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Gene Review

Lor  -  loricrin

Mus musculus

Synonyms: AI036317, Loricrin, S77319
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Disease relevance of Lor

  • Transgenic mice expressing a mutant form of loricrin reveal the molecular basis of the skin diseases, Vohwinkel syndrome and progressive symmetric erythrokeratoderma [1].
  • Antinociceptive and antiedematogenic properties and acute toxicity of Tabebuia avellanedae Lor. ex Griseb. inner bark aqueous extract [2].
  • Furthermore, in a chemical carcinogen-induced skin carcinogenesis setting, mice overexpressing human IKKalpha in the epidermis under the control of a truncated loricrin promoter developed significantly fewer SCCs and metastases than did wild-type mice [3].
  • Skin targeted loricrin 8S-LOX/C57BL/6J transgenic mice showed a more differentiated epidermal phenotype as well as a 64% reduced papilloma development in a two-stage skin carcinogenesis protocol [4].

High impact information on Lor

  • Identification of a major keratinocyte cell envelope protein, loricrin [5].
  • Analysis of Skn-1a/i gene-deleted mice reveals that the Skn-1a/i gene modulates the pattern of expression of the terminal differentiation marker loricrin and inhibits expression of genes encoding markers of the epidermal keratinocyte wounding response [6].
  • Finally, the skin of transgenic mice expressing a truncated loricrin promoter-driven dominant-negative TGFbeta type II receptor contained normal numbers of LC [7].
  • At least one of the compensatory mechanisms preventing a more severe skin phenotype in newborn Lor(-/-) mice is an increase in the expression of other CE components, such as SPRRP2D and SPRRP2H, members of the family of "small proline rich proteins", and repetin, a member of the "fused gene" subgroup of the S100 gene family [8].
  • A severe phenotype was observed in mice that lacked expression of wild-type loricrin [1].

Biological context of Lor

  • This cell differentiation-specific expression pattern suggests specific suppression of loricrin gene expression in undifferentiated keratinocytes as well as its activation in differentiated keratinocytes [9].
  • Constructs with point mutations in the putative YY1-binding motif showed increased reporter activity, indicating that YY1 negatively regulates loricrin gene transcription [9].
  • In contrast to the dramatic repression of mRNAs typical for spinous cell differentiation, activation of PKC concurrently enhances expression of mRNAs and proteins for the granular cell markers loricrin and filaggrin [10].
  • Transfection experiments indicated that the COOH-terminal domain of the mutant loricrin contains a nuclear localization signal [1].
  • By analyses of RNA and protein, we show that the human transgene is expressed in mouse epithelial tissues in an appropriate developmental manner but at an overall level about twice that of endogenous mouse loricrin [11].

Anatomical context of Lor


Associations of Lor with chemical compounds

  • Concurrently, there was diminished beta-glucocerebrosidase activity at the stratum granulosum-stratum corneum junction and a modest decrease in both involucrin and loricrin protein expression, markers of keratinocyte differentiation [15].
  • Since loricrin is rich in cysteine, L-granules account for the sulfur-rich keratohyalin granules described earlier [16].
  • To define the regulatory elements that mediate the expression of the loricrin gene, we replaced the loricrin coding sequences from a 6.5-kilobase genomic fragment with the chloramphenicol acetyltransferase gene and transfected this construct into cultured mouse keratinocytes [17].
  • The induction of filaggrin and loricrin by CS corresponds to a granular layer differentiation program, where PKC activation occurs and was blocked by the PKC inhibitor GF 109203X [18].
  • Isolation of a GC-rich cDNA identifying mRNA present in human epidermis and modulated by calcium and retinoic acid in cultured keratinocytes. Homology with murine loricrin mRNA [19].

Regulatory relationships of Lor


Other interactions of Lor

  • The basal cells of affected mice ceased to proliferate, and expressed the profilaggrin and loricrin genes which are normally transcribed only in the latest stages of epidermal differentiation [20].
  • These findings suggest that YY1 contributes to specific loricrin gene expression in differentiated keratinocytes by suppression of its transcription in undifferentiated keratinocytes [9].
  • BAPTA also inhibited the expression of K1, K10 and loricrin mRNA [21].
  • Cytokeratin 5 was localized in the lowest cell layer in the epithelial sheet, but cytokeratin 1 and loricrin were localized in the outer cell layers, resembling mouse skin [22].
  • Furthermore, the expression of both mRNA and protein for the calcium inducible keratinocyte differentiation markers, filaggrin and loricrin, were down-regulated in the epidermis of Casr(-/-) mice, whereas the number of proliferating cells were increased even though the calcium gradient within the epidermis was enhanced [23].

