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Gene Review

SEC1  -  alpha(1,2) fucosyltransferase pseudogene

Homo sapiens

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Disease relevance of SEC1

  • We have identified a human adenocarcinoma cell line, SW480, that assists in the activation of human T cells by the staphylococcal enterotoxins B (SEB), C1 (SEC1), and D (SED), but not SEA, SEC2, SEC3, or SEE [1].
  • Lymph node metastasis was not observed in the SEC1 patients but was observed in 19% of the SEC2 patients and 41% of the SEC3 patients [2].
  • We investigated the relationship between the class II binding affinities of four of these exotoxins, SEA, SEB, SEC1, and toxic shock syndrome toxin-1 and their T cell signaling capabilities [3].
  • Since no correlation was observed between the behaviour of these mutants with regard to toxin stability, emesis and T cell proliferation we conclude that SEC1-induced emesis and T cell proliferation are dependent on separate regions of the molecule [4].
  • In this study, we investigated the peripheral blood mononuclear cell (PBMC) response of patients with psoriasis vulgaris to staphylococcal superantigens (staphylococcal enterotoxin A (SEA), SEB, and SEC1) and its relationship to clinical and laboratory findings [5].

High impact information on SEC1

  • The much weaker binding to SEB than to SEC1, 2, or 3 was surprising, especially since SEB was found to actually be 3- to 10-fold more effective, on a molar basis, than the other toxins in stimulating the parental T cell hybridoma [6].
  • Sec1/Munc18 proteins: mediators of membrane fusion moving to center stage [7].
  • The amino terminus of the purified streptococcal superantigen was more homologous to the amino termini of staphylococcal enterotoxins B, C1, and C3 (SEB, SEC1, and SEC3), than to those of pyrogenic exotoxins A, B, C or other streptococcal toxins [8].
  • Mutations affecting VPS33B, a novel Sec1/Munc18 protein, have recently been linked to arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome [9].
  • Requirement of VPS33B, a member of the Sec1/Munc18 protein family, in megakaryocyte and platelet alpha-granule biogenesis [9].

Biological context of SEC1

  • Based on the activity of SEC1 mutants containing single amino acid substitutions, we concluded that the differential abilities of these native toxins to stimulate V beta 3 and V beta 13.1 was determined by the residue in position 26, located in the base of the SEC alpha 3 cavity [10].
  • One of these, termed Sec1, is a pseudogene, because translational frameshifts and termination codons interrupt potential open reading frames that would otherwise share primary sequence similarity with the H alpha(1,2)fucosyltransferase [11].
  • However, mutants with residues deleted between positions 19 and 33, although nonmitogenic themselves, were able to inhibit both SEC1-induced T-cell proliferation and binding of the native toxin to major histocompatibility complex (MHC) class II [12].
  • Here we report results of a sequence homology analysis of LRPPRC and its SEC1 domain interactive partners [13].
  • Sequence analysis of LRPPRC and its SEC1 domain interaction partners suggests roles in cytoskeletal organization, vesicular trafficking, nucleocytosolic shuttling, and chromosome activity [13].

Anatomical context of SEC1

  • These residues mapped to the putative TCR binding domain of SEC1, and suggest that subtle differences in TCR binding affinity or the topology of the SEC1-TCR interaction can compensate for the lack of MHC class II and hence promote T cell proliferation [14].
  • In contrast, SEC1 and FUT1 do not show prominently regulated expression in uterus [15].
  • Blood and lung lymphocytes were also assessed for their responsiveness to different superantigenic stimuli represented by staphylococcal enterotoxins (SEA, SEB, SEC1, SEC2, SED and SEE) [16].
  • The p-T1 tumors were subdivided into three categories: carcinoma limited to the lamina propria mucosae (19 patients, SEC1), carcinoma invading the lamina muscularis mucosae or with invasion just into the submucosa (27 patients, SEC2), and carcinoma definitely invading the submucosa (44 patients, SEC3) [2].
  • We have examined the expression of the secretor-type alpha(1,2)fucosyltransferase gene (FUT2) and a pseudogene of FUT2 (Sec1) in several tumor cell lines by northern blot and/or reverse-transcription-PCR (RT-PCR) analyses [17].

Associations of SEC1 with chemical compounds

  • For SEC, in addition to the three major SEC subtypes, i.e., SEC1, C2 and C3, other molecular variants may exist [18].
  • Phylogenetic analysis of the available H, Se, and Sec1 mammalian protein sequences demonstrates the existence of three clusters which correspond to the three genes [19].
  • The amino terminus exhibits multiple copies of leucine-rich nuclear transport signals followed by ENTH, DUF28, and SEC1 homology domains [13].
  • Here, we developed a real-time fluorescence PCR assay (TaqMan PCR) for the detection of genes encoding staphylococcal enterotoxins A, B, C1, and D (SEA, SEB, SEC1, and SED) of S. aureus as well as the mecA gene encoding methicillin resistance and the femB gene as a specific genomic marker for S. aureus [20].
  • The 314th-316th nucleotides of the Sec1 gene were CCC, which were different from the nucleotides GGG reported previously by Kelly et al [21].

