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Gene Review

TMEM158  -  transmembrane protein 158 (gene/pseudogene)

Homo sapiens

Synonyms: 40 kDa BINP-binding protein, BBP, HBBP, RIS1, Ras-induced senescence protein 1, ...
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Disease relevance of TMEM158

  • Finally, RIS1 seemed to be functionally involved in tumor development, as low-frequency MSI tumors (MSI-L) with RIS1 mutated usually were associated with a worse prognosis: 83% of them developed metastasis, and no patient with MSI-L tumor and RIS1 mutated (35.3% of MSI-L) survived >25 months after surgery (log rank P < 0.001) [1].
  • The polypeptide sequence derived from the partial RIS-1 cDNA was found to be identical to the calcium binding domain found in 'psoriasin', a gene whose expression appears to be increased in the skin of psoriasis patients [2].

High impact information on TMEM158


Biological context of TMEM158


Anatomical context of TMEM158

  • We have developed a monoclonal antibody named mAb 6A22 against the 40-kDa BINP-binding protein, p40BBP. mAb 6A22 inhibits binding between BINP and rat brain synaptosomes and abolishes the protective effect of BINP [10].

Associations of TMEM158 with chemical compounds


Other interactions of TMEM158

  • Moreover, mutations in RIS1 in MSI-H tumors correlated with the epigenetic silencing of MLH1 (P = 0.04) [1].
  • We have also previously identified a skin-specific gene (RIS-1/psoriasin) which is rapidly induced in human skin treated with RA [12].

Analytical, diagnostic and therapeutic context of TMEM158

  • HPLC analysis of the RA content of 0.1% RA-treated skin in vivo revealed significant levels at 6 h (18.8-120.6 ng RA/g wet weight tissue; approximately 240 nM), immediately preceding the time point at which the increased RIS-1 mRNA level was first seen [2].
  • A retinoic acid-inducible skin-specific gene (RIS-1/psoriasin): molecular cloning and analysis of gene expression in human skin in vivo and cultured skin cells in vitro [2].


  1. RIS1, a gene with trinucleotide repeats, is a target in the mutator pathway of colorectal carcinogenesis. Iglesias, D., Fernández-Peralta, A.M., Nejda, N., Daimiel, L., Azcoita, M.M., Oliart, S., González-Aguilera, J.J. Cancer Genet. Cytogenet. (2006) [Pubmed]
  2. A retinoic acid-inducible skin-specific gene (RIS-1/psoriasin): molecular cloning and analysis of gene expression in human skin in vivo and cultured skin cells in vitro. Tavakkol, A., Zouboulis, C.C., Duell, E.A., Voorhees, J.J. Mol. Biol. Rep. (1994) [Pubmed]
  3. Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis. Sharpless, N.E., Bardeesy, N., Lee, K.H., Carrasco, D., Castrillon, D.H., Aguirre, A.J., Wu, E.A., Horner, J.W., DePinho, R.A. Nature (2001) [Pubmed]
  4. A functional screen identifies hDRIL1 as an oncogene that rescues RAS-induced senescence. Peeper, D.S., Shvarts, A., Brummelkamp, T., Douma, S., Koh, E.Y., Daley, G.Q., Bernards, R. Nat. Cell Biol. (2002) [Pubmed]
  5. INK4a-deficient human diploid fibroblasts are resistant to RAS-induced senescence. Brookes, S., Rowe, J., Ruas, M., Llanos, S., Clark, P.A., Lomax, M., James, M.C., Vatcheva, R., Bates, S., Vousden, K.H., Parry, D., Gruis, N., Smit, N., Bergman, W., Peters, G. EMBO J. (2002) [Pubmed]
  6. Sequential activation of the MEK-extracellular signal-regulated kinase and MKK3/6-p38 mitogen-activated protein kinase pathways mediates oncogenic ras-induced premature senescence. Wang, W., Chen, J.X., Liao, R., Deng, Q., Zhou, J.J., Huang, S., Sun, P. Mol. Cell. Biol. (2002) [Pubmed]
  7. Stepwise neoplastic transformation of a telomerase immortalized fibroblast cell line. Zongaro, S., de Stanchina, E., Colombo, T., D'Incalci, M., Giulotto, E., Mondello, C. Cancer Res. (2005) [Pubmed]
  8. Identification of a candidate tumor-suppressor gene specifically activated during Ras-induced senescence. Barradas, M., Gonos, E.S., Zebedee, Z., Kolettas, E., Petropoulou, C., Delgado, M.D., León, J., Hara, E., Serrano, M. Exp. Cell Res. (2002) [Pubmed]
  9. Specific interaction of PML bodies with the TP53 locus in Jurkat interphase nuclei. Sun, Y., Durrin, L.K., Krontiris, T.G. Genomics (2003) [Pubmed]
  10. Identification and molecular cloning of a novel brain-specific receptor protein that binds to brain injury-derived neurotrophic peptide. Possible role for neuronal survival. Hama, T., Maruyama, M., Katoh-Semba, R., Takizawa, M., Iwashima, M., Nara, K. J. Biol. Chem. (2001) [Pubmed]
  11. Target genes of the WNT/beta-catenin pathway in Wilms tumors. Zirn, B., Samans, B., Wittmann, S., Pietsch, T., Leuschner, I., Graf, N., Gessler, M. Genes Chromosomes Cancer (2006) [Pubmed]
  12. Topical all-trans retinoic acid (RA) induces an early, coordinated increase in RA-inducible skin-specific gene/psoriasin and cellular RA-binding protein II mRNA levels which precedes skin erythema. Zouboulis, C.C., Voorhees, J.J., Orfanos, C.E., Tavakkol, A. Arch. Dermatol. Res. (1996) [Pubmed]
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