Analytical, diagnostic and therapeutic context of Lor


  1. Transgenic mice expressing a mutant form of loricrin reveal the molecular basis of the skin diseases, Vohwinkel syndrome and progressive symmetric erythrokeratoderma. Suga, Y., Jarnik, M., Attar, P.S., Longley, M.A., Bundman, D., Steven, A.C., Koch, P.J., Roop, D.R. J. Cell Biol. (2000) [Pubmed]
  2. Antinociceptive and antiedematogenic properties and acute toxicity of Tabebuia avellanedae Lor. ex Griseb. inner bark aqueous extract. de Miranda, F.G., Vilar, J.C., Alves, I.A., Cavalcanti, S.C., Antoniolli, A.R. BMC Pharmacol. (2001) [Pubmed]
  3. A critical role for I{kappa}B kinase {alpha} in the development of human and mouse squamous cell carcinomas. Liu, B., Park, E., Zhu, F., Bustos, T., Liu, J., Shen, J., Fischer, S.M., Hu, Y. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  4. An antitumorigenic role for murine 8S-lipoxygenase in skin carcinogenesis. Kim, E., Rundhaug, J.E., Benavides, F., Yang, P., Newman, R.A., Fischer, S.M. Oncogene (2005) [Pubmed]
  5. Identification of a major keratinocyte cell envelope protein, loricrin. Mehrel, T., Hohl, D., Rothnagel, J.A., Longley, M.A., Bundman, D., Cheng, C., Lichti, U., Bisher, M.E., Steven, A.C., Steinert, P.M. Cell (1990) [Pubmed]
  6. Functions of the POU domain genes Skn-1a/i and Tst-1/Oct-6/SCIP in epidermal differentiation. Andersen, B., Weinberg, W.C., Rennekampff, O., McEvilly, R.J., Bermingham, J.R., Hooshmand, F., Vasilyev, V., Hansbrough, J.F., Pittelkow, M.R., Yuspa, S.H., Rosenfeld, M.G. Genes Dev. (1997) [Pubmed]
  7. A role for TGFbeta1 in langerhans cell biology. Further characterization of the epidermal Langerhans cell defect in TGFbeta1 null mice. Borkowski, T.A., Letterio, J.J., Mackall, C.L., Saitoh, A., Wang, X.J., Roop, D.R., Gress, R.E., Udey, M.C. J. Clin. Invest. (1997) [Pubmed]
  8. Lessons from loricrin-deficient mice: compensatory mechanisms maintaining skin barrier function in the absence of a major cornified envelope protein. Koch, P.J., de Viragh, P.A., Scharer, E., Bundman, D., Longley, M.A., Bickenbach, J., Kawachi, Y., Suga, Y., Zhou, Z., Huber, M., Hohl, D., Kartasova, T., Jarnik, M., Steven, A.C., Roop, D.R. J. Cell Biol. (2000) [Pubmed]
  9. Yin-yang 1 negatively regulates the differentiation-specific transcription of mouse loricrin gene in undifferentiated keratinocytes. Xu, X., Kawachi, Y., Nakamura, Y., Sakurai, H., Hirota, A., Banno, T., Takahashi, T., Roop, D.R., Otsuka, F. J. Invest. Dermatol. (2004) [Pubmed]
  10. Coordinate changes in gene expression which mark the spinous to granular cell transition in epidermis are regulated by protein kinase C. Dlugosz, A.A., Yuspa, S.H. J. Cell Biol. (1993) [Pubmed]
  11. Overexpression of human loricrin in transgenic mice produces a normal phenotype. Yoneda, K., Steinert, P.M. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  12. Loricrin expression is coordinated with other epidermal proteins and the appearance of lipid lamellar granules in development. Bickenbach, J.R., Greer, J.M., Bundman, D.S., Rothnagel, J.A., Roop, D.R. J. Invest. Dermatol. (1995) [Pubmed]
  13. Characterization of the mouse loricrin gene: linkage with profilaggrin and the flaky tail and soft coat mutant loci on chromosome 3. Rothnagel, J.A., Longley, M.A., Bundman, D.S., Naylor, S.L., Lalley, P.A., Jenkins, N.A., Gilbert, D.J., Copeland, N.G., Roop, D.R. Genomics (1994) [Pubmed]
