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Gene Review

Krt5  -  keratin 5

Mus musculus

Synonyms: 3300001P10Rik, AW146334, CK-5, CK5, Cytokeratin-5, ...
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Disease relevance of Krt5

  • We suggest that K5 null mutations may be lethal in human epidermolysis bullosa simplex patients [1].
  • Nulliparous transgenic females developed mammary hyperplasia that comprised undifferentiated basal (K5/14-positive, K8- and alpha-smooth muscle-actin-negative) cells [2].
  • Antibodies to the basal cell keratins, K5 and K14, stained both basal and suprabasal cells in hyperplastic epidermis and papillomas [3].
  • In addition, as a consequence of transgene expression in other ectodermally derived epithelia, K5-GR mice exhibited further abnormalities that strikingly resemble the clinical findings in patients with ectodermal dysplasia, which includes aplasia cutis congenita [4].
  • Inducible expression of a mutated K-ras gene under the control of the K5 promoter led to the development of hyperplastic and dysplastic epithelial lesions and carcinomas, with an incidence of 100% and a minimum latency of a week [5].

High impact information on Krt5

  • This study describes abnormalities of the thymus in mice in which the Stat3 gene has been specifically disrupted behind the keratin 5 promoter [6].
  • METHODS: The pathologic changes of transgenic mouse pancreas with keratin 5-promoter-driven expression and activity of COX-2 were characterized [7].
  • Surprisingly, our transgenic mice expressing wild-type TGFbeta1 in the epidermis using a keratin 5 promoter (K5.TGFbeta1(wt)) developed inflammatory skin lesions, with gross appearance of psoriasis-like plaques, generalized scaly erythema, and Koebner's phenomenon [8].
  • Transfection of K10 in combination with K5 or K1 resulted in cytoplasmic agglomerates, but not a cytoskeleton [9].
  • Keratinocyte-specific expression of the transgene was achieved by using a keratin 5 promoter [10].

Biological context of Krt5

  • Thymus Medulla Formation and Central Tolerance Are Restored in IKK{alpha}-/- Mice That Express an IKK{alpha} Transgene in Keratin 5+ Thymic Epithelial Cells [11].
  • In contrast to the K14(-/-) mice, we detected a strong induction of the wound-healing keratin K6 in the suprabasal epidermis of cytolyzed areas of postnatal K5(-/-) mice [1].
  • We have focused on tooth development in K5-GR mice and found that an inhibitor of steroid synthesis partially reversed the abnormal phenotype [12].
  • We have used a recently described model in which a ras oncogene is expressed in cytokeratin 5 (K5)-expressing cells on doxycycline administration to explore the effects of this oncogene in salivary glands of adult mice [5].
  • To explore the emergence of TEC subsets during ontogeny, we analyzed keratin 8 and keratin 5 expression at several stages of fetal development in normal C57BL/6J mice [13].

Anatomical context of Krt5

  • Moreover, we show that in the absence of K5 and other type II keratins, residual K14 and K15 aggregated along hemidesmosomes, demonstrating that individual keratins without a partner are stable in vivo [1].
  • The levels of K15 and K16 were not different in the MKC-5 and MKC-6 cell lines, suggesting that they are not contributing factors to the stabilization of K5 in the mutant cells [14].
  • K5/14 persisted suprabasally at elevated protein levels, whereas their mRNAs remained restricted to the basal keratinocytes [15].
  • Here, we report that K5-GR mice exhibit multiple epithelial defects in hair follicle, tooth, and palate development [12].
  • K5 protein expression starts in the forelimb surface ectoderm as early as E9.25, while the expression of its partner, K14, begins at E9.75 [16].

Associations of Krt5 with chemical compounds

  • Early vitamin A deficiency caused the appearance of single subcolumnar reserve cells expressing K5 mRNA [17].
  • In the study presented here, the effects of constitutive COX-2 overexpression in keratin 5-positive myoepithelial and luminal cells, driven by the keratin 5 promoter in a hormone-independent manner, was investigated [18].
  • [3H]ATMP failed to bind to K5 after removal of GlcNAc [19].
  • K5 failed to bind to ATMP when the third proline was substituted with threonine, as in some cases of human X-linked amelogenesis imperfecta or when tyrosyl residues were substituted with phenylalanine [19].
  • Immunohistochemistry revealed that the CD44(+) cancer cells have a primitive cellular morphology and costain with the basal cell marker Cytokeratin 5/14, whereas the CD44(-) cancer cells resemble differentiated squamous epithelium and express the differentiation marker Involucrin [20].

