Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of H2-Ab1. (This text reflects annotations as of Wednesday, January 23, 2013.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] HLA-DQB1 belongs to the HLA class II beta chain paralogs. This class II molecule is a heterodimer consisting of an alpha (DQA) and a beta chain (DQB), both anchored in the membrane. It plays a central role in the immune system by presenting peptides derived from extracellular proteins. Class II molecules are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). The beta chain is approximately 26-28 kDa and it contains six exons. Exon 1 encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and exon 5 encodes the cytoplasmic tail. Within the DQ molecule both the alpha chain and the beta chain contain the polymorphisms specifying the peptide binding specificities, resulting in up to four different molecules. Typing for these polymorphisms is routinely done for bone marrow transplantation. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Sep 2011]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of H2-Ab1
  • participates in the following biological processes:
    • antigen processing and presentation ^[11]
    • antigen processing and presentation of exogenous peptide antigen via MHC class II ^{[1, 11, 15, 17, 19, 21, 25, 27]}
    • antigen processing and presentation of peptide antigen ^[21]
    • B cell affinity maturation ^[18]
    • cellular response to interferon-gamma ^{[2, 4, 6, 7, 23]}
    • positive regulation of alpha-beta T cell activation ^[13]
    • positive regulation of antigen processing and presentation ^[13]
    • positive regulation of T-helper 1 type immune response ^[13]
  • performs the following molecular functions:
    • peptide antigen binding ^{[11, 21]}
    • transcription factor binding ^[5]
  • is located in the following cellular components:
    • early endosome ^[12]
    • external side of plasma membrane ^{[9, 11, 15, 17, 19, 25, 26, 28, 29]}
    • Golgi apparatus ^[25]
    • integral to membrane ^[16]
    • intracellular ^[14]
    • MHC class II protein complex ^{[9, 10, 11, 15, 17, 19, 25, 26]}
    • multivesicular body ^[12]
    • plasma membrane ^{[9, 10, 12, 14, 25]}
• The gene product of H2-Ab1 has been shown to bind to the gene products of Cd74, H2-Aa. ^[10] Researchers have inferred, based on physical interactions, that the gene product of H2-Ab1
  • performs the following molecular functions:
    • repressing transcription factor binding ^[3]
    • toxin binding ^[22]
    • ubiquitin protein ligase binding ^[20]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of H2-Ab1
  • participates in the following biological processes:
    • immune response ^[8]
    • positive regulation of alpha-beta T cell activation ^[24]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of H2-Ab1:
  • participates in the following biological processes:
    • humoral immune response mediated by circulating immunoglobulin
    • immunoglobulin production involved in immunoglobulin mediated immune response
    • negative regulation of T cell proliferation
  • performs the following molecular functions:
    • protein heterodimerization activity
  • is located in the following cellular components:
    • cell surface

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Summary text based on GO annotations supported by structural data

• H2-Ab1 encodes a protein or proteins that contain the following InterPro domains: Immunoglobulin C1-set, Immunoglobulin-like, Immunoglobulin-like fold, Immunoglobulin/major histocompatibility complex, conserved site, MHC class II, alpha/beta chain, N-terminal, MHC class II, beta chain, N-terminal, MHC classes I/II-like antigen recognition protein, indicating that the gene product:
  • is located in the following cellular components:
    • membrane

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe H2-Ab1 indicates that it:
  • participates in the following biological processes:
    • antigen processing and presentation of peptide or polysaccharide antigen via MHC class II
  • is located in the following cellular components:
    • membrane

