the inability of thymocytes from the H-2L-deletion mutant (H-2dm2) to rosette with syngeneic, allogeneic (rat) erythrocytes [6].
  • With erythrocyte sonicates from recombinant mouse strains it was demonstrated that rosetting with syngeneic erythrocytes was mediated by H-2L and/or H-2D region-restricted receptors [6].
 

Biological context of H2-L

  • H-2L-like sequences are found in mutant H-2Kb molecules, suggesting that gene conversion or reciprocal recombination may play a role in the development of H-2 polymorphism [7].
  • Implication of the H-2L locus in hybrid histocompatibility (Hh-1) [8].
  • These findings explain the previously widely reported selective down-regulation of certain MHC class I-encoded glycoproteins (H-2K, bur not H-2D or H-2L) during tumor progression [9].
  • In order to study the fine structure of H-2L, the third H-2 locus of the mouse major histocompatibility complex, we have produced and characterized the monoclonal anti-Ld antibodies secreted by 3 different hybridoma cell lines [10].
  • Mutant H chains, expressed in the presence of excess L chain, associate with Ig binding protein (BiP) and GRP94 and fail to form HL and H2L assembly intermediates efficiently [11].
 

Anatomical context of H2-L

  • Even though mutant lymphocytes, which lack H-2L but not H-2D antigens, are not cytotoxically lysed by D28b (as are parental H-2d cells), D28b appears to precipitate H-2D antigens from NP-40 extracts of mutant splenocytes [12].
  • It was found that subpopulations of both T and B lymphocytes autorosette via H-2L restricted receptors [13].
  • In contrast, H2L was unable to counteract BoNT-induced paralysis at the murine neuromuscular junction [14].
  • To test whether the major histocompatibility complex class I genes are involved in the regulation of hemopoiesis, the stem cell activities of BALB/c-H-2dm2 (Dm2) mice, which are defective in the expression of H-2L antigens, have been compared with those of the wild-type, BALB/c-Kh, in in vivo and in vitro stem cell assays [15].
  • The human colon adenocarcinoma-derived cell line CaCo-2 was used as a model system to study the effects of copper (II), tetradentate N-alkyl ligand (H2L) and their complex [16].
 

Associations of H2-L with chemical compounds

  • The H-2L locus is closely linked to H-2D and codes for antigenic specificities present on a 45,000 mol wt glycoprotein that is distinct from the molecule which bears the D region private specificity [1].
  • Other studies show that the tyrosine in the cytoplasmic domain is accessible to radioiodination on only a subset of H-2Ld molecules, and that the two-dimensional electrophoretic profiles of phosphorylated H-2L/Db molecules, of R4-reactive molecules, and of H-2Ld molecules radiolabeled on this cytoplasmic domain tyrosine are virtually identical [17].
  • BALB/c spleen cells treated for 1 to 2 hr with cholesteryl hemisuccinate (CHS) displayed reduced levels of all tested H-2 determinants (H-2L, H-2K, and H-2D) as evaluated by flow microfluorometry and increased membrane lipid packing density as determined by 1,6-diphenyl-1,3,5-hexatriene (DPH) fluorescence polarization [18].
  • In comparing the tryptic peptide maps of the H-2L and H-2D glycoprotein antigens isolated from NP-40 lysates of RADA1 (H-2 alpha) leukemic cells, no more than 37% of the observed arginine-containing tryptic peptides are found to be homologous [12].
  • The six molecular components of the reoxidation--L (light chain), H (heavy chain), HL, H2, H2L, H2L2--are quantitatively determined from polyacrylamide gels containing sodium dodecyl sulfate and the time-dependent sulfhydryl titer is measured with 5,5'-dithiobis-(2-nitrobenzoic acid) [19].
 

Physical interactions of H2-L

  • With the s haplotype the rosetting receptor was mapped to the H-2L/H-2D region, whereas with the b and q haplotypes rosetting was only mapped to the D end of the H-2 complex [6].
 

Other interactions of H2-L

  • These experiments show that the presently defined H-2K, H-2D and H-2L antigens as well as some Ia antigens are themselves not the C3d receptors [20].
  • These structural analyses further substantiate the functional studies that define the H-2L molecule as the "third" major histocompatibility molecule of the mouse [21].
 