Other interactions of Krt5

  • The distribution of K5, the natural partner of K14, at the immunofluorescence level was also normal looking in the K14-/- MKC-5 cells, but with fewer filaments detectable, consistent with the approximately 20% reduction in K5 detectable on immunoblots [14].
  • The localization of both K5 and K1 proteins in these same cell layers, and above, is consistent with transcriptional regulation of these keratins [17].
  • From E9.25 to E9.75, K5 forms atypical filaments with K18 [16].
  • While CK5 expression in Wnt10b transgenic tissue was still confined to the lining cell layer, its expression in Int2 transgenic tissue was completely disorganized [21].
  • K5 was much stronger in the conjunctiva of the IKKalpha(-/-) mice [22].

Analytical, diagnostic and therapeutic context of Krt5


  1. Complete cytolysis and neonatal lethality in keratin 5 knockout mice reveal its fundamental role in skin integrity and in epidermolysis bullosa simplex. Peters, B., Kirfel, J., Büssow, H., Vidal, M., Magin, T.M. Mol. Biol. Cell (2001) [Pubmed]
  2. Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia. Teulière, J., Faraldo, M.M., Deugnier, M.A., Shtutman, M., Ben-Ze'ev, A., Thiery, J.P., Glukhova, M.A. Development (2005) [Pubmed]
  3. Ornithine decarboxylase expression in cutaneous papillomas in SENCAR mice is associated with altered expression of keratins 1 and 10. Sundberg, J.P., Erickson, A.A., Roop, D.R., Binder, R.L. Cancer Res. (1994) [Pubmed]
  4. Altered skin development and impaired proliferative and inflammatory responses in transgenic mice overexpressing the glucocorticoid receptor. Pérez, P., Page, A., Bravo, A., Del Río, M., Giménez-Conti, I., Budunova, I., Slaga, T.J., Jorcano, J.L. FASEB J. (2001) [Pubmed]
  5. Rapid Development of Salivary Gland Carcinomas upon Conditional Expression of K-ras Driven by the Cytokeratin 5 Promoter. Raimondi, A.R., Vitale-Cross, L., Amornphimoltham, P., Gutkind, J.S., Molinolo, A. Am. J. Pathol. (2006) [Pubmed]
  6. Stat3 in thymic epithelial cells is essential for postnatal maintenance of thymic architecture and thymocyte survival. Sano, S., Takahama, Y., Sugawara, T., Kosaka, H., Itami, S., Yoshikawa, K., Miyazaki, J., van Ewijk, W., Takeda, J. Immunity (2001) [Pubmed]
  7. Preinvasive duct-derived neoplasms in pancreas of keratin 5-promoter cyclooxygenase-2 transgenic mice. Müller-Decker, K., Fürstenberger, G., Annan, N., Kucher, D., Pohl-Arnold, A., Steinbauer, B., Esposito, I., Chiblak, S., Friess, H., Schirmacher, P., Berger, I. Gastroenterology (2006) [Pubmed]
  8. Latent TGFbeta1 overexpression in keratinocytes results in a severe psoriasis-like skin disorder. Li, A.G., Wang, D., Feng, X.H., Wang, X.J. EMBO J. (2004) [Pubmed]
  9. Mouse differentiation-specific keratins 1 and 10 require a preexisting keratin scaffold to form a filament network. Kartasova, T., Roop, D.R., Holbrook, K.A., Yuspa, S.H. J. Cell Biol. (1993) [Pubmed]
  10. Skin-specific expression of a truncated E1a oncoprotein binding to p105-Rb leads to abnormal hair follicle maturation without increased epidermal proliferation. Missero, C., Serra, C., Stenn, K., Dotto, G.P. J. Cell Biol. (1993) [Pubmed]
  11. Thymus Medulla Formation and Central Tolerance Are Restored in IKK{alpha}-/- Mice That Express an IKK{alpha} Transgene in Keratin 5+ Thymic Epithelial Cells. Lomada, D., Liu, B., Coghlan, L., Hu, Y., Richie, E.R. J. Immunol. (2007) [Pubmed]
