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Gene Review

SLURP1  -  secreted LY6/PLAUR domain containing 1

Homo sapiens

Synonyms: ANUP, ARS, ARS component B, ARS(component B)-81/S, Anti-neoplastic urinary protein, ...
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Disease relevance of SLURP1

  • Mutations in the SLURP1 gene are the cause of Mal de Meleda (MDM), a rare autosomal recessive genetic disease, characterized by inflammatory palmoplantar keratoderma [1].
  • Conditions that typically occur late in the course of AIDS such as Mycobacterium avium infection and cytomegalovirus disease, were more frequently recorded by ASD than by ARS [2].
  • PATIENTS AND METHODS: Sera from patients with polymyositis and sera found to contain anticytoplasmic antibodies were screened for antibody to PL-12 by testing for inhibition of ARS enzymatic activity by serum, and by immunoprecipitation [3].
  • BACKGROUND: Tibial muscular dystrophy (TMD), a late-onset dominant distal myopathy, is caused by yet unknown mutations on chromosome 2q, whereas MD with myositis (MDM) is a muscular dystrophy of the mouse, also progressing with age and linked to mouse chromosome 2 [4].
  • Comparison of the histologic and clinical prognostic indicators of mortality in patients who have malignant melanoma with the clinical and pathologic features seen in this series of 21 patients would appear to indicate a diminished tendency toward metastatic or recurrent disease in patients with MDM and BM [5].

Psychiatry related information on SLURP1


High impact information on SLURP1

  • The arsenic resistance efflux system transports arsenite, using alternatively either a two-component (ArsA and ArsB) ATPase or a single polypeptide (ArsB) functioning as a chemiosmotic transporter [7].
  • In vitro experiments revealed that ArsB and ArsC, sharing 71% amino acid sequence identity, were an alkylresorcinol synthase and an alkylpyrone synthase, respectively, indicating that ArsB and ArsC are not isozymes but enzymatically distinct polyketide synthases [8].
  • The ars operon consisted of four genes, two of which encoded a type III polyketide synthase, ArsB and ArsC [8].
  • It has been shown recently that amino acid substitution at the antigen recognition site (ARS) is more rapid than synonymous substitution, suggesting some kind of positive natural selection working at the ARS [9].
  • These results identify SLURP-1 as a secreted epidermal neuromodulator which is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing [10].

Chemical compound and disease context of SLURP1

  • METHODS: Patients with a history of immediate allergic reactions to penicillins were studied with: skin tests with major and minor determinants of benzylpenicillin (BPO/MDM), amoxicillin, and ampicillin; in vitro determination of specific IgE; and controlled administration for those with a positive history but negative skin and in vitro tests [11].
  • Sixteen Pseudomonas aeruginosa strains, including patent strain NRRL B-18602, three recent isolates from composted materials amended with ricinoleic acid, and 12 randomly selected from the holdings of the ARS Culture Collection, were examined for their fatty acid converting abilities [12].

Biological context of SLURP1

  • Transfected human embryonic kidney 293T cells expressed the MDM mutant SLURP1 containing the single amino-acid substitution G86R but did not tolerate the MDM mutation W15R located in the signal peptide [1].
  • We report the refinement of our previously described interval of MDM on chromosome 8qter, and the identification of mutations in affected individuals in the ARS (component B) gene, encoding a protein named SLURP-1, for secreted Ly-6/uPAR related protein 1 [13].
  • Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda [10].
  • SLURP-1 belongs to the Ly-6/uPAR superfamily of receptor and secreted proteins, which participate in signal transduction, immune cell activation or cellular adhesion [10].
  • Thus, the changes in the cell state induced by SLURP-1 could result from nAChR-mediated effects on the KC gene expression [14].