Other interactions of SEC1

  • The phylogenetic analysis also suggests that Sec1 has a higher evolutionary rate than FUT2 and FUT1 [19].
  • Other superantigens (SEA, SEC1, SEC2) but not mite antigen (Dermatophagoides) also induced ICAM-1 expression both at protein and mRNA level [22].
  • Socio-economic inequalities remain: the death rate from all external causes for children of parents classified as never having worked or as long-term unemployed (NS-SEC 8) was 13.1 (10.3-16.5) times that for children in NS-SEC 1 (higher managerial/professional occupations) [23].

Analytical, diagnostic and therapeutic context of SEC1

  • In this study, four polymerase chain reaction (PCR) primers used in pairs (ENTC1/ENTCR, ENTC2/ENTCR and ENTC3/ENTCR) for the specific detection of SEC1, C2 and C3 genes of S. aureus strains were developed [18].
  • On the other hand, RT-PCR indicated that Sec1 was expressed in all these tumor cells, including all hematopoietic cells studied [17].
  • In the ELISA for SEB, cross-reactive antibodies to SEC were removed by absorption in a biotin-streptavidin-agarose column (SEC1 at concentrations to 100,000 ng/mL could not be detected) [24].
  • To address the role of antibodies in protection against BSAgs, we screened the sera of 29 human volunteers for antibodies to the SAgs staphylococcal enterotoxin A (SEA), SEB, SEC1, and toxic shock syndrome toxin 1 (TSST-1) [25].
  • RESULTS: Thirty-eight per cent of the AD patients showed a selective deficiency in IgG2 antibodies against SEC1 compared with only 14% in the control group [26].