  12. Ectoderm-targeted overexpression of the glucocorticoid receptor induces hypohidrotic ectodermal dysplasia. Cascallana, J.L., Bravo, A., Donet, E., Leis, H., Lara, M.F., Paramio, J.M., Jorcano, J.L., Pérez, P. Endocrinology (2005) [Pubmed]
  13. Cutting edge: thymocyte-independent and thymocyte-dependent phases of epithelial patterning in the fetal thymus. Klug, D.B., Carter, C., Gimenez-Conti, I.B., Richie, E.R. J. Immunol. (2002) [Pubmed]
  14. In vitro characteristics of early epidermal progenitors isolated from keratin 14 (K14)-deficient mice: insights into the role of keratin 17 in mouse keratinocytes. Troy, T.C., Turksen, K. J. Cell. Physiol. (1999) [Pubmed]
  15. Formation of a normal epidermis supported by increased stability of keratins 5 and 14 in keratin 10 null mice. Reichelt, J., Büssow, H., Grund, C., Magin, T.M. Mol. Biol. Cell (2001) [Pubmed]
  16. Type II keratins precede type I keratins during early embryonic development. Lu, H., Hesse, M., Peters, B., Magin, T.M. Eur. J. Cell Biol. (2005) [Pubmed]
  17. Retinoid status controls the appearance of reserve cells and keratin expression in mouse cervical epithelium. Darwiche, N., Celli, G., Sly, L., Lancillotti, F., De Luca, L.M. Cancer Res. (1993) [Pubmed]
  18. Cystic duct dilatations and proliferative epithelial lesions in mouse mammary glands upon keratin 5 promoter-driven overexpression of cyclooxygenase-2. Müller-Decker, K., Berger, I., Ackermann, K., Ehemann, V., Zoubova, S., Aulmann, S., Pyerin, W., Fürstenberger, G. Am. J. Pathol. (2005) [Pubmed]
  19. Amelogenin interacts with cytokeratin-5 in ameloblasts during enamel growth. Ravindranath, R.M., Basilrose, R.M., Ravindranath, N.H., Vaitheesvaran, B. J. Biol. Chem. (2003) [Pubmed]
  20. Identification of a subpopulation of cells with cancer stem cell properties in head and neck squamous cell carcinoma. Prince, M.E., Sivanandan, R., Kaczorowski, A., Wolf, G.T., Kaplan, M.J., Dalerba, P., Weissman, I.L., Clarke, M.F., Ailles, L.E. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  21. Activation of different Wnt/beta-catenin signaling components in mammary epithelium induces transdifferentiation and the formation of pilar tumors. Miyoshi, K., Rosner, A., Nozawa, M., Byrd, C., Morgan, F., Landesman-Bollag, E., Xu, X., Seldin, D.C., Schmidt, E.V., Taketo, M.M., Robinson, G.W., Cardiff, R.D., Hennighausen, L. Oncogene (2002) [Pubmed]
  22. IkappaB kinase alpha is essential for development of the mammalian cornea and conjunctiva. Yoshida, K., Hu, Y., Karin, M. Invest. Ophthalmol. Vis. Sci. (2000) [Pubmed]
  23. A novel type II cytokeratin, mK6irs, is expressed in the Huxley and Henle layers of the mouse inner root sheath. Aoki, N., Sawada, S., Rogers, M.A., Schweizer, J., Shimomura, Y., Tsujimoto, T., Ito, K., Ito, M. J. Invest. Dermatol. (2001) [Pubmed]
  24. Real-time monitoring of keratin 5 expression during burn re-epithelialization. Bruen, K.J., Campbell, C.A., Schooler, W.G., deSerres, S., Cairns, B.A., Hultman, C.S., Meyer, A.A., Randell, S.H. J. Surg. Res. (2004) [Pubmed]
  25. Circulating progenitor epithelial cells traffic via CXCR4/CXCL12 in response to airway injury. Gomperts, B.N., Belperio, J.A., Rao, P.N., Randell, S.H., Fishbein, M.C., Burdick, M.D., Strieter, R.M. J. Immunol. (2006) [Pubmed]
  26. Kringle 5 of human plasminogen suppresses hepatocellular carcinoma growth both in grafted and xenografted mice by anti-angiogenic activity. Yang, X., Cheng, R., Li, C., Cai, W., Ma, J.X., Liu, Q., Yang, Z., Song, Z., Liu, Z., Gao, G. Cancer Biol. Ther. (2006) [Pubmed]
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