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Gene Review

CRNN  -  cornulin

Homo sapiens

Synonyms: 53 kDa squamous epithelial-induced stress protein, 58 kDa heat shock protein, C1orf10, Cornulin, DRC1, ...
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Disease relevance of CRNN

  • These findings suggest that expression of C1orf10 is unique to esophageal cells and that loss of its expression may play a role in the development of esophageal cancer [1].
  • In this study, to determine whether the loss of C1orf10 gene function could contribute to the development of oral squamous cell carcinoma (OSCC), we have evaluated the expression status of this gene by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and quantitative real-time PCR analysis [2].
  • The patients with laryngeal cancer had significantly lower levels of Sep70, Sep53 (p < .01), and Hsp70 (p < .05) than the normal control subjects [3].
  • CRNN was found to be differentially expressed in ESCC tumors as compared to normal esophageal epithelia in a quantitative proteomic analysis of ESCC tissue [4].
  • CRNN is a potential tumor suppressor in ESCC via arresting cell cycle progression at G1/S checkpoint by upregulating P21WAF1/CIP1 and Rb [5].

High impact information on CRNN


Biological context of CRNN

  • Using a radiation hybrid panel, C1orf10 was found to be located on chromosome 1q21 [1].
  • The amino acid sequence of C1orf10 is characterized by the presence of a calcium-binding motif of about 90 amino acids at its N-terminal and a conserved consecutive repeat sequence of 60 amino acids that was identified previously only in bacterial ice nucleation proteins [1].
  • The C1orf10 gene, which spans 5 kb in length, is composed of three exons [1].
  • Two of the three heat shock proteins were identified by mass spectrometric sequencing to be the calcium-calmodulin homologue transglutaminase-3 (78 kDa) and a recently cloned oesophageal-specific gene called C1orf10, which encodes a 53-kDa putative calcium binding protein we have named squamous epithelial heat shock protein 53 (SEP53) [6].
  • Clonogenic assays were used to show that SEP53 can function as a survival factor in mammalian cell lines, can attenuate DCA-induced apoptotic cell death, and can attenuate DCA-mediated increases in intracellular free calcium [7].

Anatomical context of CRNN

  • In normal adult tissues, C1orf10 is highly expressed only in the esophagus and was undetectable in a total of 15 other tissues examined, suggesting its important role in esophageal cells [1].
  • The expression of C1orf10 is either dramatically reduced or absent in esophageal cancer cell lines (3/3) as well as primary esophageal cancer tissues (35/37) compared with the corresponding normal esophageal mucosa [1].
  • Given the role of deoxycholic acid (DCA) as a potential damaging agent in squamous epithelium, we developed assays measuring the effects of DCA on SEP53-mediated responses to damage [7].
  • Oesophageal squamous epithelial cells have evolved an atypical stress response that results in the synthesis of a 53 kDa protein of undefined function named squamous epithelial-induced stress protein of 53 kDa (SEP53) [7].
  • Expression of CRNN is localized to the differentiated layers (functional and prickle layers) in normal esophageal epithelia. More specifically its sub-cellular localization is cytoplasmic and peri-nuclear in epithelial cells. Expression of CRNN is not detectable in majority of Grade II and III ESCC tumors. However, expression of CRNN is seen in keratinized foci referred to as keratin pearls in well differentiated ESCC tumors (Grade I) [8].

Associations of CRNN with chemical compounds

  • The calcium-binding domain of the stress protein SEP53 is required for survival in response to deoxycholic acid-mediated injury [7].

Other interactions of CRNN

  • Deletion of the highly conserved EF-hand calcium-binding domain in SEP53 neutralizes the colony survival activity of the protein, neutralizes the protective effects of SEP53 after DCA exposure, and permits calcium elevation in response to DCA challenge [7].

Analytical, diagnostic and therapeutic context of CRNN

  • We have identified a novel human gene, designated C1orf10, using modified differential display PCR [1].
  • Using the organ culture model, we demonstrated that laryngeal Sep70 and Sep53 proteins are induced after exposure to low pH [3].


  1. Novel human esophagus-specific gene c1orf10: cDNA cloning, gene structure, and frequent loss of expression in esophageal cancer. Xu, Z., Wang, M.R., Xu, X., Cai, Y., Han, Y.L., Wu, K.M., Wang, J., Chen, B.S., Wang, X.Q., Wu, M. Genomics (2000) [Pubmed]
  2. Chromosome 1 open reading frame 10 (C1orf10) gene is frequently down-regulated and inhibits cell proliferation in oral squamous cell carcinoma. Imai, F.L., Uzawa, K., Nimura, Y., Moriya, T., Imai, M.A., Shiiba, M., Bukawa, H., Yokoe, H., Tanzawa, H. Int. J. Biochem. Cell Biol. (2005) [Pubmed]
  3. Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: role in laryngopharyngeal reflux disease. Johnston, N., Dettmar, P.W., Lively, M.O., Postma, G.N., Belafsky, P.C., Birchall, M., Koufman, J.A. The Annals of otology, rhinology, and laryngology. (2006) [Pubmed]
  4. Quantitative tissue proteomics of esophageal squamous cell carcinoma for novel biomarker discovery. Pawar, H., Kashyap, M.K., Sahasrabuddhe, N.A., Renuse, S., Harsha, H.C., Kumar, P., Sharma, J., Kandasamy, K., Marimuthu, A., Nair, B., Rajagopalan, S., Maharudraiah, J., Premalatha, C.S., Kumar, K.V., Vijayakumar, M., Chaerkady, R., Prasad, T.S., Kumar, R.V., Kumar, R.V., Pandey, A. Cancer. Biol. Ther. (2011) [Pubmed]
  5. Characterization of tumor suppressive function of cornulin in esophageal squamous cell carcinoma. Chen, K., Li, Y., Dai, Y., Li, J., Qin, Y., Zhu, Y., Zeng, T., Ban, X., Fu, L., Guan, X.Y. PLoS. One. (2013) [Pubmed]
  6. The human oesophageal squamous epithelium exhibits a novel type of heat shock protein response. Yagui-Beltran, A., Craig, A.L., Lawrie, L., Thompson, D., Pospisilova, S., Johnston, D., Kernohan, N., Hopwood, D., Dillon, J.F., Hupp, T.R. Eur. J. Biochem. (2001) [Pubmed]
  7. The calcium-binding domain of the stress protein SEP53 is required for survival in response to deoxycholic acid-mediated injury. Darragh, J., Hunter, M., Pohler, E., Nelson, L., Dillon, J.F., Nenutil, R., Vojtesek, B., Ross, P.E., Kernohan, N., Hupp, T.R. FEBS J. (2006) [Pubmed]
  8. Downregulation of cornulin in esophageal squamous cell carcinoma. Pawar, H., Maharudraiah, J., Kashyap, M.K., Sharma, J., Srikanth, S.M., Choudhary, R., Chavan, S., Sathe, G., Manju, H.C., Kumar, K.V., Vijayakumar, M., Sirdeshmukh, R., Harsha, H.C., Prasad, T.S., Pandey, A., Kumar, R.V. Acta. Histochem. (2013) [Pubmed]
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