  1. Intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 provide costimulation for superantigen-induced T lymphocyte proliferation in the absence of a specific presenting molecule. Lamphear, J.G., Stevens, K.R., Rich, R.R. J. Immunol. (1998) [Pubmed]
  2. Detection of lymph node metastasis using desmoglein 1 expression in superficial esophageal cancer in relation to the endoscopic mucosal resection. Nakano, S., Baba, M., Natsugoe, S., Kijima, F., Nakashima, S., Shimada, M., Shirao, K., Kusano, C., Yoshinaka, H., Fukumoto, T., Aikou, T. Dis. Esophagus (1998) [Pubmed]
  3. Staphylococcal exotoxin activation of T cells. Role of exotoxin-MHC class II binding affinity and class II isotype. Mollick, J.A., Chintagumpala, M., Cook, R.G., Rich, R.R. J. Immunol. (1991) [Pubmed]
  4. Investigation of the role of the disulphide bond in the activity and structure of staphylococcal enterotoxin C1. Hovde, C.J., Marr, J.C., Hoffmann, M.L., Hackett, S.P., Chi, Y.I., Crum, K.K., Stevens, D.L., Stauffacher, C.V., Bohach, G.A. Mol. Microbiol. (1994) [Pubmed]
  5. Clinical analysis of staphylococcal superantigen hyper-reactive patients with psoriasis vulgaris. Yamamoto, T., Katayama, I., Nishioka, K. European journal of dermatology : EJD. (1998) [Pubmed]
  6. Superantigen binding to a T cell receptor beta chain of known three-dimensional structure. Malchiodi, E.L., Eisenstein, E., Fields, B.A., Ohlendorf, D.H., Schlievert, P.M., Karjalainen, K., Mariuzza, R.A. J. Exp. Med. (1995) [Pubmed]
  7. Sec1/Munc18 proteins: mediators of membrane fusion moving to center stage. Jahn, R. Neuron (2000) [Pubmed]
  8. A novel superantigen isolated from pathogenic strains of Streptococcus pyogenes with aminoterminal homology to staphylococcal enterotoxins B and C. Mollick, J.A., Miller, G.G., Musser, J.M., Cook, R.G., Grossman, D., Rich, R.R. J. Clin. Invest. (1993) [Pubmed]
  9. Requirement of VPS33B, a member of the Sec1/Munc18 protein family, in megakaryocyte and platelet alpha-granule biogenesis. Lo, B., Li, L., Gissen, P., Christensen, H., McKiernan, P.J., Ye, C., Abdelhaleem, M., Hayes, J.A., Williams, M.D., Chitayat, D., Kahr, W.H. Blood (2005) [Pubmed]
  10. Subtype-specific interactions of type C staphylococcal enterotoxins with the T-cell receptor. Deringer, J.R., Ely, R.J., Stauffacher, C.V., Bohach, G.A. Mol. Microbiol. (1996) [Pubmed]
  11. Sequence and expression of a candidate for the human Secretor blood group alpha(1,2)fucosyltransferase gene (FUT2). Homozygosity for an enzyme-inactivating nonsense mutation commonly correlates with the non-secretor phenotype. Kelly, R.J., Rouquier, S., Giorgi, D., Lennon, G.G., Lowe, J.B. J. Biol. Chem. (1995) [Pubmed]
  12. Predictions of T-cell receptor- and major histocompatibility complex-binding sites on staphylococcal enterotoxin C1. Hoffmann, M.L., Jablonski, L.M., Crum, K.K., Hackett, S.P., Chi, Y.I., Stauffacher, C.V., Stevens, D.L., Bohach, G.A. Infect. Immun. (1994) [Pubmed]
  13. Sequence analysis of LRPPRC and its SEC1 domain interaction partners suggests roles in cytoskeletal organization, vesicular trafficking, nucleocytosolic shuttling, and chromosome activity. Liu, L., McKeehan, W.L. Genomics (2002) [Pubmed]
  14. Structural dichotomy of staphylococcal enterotoxin C superantigens leading to MHC class II-independent activation of T lymphocytes. Lamphear, J.G., Bohach, G.A., Rich, R.R. J. Immunol. (1998) [Pubmed]
  15. Molecular cloning, genomic mapping, and expression of two secretor blood group alpha (1,2)fucosyltransferase genes differentially regulated in mouse uterine epithelium and gastrointestinal tract. Domino, S.E., Zhang, L., Lowe, J.B. J. Biol. Chem. (2001) [Pubmed]
  16. Skewing of the T-cell receptor repertoire in the lung of patients with HIV-1 infection. Trentin, L., Zambello, R., Facco, M., Sancetta, R., Cerutti, A., Milani, A., Tassinari, C., Crivellaro, C., Cipriani, A., Agostini, C., Semenzato, G. AIDS (1996) [Pubmed]
  17. Structure and expression of the gene encoding secretor-type galactoside 2-alpha-L-fucosyltransferase (FUT2). Koda, Y., Soejima, M., Wang, B., Kimura, H. Eur. J. Biochem. (1997) [Pubmed]
  18. Development and use of PCR primers for the investigation of C1, C2 and C3 enterotoxin types of Staphylococcus aureus strains isolated from food-borne outbreaks. Chen, T.R., Hsiao, M.H., Chiou, C.S., Tsen, H.Y. Int. J. Food Microbiol. (2001) [Pubmed]
  19. Evolution of alpha 2-fucosyltransferase genes in primates: relation between an intronic Alu-Y element and red cell expression of ABH antigens. Apoil, P.A., Roubinet, F., Despiau, S., Mollicone, R., Oriol, R., Blancher, A. Mol. Biol. Evol. (2000) [Pubmed]
  20. Detection of Staphylococcus aureus enterotoxins A to D by real-time fluorescence PCR assay. Klotz, M., Opper, S., Heeg, K., Zimmermann, S. J. Clin. Microbiol. (2003) [Pubmed]
  21. Se genotyping following allele-specific polymerase chain reaction amplification. Mitani, T., Tsujita, H., Sonoda, S., Akane, A. Legal medicine (Tokyo, Japan) (2002) [Pubmed]
  22. Superantigen-induced cytokine expression in organ-cultured human skin. Matsunaga, T., Katayama, I., Yokozeki, H., Nishioka, K. J. Dermatol. Sci. (1996) [Pubmed]
  23. Deaths from injury in children and employment status in family: analysis of trends in class specific death rates. Reading, R. Child: care, health and development. (2006) [Pubmed]
  24. Detection of staphylococcal enterotoxin B among toxic shock syndrome (TSS)- and non-TSS-associated Staphylococcus aureus isolates. Lee, V.T., Chang, A.H., Chow, A.W. J. Infect. Dis. (1992) [Pubmed]
  25. Human antibodies to bacterial superantigens and their ability to inhibit T-cell activation and lethality. LeClaire, R.D., Bavari, S. Antimicrob. Agents Chemother. (2001) [Pubmed]
  26. Deficiency in immunoglobulin G2 antibodies against staphylococcal enterotoxin C1 defines a subgroup of patients with atopic dermatitis. Mrabet-Dahbi, S., Breuer, K., Klotz, M., Herz, U., Heeg, K., Werfel, T., Renz, H. Clin. Exp. Allergy (2005) [Pubmed]
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