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Daf2  -  decay accelerating factor 2

Mus musculus

Synonyms: AI323748, Cd55b, Complement decay-accelerating factor transmembrane isoform, DAF-TM, Daf, ...
 
 
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High impact information on Daf2

  • We demonstrate that during primary T cell activation, the absence of Daf on antigen-presenting cells (APCs) and on T cells enhances T cell proliferation and augments the induced frequency of effector cells [1].
  • We show that cognate T cell-APC interactions are accompanied by rapid production of alternative pathway components and down-regulation of Daf expression [1].
  • Decay-accelerating factor (Daf) dissociates C3/C5 convertases that assemble on host cells and thereby prevents complement activation on their surfaces [1].
  • Chromosome localization studies mapped the mouse Daf genes to chromosome 1, where they segregated with the C4-binding protein (C4bp) gene [2].
  • Molecular cloning of mouse decay accelerating factor (DAF; CD55) predicted two forms of the molecule, one transmembrane (TM) and the other glycosylphosphatidylinositol (GPI)-anchored; these are encoded by separate genes termed Daf-GPI and Daf-TM [3].
 

Anatomical context of Daf2

  • Northern blot analysis indicated that rat GPI-DAF mRNA was present in all tissues examined except for liver, while rat TM-DAF mRNA was preferentially expressed in testis [4].
  • Examination of the fetoplacental unit at the day 7.5 stage revealed that GPI-DAF but not the TM-DAF gene is expressed in the maternal decidua cells surrounding the trophoectoderm of the embryo [5].
  • These findings suggest that although the TM-DAF gene is irrelevant on mouse blood cells, the two DAF genes may have different roles in germ cell development and/or mature sperm function [5].
  • In this study, we transfected cDNA of mouse GPI-DAF or TM-DAF into Chinese hamster ovary (CHO) cells [6].
  • The findings argue that local alternative pathway activation and surface Daf protein function respectively as a costimulator and a negative modulator of T cell immunity and explain previously reported observations linking complement to T cell function [1].
 

Other interactions of Daf2

  • In mice, both GPI-anchored and transmembrane-anchored DAF proteins are produced, each of which can be derived from two different genes (Daf1 and Daf2) [7].

References

  1. Decay-accelerating factor modulates induction of T cell immunity. Heeger, P.S., Lalli, P.N., Lin, F., Valujskikh, A., Liu, J., Muqim, N., Xu, Y., Medof, M.E. J. Exp. Med. (2005) [Pubmed]
  2. Molecular cloning and chromosomal localization of the mouse decay-accelerating factor genes. Duplicated genes encode glycosylphosphatidylinositol-anchored and transmembrane forms. Spicer, A.P., Seldin, M.F., Gendler, S.J. J. Immunol. (1995) [Pubmed]
  3. Molecular and functional analysis of mouse decay accelerating factor (CD55). Harris, C.L., Rushmere, N.K., Morgan, B.P. Biochem. J. (1999) [Pubmed]
  4. Alternative exon usage in the 3' region of a single gene generates glycosylphosphatidylinositol-anchored and transmembrane forms of rat decay-accelerating factor. Miwa, T., Okada, N., Okada, H. Immunogenetics (2000) [Pubmed]
  5. Characterization of glycosylphosphatidylinositol-anchored decay accelerating factor (GPI-DAF) and transmembrane DAF gene expression in wild-type and GPI-DAF gene knockout mice using polyclonal and monoclonal antibodies with dual or single specificity. Miwa, T., Sun, X., Ohta, R., Okada, N., Harris, C.L., Morgan, B.P., Song, W.C. Immunology (2001) [Pubmed]
  6. Characterization of mouse DAF on transfectant cells using monoclonal antibodies which recognize different epitopes. Ohta, R., Imai, M., Fukuoka, Y., Miwa, T., Okada, N., Okada, H. Microbiol. Immunol. (1999) [Pubmed]
  7. Tissue distribution of products of the mouse decay-accelerating factor (DAF) genes. Exploitation of a Daf1 knock-out mouse and site-specific monoclonal antibodies. Lin, F., Fukuoka, Y., Spicer, A., Ohta, R., Okada, N., Harris, C.L., Emancipator, S.N., Medof, M.E. Immunology (2001) [Pubmed]
 
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