Anatomical context of SLURP1


Associations of SLURP1 with chemical compounds

  • We found that SLURP-1 potentiates the human alpha 7 nicotinic acetylcholine receptors that are present in keratinocytes [10].
  • In the presence of the agonist carbachol, the effects of SLURP-1 on gene expression were augmented, which is in keeping with the notion that SLURP-1 acts as an allosteric agonist at the KC nAChR [14].
  • Since the SLURP-1 gene maps to the same chromosomal region as several members of the Ly-6/uPAR subfamily of glycoprotein receptors, it is suggested that both biologically distinct subfamilies might have co-evolved from local chromosomal duplication events [19].
  • ArsA is the catalytic subunit of the arsenical pump, coupling ATP hydrolysis to the efflux of arsenicals through the ArsB membrane protein [20].
  • METHODS: After initial treatment of reflux oesophagitis with omeprazole to control symptoms and to heal oesophagitis, 154 patients were randomised to continue treatment with omeprazole (20 or 40 mg daily) and 144 patients to have an open antireflux operation (ARS) [21].

Other interactions of SLURP1

  • A recurrent mutation in the ARS (component B) gene encoding SLURP-1 in Turkish families with mal de Meleda: evidence of a founder effect [22].
  • The high degree of structural similarity between SLURP-1 and the three fingers motif of snake neurotoxins and Lynx1 suggests that this protein interacts with the neuronal acetylcholine receptors [10].