Analytical, diagnostic and therapeutic context of H2-L

References

  1. Involvement of H-2L gene products in virus-immune T-cell recognition. Evidence for an H-2L-restricted T-cell response. Biddison, W.E., Hansen, T.H., Levy, R.B., Doherty, P.C. J. Exp. Med. (1978) [Pubmed]
  2. H-2L-restricted recognition of viral antigens In the H-2d haplotype, anti-vesicular stomatitis virus cytotoxic T cells are restricted solely by H-2L. Ciavarra, R., Forman, J. J. Exp. Med. (1982) [Pubmed]
  3. Alteration in natural defense activity against NK-susceptible B16 melanoma cells after treatment with Corynebacterium parvum. Karashima, A., Taniguchi, K., Yoshikai, Y., Nomoto, K. Immunobiology (1991) [Pubmed]
  4. Alternative RNA splicing in expression of the H-2K gene. Kress, M., Glaros, D., Khoury, G., Jay, G. Nature (1983) [Pubmed]
  5. Molecular evidence that the H-2D and H-2L genes arose by duplication. Differences between the evolution of the class I genes in mice and humans. Rubocki, R.J., Lee, D.R., Lie, W.R., Myers, N.B., Hansen, T.H. J. Exp. Med. (1990) [Pubmed]
  6. Anti-self receptors. I. Direct detection of H-2L region-restricted receptors on murine thymocytes. Sia, D.Y., Parish, C.R. J. Exp. Med. (1980) [Pubmed]
  7. Structure and expression of a mouse major histocompatibility antigen gene, H-2Ld. Evans, G.A., Margulies, D.H., Camerini-Otero, R.D., Ozato, K., Seidman, J.G. Proc. Natl. Acad. Sci. U.S.A. (1982) [Pubmed]
  8. Implication of the H-2L locus in hybrid histocompatibility (Hh-1). Morgan, G.M., McKenzie, I.F. Transplantation (1981) [Pubmed]
  9. Attenuation of the Fas-L independent b16bL6 melanoma lymphocidic capacity by H-2K class I molecules. Kellman-Pressman, S., Fishman, D., Tsory, S., Segal, S. Immunol. Lett. (2005) [Pubmed]
  10. Monoclonal antibodies to mouse MHC antigens. II. Antibodies to the H-2Ld antigen, the products of a third polymorphic locus of the mouse major histocompatibility complex. Ozato, K., Hansen, T.H., Sachs, D.H. J. Immunol. (1980) [Pubmed]
  11. Mutation of a single conserved residue in VH complementarity-determining region 2 results in a severe Ig secretion defect. Wiens, G.D., Lekkerkerker, A., Veltman, I., Rittenberg, M.B. J. Immunol. (2001) [Pubmed]
  12. Biochemical evidence for a separate, MHC-linked locus encoding H-2.28 antigens. Sears, D.W., Polizzi, C.M. Immunogenetics (1980) [Pubmed]
  13. Anti-self receptors. II. Demonstration of H-2L region-restricted receptors on subpopulations of peripheral T and B lymphocytes. Sia, D.Y., Parish, C.R. J. Immunol. (1980) [Pubmed]
  14. Multiple domains of botulinum neurotoxin contribute to its inhibition of transmitter release in Aplysia neurons. Poulain, B., Wadsworth, J.D., Shone, C.C., Mochida, S., Lande, S., Melling, J., Dolly, J.O., Tauc, L. J. Biol. Chem. (1989) [Pubmed]
  15. Influence of major histocompatibility complex H-2LD class I molecules on spleen colony-forming units. Tange, T., Ahmed-Ansari, A., Hansen, T., Tse, H.Y. J. Immunol. (1988) [Pubmed]
  16. Stability, toxicity and cytotoxicity of a cupric complex towards cultured CaCo-2 cells. Thanh, X.D., Djebbar-Sid, S., Benali-Baïtich, O., Pehu, G., Khan, M.A., Bouet, G. Anticancer Res. (2000) [Pubmed]
  17. The cytoplasmic domain of the H-2Ld class I major histocompatibility complex molecule is differentially accessible to immunological and biochemical probes during transport to the cell surface. Capps, G.G., Zúñiga, M.C. J. Biol. Chem. (1993) [Pubmed]
  18. Changes in cell-surface expression of MHC and Thy-1.2 determinants following treatment with lipid modulating agents. Muller, C.P., Stephany, D.A., Shinitzky, M., Wunderlich, J.R. J. Immunol. (1983) [Pubmed]
  19. A kinetic study in vitro of the reoxidation of interchain disulfide bonds in a human immunoglobulin IgGLk. Correlation between sulfhydryl disappearance and intermediates in covalent assembly of H2L2. Sears, D.W., Mohrer, J., Beychok, S. Proc. Natl. Acad. Sci. U.S.A. (1975) [Pubmed]
  20. The blocking effect of antibodies against the products of the H-2 gene complex on lymphocyte complement (C3d) receptors. complement dependence and specificity. Bishop, C., Démant, P., Capel, P.J. Tissue Antigens (1980) [Pubmed]
  21. Structural relation of murine "third locus" (H-2L) major histocompatibility antigens to the products of H-2K and H-2D loci. Rose, S.M., Hansen, T.H., Cullen, S.E. J. Immunol. (1980) [Pubmed]
  22. Skin graft enhancement studies with antigenic differences arising from the H-2K, H-2D, and H-2L loci. McKenzie, I.F., Henning, M.M., Morgan, G.M. Transplantation (1980) [Pubmed]
  23. Enumeration of H-2-gene products: failure to detect L molecules in the H-2b haplotype. Hansen, T.H., Ozato, K., Sachs, D.H. Ann. Immunol. (Paris) (1980) [Pubmed]
  24. Enhancement and antibody-mediated rejection of mouse skin allografts with anti-H-2K, H-2D, H-2L antibodies. Capel, P.J., de Waal, R.M., Démant, P., Koene, R.A. Transplant. Proc. (1981) [Pubmed]
 
WikiGenes - Universities