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References

1. Alfonso C et al. (2001) The Impact of H2-DM on Humoral Immune Responses. J Immunol, 167:6348-55. (PubMed:11714799)
2. Barrera LF et al. (1997) I-A beta gene expression regulation in macrophages derived from mice susceptible or resistant to infection with M. bovis BCG. Mol Immunol, 34:343-55. (PubMed:9244347)
3. Borras FE et al. (1995) Repression of I-A beta gene expression by the transcription factor PU.1. J Biol Chem, 270:24385-91. (PubMed:7592651)
4. Celada A et al. (1989) The expression of I-A correlates with the uptake of interferon-gamma by macrophages. Eur J Immunol, 19:205-8. (PubMed:2493384)
5. Celada A et al. (1996) Identification of a transcription factor that binds to the S box of the I-A beta gene of the major histocompatibility complex. Biochem J, 313:737-44. (PubMed:8611149)
6. Celada A et al. (1991) IFN-gamma induces the expression of the genes for MHC class II I-A beta and tumor necrosis factor through a protein kinase C-independent pathway. J Immunol, 146:114-20. (PubMed:1845803)
7. Celada A et al. (1989) Interferon-gamma activates multiple pathways to regulate the expression of the genes for major histocompatibility class II I-A beta, tumor necrosis factor and complement component C3 in mouse macrophages. Eur J Immunol, 19:1103-9. (PubMed:2502420)
8. Cosgrove D et al. (1991) Mice lacking MHC class II molecules. Cell, 66:1051-66. (PubMed:1909605)
9. Fung-Leung WP et al. (1996) Antigen presentation and T cell development in H2-M-deficient mice. Science, 271:1278-81. (PubMed:8638109)
10. Karlsson L et al. (1994) Reconstitution of an operational MHC class II compartment in nonantigen-presenting cells. Science, 266:1569-73. (PubMed:7985028)
11. Kovats S et al. (1998) Invariant chain-independent function of H-2M in the formation of endogenous peptide-major histocompatibility complex class II complexes in vivo. J Exp Med, 187:245-51. (PubMed:9432982)
12. Lankar D et al. (2002) Dynamics of major histocompatibility complex class II compartments during B cell receptor-mediated cell activation. J Exp Med, 195:461-72. (PubMed:11854359)
13. Lemos MP et al. (2003) CD8alpha+ and CD11b+ dendritic cell-restricted MHC class II controls Th1 CD4+ T cell immunity. J Immunol, 171:5077-84. (PubMed:14607905)
14. Liljedahl M et al. (1996) HLA-DO is a lysosomal resident which requires association with HLA-DM for efficient intracellular transport. EMBO J, 15:4817-24. (PubMed:8890155)
15. Liljedahl M et al. (1998) Altered antigen presentation in mice lacking H2-O. Immunity, 8:233-43. (PubMed:9492004)
16. Lindstedt R et al. (1995) The MHC class II molecule H2-M is targeted to an endosomal compartment by a tyrosine-based targeting motif. Immunity, 3:561-72. (PubMed:7584146)
17. Martin WD et al. (1996) H2-M mutant mice are defective in the peptide loading of class II molecules, antigen presentation, and T cell repertoire selection. Cell, 84:543-50. (PubMed:8598041)
18. Miki N et al. (1992) Role of I-A molecules in early stages of B cell maturation. J Immunol, 149:801-7. (PubMed:1378867)
19. Miyazaki T et al. (1996) Mice lacking H2-M complexes, enigmatic elements of the MHC class II peptide-loading pathway. Cell, 84:531-41. (PubMed:8598040)
20. Ohmura-Hoshino M et al. (2006) Inhibition of MHC class II expression and immune responses by c-MIR. J Immunol, 177:341-54. (PubMed:16785530)
21. Perraudeau M et al. (2000) Altered major histocompatibility complex class II peptide loading in H2-O-deficient mice Eur J Immunol, 30:2871-80. (PubMed:11069069)
22. Russell JK et al. (1990) The I-A beta b region (65-85) is a binding site for the superantigen, staphylococcal enterotoxin A. Biochem Biophys Res Commun, 168:696-701. (PubMed:2159298)
23. Sanderson IR et al. (1993) Differential regulation of B7 mRNA in enterocytes and lymphoid cells. Immunology, 79:434-8. (PubMed:7691725)
24. Schito ML et al. (1998) Major histocompatibility complex class I- and II-deficient knock-out mice are resistant to primary but susceptible to secondary Eimeria papillata infections. Parasitol Res, 84:394-8. (PubMed:9610637)
25. Viville S et al. (1993) Mice lacking the MHC class II-associated invariant chain. Cell, 72:635-48. (PubMed:7679955)
26. Walter W et al. (2001) H2-Mbeta 1 and H2-Mbeta 2 heterodimers equally promote clip removal in I-A(q) molecules from autoimmune-prone DBA/1 mice. J Biol Chem, 276:11086-91. (PubMed:11148202)
27. Walter W et al. (2000) MHC class II antigen presentation pathway in murine tumours: tumour evasion from immunosurveillance? Br J Cancer, 83:1192-201. (PubMed:11027433)
28. Yada A et al. (2003) Accelerated antigen presentation and elicitation of humoral response in vivo by FcgammaRIIB- and FcgammaRI/III-mediated immune complex uptake. Cell Immunol, 225:21-32. (PubMed:14643301)
29. Yokota A et al. (2003) Cell-mediated fas-based lysis of dendritic cells which are apparently resistant to anti-Fas antibody. Microbiol Immunol, 47:285-93. (PubMed:12801066)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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