  14. Spatial distributions of sulfur-rich proteins in cornifying epithelia. Leapman, R.D., Jarnik, M., Steven, A.C. J. Struct. Biol. (1997) [Pubmed]
  15. Role of peroxisome proliferator-activated receptor alpha in epidermal development in utero. Schmuth, M., Schoonjans, K., Yu, Q.C., Fluhr, J.W., Crumrine, D., Hachem, J.P., Lau, P., Auwerx, J., Elias, P.M., Feingold, K.R. J. Invest. Dermatol. (2002) [Pubmed]
  16. Biosynthetic pathways of filaggrin and loricrin--two major proteins expressed by terminally differentiated epidermal keratinocytes. Steven, A.C., Bisher, M.E., Roop, D.R., Steinert, P.M. J. Struct. Biol. (1990) [Pubmed]
  17. The proximal promoter of the mouse loricrin gene contains a functional AP-1 element and directs keratinocyte-specific but not differentiation-specific expression. DiSepio, D., Jones, A., Longley, M.A., Bundman, D., Rothnagel, J.A., Roop, D.R. J. Biol. Chem. (1995) [Pubmed]
  18. Cholesterol sulfate activates multiple protein kinase C isoenzymes and induces granular cell differentiation in cultured murine keratinocytes. Denning, M.F., Kazanietz, M.G., Blumberg, P.M., Yuspa, S.H. Cell Growth Differ. (1995) [Pubmed]
  19. Isolation of a GC-rich cDNA identifying mRNA present in human epidermis and modulated by calcium and retinoic acid in cultured keratinocytes. Homology with murine loricrin mRNA. Magnaldo, T., Pommes, L., Asselineau, D., Darmon, M. Mol. Biol. Rep. (1990) [Pubmed]
  20. Regulation of epidermal differentiation by a Distal-less homeodomain gene. Morasso, M.I., Markova, N.G., Sargent, T.D. J. Cell Biol. (1996) [Pubmed]
  21. Chelation of intracellular Ca2+ inhibits murine keratinocyte differentiation in vitro. Li, L., Tucker, R.W., Hennings, H., Yuspa, S.H. J. Cell. Physiol. (1995) [Pubmed]
  22. Mouse epidermal keratinocytes in three-dimensional organotypic coculture with dermal fibroblasts form a stratified sheet resembling skin. Ikuta, S., Sekino, N., Hara, T., Saito, Y., Chida, K. Biosci. Biotechnol. Biochem. (2006) [Pubmed]
  23. Epidermal expression of the full-length extracellular calcium-sensing receptor is required for normal keratinocyte differentiation. Komuves, L., Oda, Y., Tu, C.L., Chang, W.H., Ho-Pao, C.L., Mauro, T., Bikle, D.D. J. Cell. Physiol. (2002) [Pubmed]
  24. Genomic organization and mapping of the human and mouse neuronal beta2-nicotinic acetylcholine receptor genes. Lueders, K.K., Elliott, R.W., Marenholz, I., Mischke, D., DuPree, M., Hamer, D. Mamm. Genome (1999) [Pubmed]
  25. Modulations in epidermal calcium regulate the expression of differentiation-specific markers. Elias, P.M., Ahn, S.K., Denda, M., Brown, B.E., Crumrine, D., Kimutai, L.K., Kömüves, L., Lee, S.H., Feingold, K.R. J. Invest. Dermatol. (2002) [Pubmed]
  26. Phytosphingosine stimulates the differentiation of human keratinocytes and inhibits TPA-induced inflammatory epidermal hyperplasia in hairless mouse skin. Kim, S., Hong, I., Hwang, J.S., Choi, J.K., Rho, H.S., Kim, D.H., Chang, I., Lee, S.H., Lee, M.O., Hwang, J.S. Mol. Med. (2006) [Pubmed]
  27. In utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin causes accelerated terminal differentiation in fetal mouse skin. Loertscher, J.A., Lin, T.M., Peterson, R.E., Allen-Hoffmann, B.L. Toxicol. Sci. (2002) [Pubmed]
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