Analytical, diagnostic and therapeutic context of SLURP1


  1. SLURP1 is a late marker of epidermal differentiation and is absent in Mal de Meleda. Favre, B., Plantard, L., Aeschbach, L., Brakch, N., Christen-Zaech, S., de Viragh, P.A., Sergeant, A., Huber, M., Hohl, D. J. Invest. Dermatol. (2007) [Pubmed]
  2. Surveillance of AIDS-defining conditions in the United States. Adult/Adolescent Spectrum of HIV Disease Project Group. Jones, J.L., Hanson, D.L., Chu, S.Y., Fleming, P.L., Hu, D.J., Ward, J.W. AIDS (1994) [Pubmed]
  3. Clinical manifestations in patients with antibody to PL-12 antigen (alanyl-tRNA synthetase). Targoff, I.N., Arnett, F.C. Am. J. Med. (1990) [Pubmed]
  4. Secondary calpain3 deficiency in 2q-linked muscular dystrophy: titin is the candidate gene. Haravuori, H., Vihola, A., Straub, V., Auranen, M., Richard, I., Marchand, S., Voit, T., Labeit, S., Somer, H., Peltonen, L., Beckmann, J.S., Udd, B. Neurology (2001) [Pubmed]
  5. The spectrum of minimal deviation melanoma: a clinicopathologic study of 21 cases. Phillips, M.E., Margolis, R.J., Merot, Y., Sober, A.J., Reed, R.J., Muhlbauer, J.E., Mihm, M.C. Hum. Pathol. (1986) [Pubmed]
  6. The SCS/ARS/CES pesticide properties database for environmental decision-making. Wauchope, R.D., Buttler, T.M., Hornsby, A.G., Augustijn-Beckers, P.W., Burt, J.P. Reviews of environmental contamination and toxicology. (1992) [Pubmed]
  7. Bacterial heavy metal resistance: new surprises. Silver, S., Phung, L.T. Annu. Rev. Microbiol. (1996) [Pubmed]
  8. Phenolic lipid synthesis by type III polyketide synthases is essential for cyst formation in Azotobacter vinelandii. Funa, N., Ozawa, H., Hirata, A., Horinouchi, S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  9. Role of diversifying selection and gene conversion in evolution of major histocompatibility complex loci. Ohta, T. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  10. Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda. Chimienti, F., Hogg, R.C., Plantard, L., Lehmann, C., Brakch, N., Fischer, J., Huber, M., Bertrand, D., Hohl, D. Hum. Mol. Genet. (2003) [Pubmed]
  11. Diagnostic evaluation of a large group of patients with immediate allergy to penicillins: the role of skin testing. Torres, M.J., Romano, A., Mayorga, C., Moya, M.C., Guzman, A.E., Reche, M., Juarez, C., Blanca, M. Allergy (2001) [Pubmed]
  12. Diversity of oleic acid, ricinoleic acid and linoleic acid conversions among Pseudomonas aeruginosa strains. Kuo, T.M., Nakamura, L.K. Curr. Microbiol. (2004) [Pubmed]
  13. Mutations in the gene encoding SLURP-1 in Mal de Meleda. Fischer, J., Bouadjar, B., Heilig, R., Huber, M., Lefèvre, C., Jobard, F., Macari, F., Bakija-Konsuo, A., Ait-Belkacem, F., Weissenbach, J., Lathrop, M., Hohl, D., Prud'homme, J.F. Hum. Mol. Genet. (2001) [Pubmed]
  14. Biological effects of SLURP-1 on human keratinocytes. Arredondo, J., Chernyavsky, A.I., Webber, R.J., Grando, S.A. J. Invest. Dermatol. (2005) [Pubmed]
  15. ARS Component B: structural characterization, tissue expression and regulation of the gene and protein (SLURP-1) associated with Mal de Meleda. Mastrangeli, R., Donini, S., Kelton, C.A., He, C., Bressan, A., Milazzo, F., Ciolli, V., Borrelli, F., Martelli, F., Biffoni, M., Serlupi-Crescenzi, O., Serani, S., Micangeli, E., El Tayar, N., Vaccaro, R., Renda, T., Lisciani, R., Rossi, M., Papoian, R. European journal of dermatology : EJD. (2003) [Pubmed]
  16. Novel mutations in the gene encoding secreted lymphocyte antigen-6/urokinase-type plasminogen activator receptor-related protein-1 (SLURP-1) and description of five ancestral haplotypes in patients with Mal de Meleda. Marrakchi, S., Audebert, S., Bouadjar, B., Has, C., Lefèvre, C., Munro, C., Cure, S., Jobard, F., Morlot, S., Hohl, D., Prud'homme, J.F., Zahaf, A., Turki, H., Fischer, J. J. Invest. Dermatol. (2003) [Pubmed]
  17. Partial N-terminal amino acid sequence of the anti-neoplastic urinary protein (ANUP) and the anti-tumour effect of the N-terminal nonapeptide of the unique cytokine present in human granulocytes. Ridge, R.J., Sloane, N.H. Cytokine (1996) [Pubmed]
  18. Antineoplastic urinary protein inhibits Kaposi's sarcoma and angiogenesis in vitro and in vivo. Masood, R., McGarvey, M.E., Zheng, T., Cai, J., Arora, N., Smith, D.L., Sloane, N., Gill, P.S. Blood (1999) [Pubmed]
  19. Structural and phylogenetic characterization of human SLURP-1, the first secreted mammalian member of the Ly-6/uPAR protein superfamily. Adermann, K., Wattler, F., Wattler, S., Heine, G., Meyer, M., Forssmann, W.G., Nehls, M. Protein Sci. (1999) [Pubmed]
  20. A kinetic model for the action of a resistance efflux pump. Walmsley, A.R., Zhou, T., Borges-Walmsley, M.I., Rosen, B.P. J. Biol. Chem. (2001) [Pubmed]
  21. The cost of long term therapy for gastro-oesophageal reflux disease: a randomised trial comparing omeprazole and open antireflux surgery. Myrvold, H.E., Lundell, L., Miettinen, P., Pedersen, S.A., Liedman, B., Hatlebakk, J., Julkunen, R., Levander, K., Lamm, M., Mattson, C., Carlsson, J., Ståhlhammar, N.O. Gut (2001) [Pubmed]
  22. A recurrent mutation in the ARS (component B) gene encoding SLURP-1 in Turkish families with mal de Meleda: evidence of a founder effect. Hu, G., Yildirim, M., Baysal, V., Yerebakan, O., Yilmaz, E., Inaloz, H.S., Martinez-Mir, A., Christiano, A.M., Celebi, J.T. J. Invest. Dermatol. (2003) [Pubmed]
  23. Natural evolution of skin test sensitivity in patients allergic to beta-lactam antibiotics. Blanca, M., Torres, M.J., García, J.J., Romano, A., Mayorga, C., de Ramon, E., Vega, J.M., Miranda, A., Juarez, C. J. Allergy Clin. Immunol. (1999) [Pubmed]
  24. Anaphylaxis to penicillins after non-therapeutic exposure: an immunological investigation. Blanca, M., Garcia, J., Vega, J.M., Miranda, A., Carmona, M.J., Mayorga, C., Moreno, F., Juarez, C. Clin. Exp. Allergy (1996) [Pubmed]
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