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Gene Review

Krt10  -  keratin 10

Mus musculus

Synonyms: 56 kDa cytokeratin, CK-10, Cytokeratin-10, D130054E02Rik, K10, ...
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Disease relevance of Krt10

  • In early papillomas, K1 staining was patchy, and K10 staining occurred in very limited focal areas or was negative, such that the absence of staining delineated the lesions [1].
  • An unexpected role for keratin 10 end domains in susceptibility to skin cancer [2].
  • Transgenic mice expressing a mutant keratin 10 gene reveal the likely genetic basis for epidermolytic hyperkeratosis [3].
  • Positive reaction was obtained for CK4, CK34betaE12, CK10, CK14 in skin and cholesteatoma epithelium [4].
  • To generate paucibacillary infection, C57BL/6 mice were artificially infected with Mycobacterium avium subsp. paratuberculosis strain K10 and M. tuberculosis H37Rv, yielding tissues harboring fewer than one bacillus per oil immersion field [5].

High impact information on Krt10

  • A second form, Skn-1a, contains an alternative amino terminus and serves to activate cytokeratin 10 (K10) gene expression [6].
  • Driven by the suprabasal-specific keratin-10 gene promoter, expression of dnRXR alpha severely reduced the ability of RAR-selective ligands tRA and CD367 to induce epidermal mRNA levels of the CRABPII, CRBPI, and CRBPII genes, which contain RA-responsive elements (RAREs) DR1 and/or DR2 [7].
  • Transgenic mice were generated using a keratin 10 (K10) gene promoter to drive constitutive expression of TGF-beta 1 in the suprabasal keratinocyte compartment [8].
  • This genetic model allows activation of a somatic K10 mutation in epidermal stem cells in a spatially and temporally controlled manner using an inducible Cre recombinase [9].
  • We constitutively overexpressed BMP-6 in suprabasal layers of interfollicular epidermis in transgenic mice using a keratin 10 promoter [10].

Biological context of Krt10

  • Transfection of K10 in combination with K5 or K1 resulted in cytoplasmic agglomerates, but not a cytoskeleton [11].
  • The mild phenotype of K10(-/-) mice suggests that there is a considerable redundancy in the keratin gene family [12].
  • Here, we show that the loss of K10, the most prominent epidermal protein, allowed the formation of a normal epidermis in neonatal mice without signs of fragility or wound-healing response [12].
  • Furthermore, the ability of K10 to suppress cell proliferation was mapped to its unique N- and C-terminal protein domains [2].
  • Unlike most keratin mutant mice, the epidermis of adult K10-/- mice showed no cytolysis but displayed hyperproliferation of basal keratinocytes and an increased cell size [13].

Anatomical context of Krt10

  • Keratins 1 (K1) and 10 (K10) are the predominant cytoskeletal intermediate filaments of epidermal cells during transition from the proliferative to the terminal differentiation stage [11].
  • Transient and stable transfectants, as well as heterokaryons produced by fusions with epithelial cells, were evaluated for expression of K1 and K10 proteins and filament formation using specific antibodies [11].
  • The major differentiation products in suprabasal keratinocytes are keratins, K1 and K10 [1].
  • Sebaceous gland cells of K10-/- mice showed an accelerated turnover and secreted more sebum including wax esters, triglycerides, and cholesterol esters [14].
  • Forced expression of K10, a keratin normally expressed in postmitotic, terminally differentiating epidermal keratinocytes, inhibits the progression of the cell cycle in cultured cells (Paramio, J. M., Casanova, M. Ll., Segrelles, C., Mittnacht, S., Lane, E. B., and Jorcano, J. L. (1999) Mol. Cell. Biol. 19, 3086-3094) [15].

Associations of Krt10 with chemical compounds

  • The treatment of basal cells with retinoic acid at pharmacological concentrations prevented the expression of K1 and K10 when cells were challenged by 1.4 mM Ca2+ [16].
  • At doses which activate PKC, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1-oleoyl-2-acetylglycerol block Ca(2+)-mediated induction of the spinous cell markers keratins K1 and K10 at both the protein and mRNA level [17].
  • By use of cross-linking, high resolution polyacrylamide gel electrophoresis and blotting for 3H-labeled keratins or with an anti-mouse keratin 10 antibody, it was found that individual keratin chains form type I or type II homodimers and homotetramers in solution that do not assemble into KIF in vitro [18].
  • Moreover, differentiation-specific markers such as cytokeratin 10, involucrin, and filaggrin were shown to be expressed in an ordered succession [19].
  • Most importantly, the analysis of ceramide subpopulations revealed that the total amount of ceramide 2 was elevated in keratin 10-deficient mice, whereas ceramides 1, 3, 4, and 5 were decreased among total stratum corneum lipids [20].

Regulatory relationships of Krt10

  • After orthotopic transplantation to the floor of the mouth in athymic mice, cells containing dn TbetaR-II formed comparable numbers of primary tumours at the site of inoculation as controls but the tumours were less differentiated as demonstrated by the absence of keratin 10 immunostaining [21].

Other interactions of Krt10

  • In situ, formation of the K1/K10 intermediate filament network occurs in the cytoplasm of cells with a preexisting cytoskeleton composed of keratins 5 and 14 [11].
  • This intense staining for ODC occurred consistently in areas with decreased K1 and K10 expression, and, therefore, was associated with an altered pattern of differentiation [1].
  • BAPTA also inhibited the expression of K1, K10 and loricrin mRNA [22].
  • Although K10(-/-) mice show significant epidermal hyperproliferation, accompanied by an activation of the mitogen-activated protein kinase (MAPK) pathway, they formed no spontaneous tumors [23].
  • In newborn mutant epidermis, K6 and K16 are found to be most abundant in the outermost epidermal cells, a distribution opposite to that of K1 and K10 [24].

Analytical, diagnostic and therapeutic context of Krt10


  1. 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]
  2. An unexpected role for keratin 10 end domains in susceptibility to skin cancer. Chen, J., Cheng, X., Merched-Sauvage, M., Caulin, C., Roop, D.R., Koch, P.J. J. Cell. Sci. (2006) [Pubmed]
  3. Transgenic mice expressing a mutant keratin 10 gene reveal the likely genetic basis for epidermolytic hyperkeratosis. Fuchs, E., Esteves, R.A., Coulombe, P.A. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  4. Comparative cytokeratin distribution patterns in cholesteatoma epithelium. Olszewska, E., Sudhoff, H. Histol. Histopathol. (2007) [Pubmed]
  5. Evaluation of in situ methods used to detect Mycobacterium avium subsp. paratuberculosis in samples from patients with Crohn's disease. Jeyanathan, M., Alexander, D.C., Turenne, C.Y., Girard, C., Behr, M.A. J. Clin. Microbiol. (2006) [Pubmed]
  6. Skn-1a and Skn-1i: two functionally distinct Oct-2-related factors expressed in epidermis. Andersen, B., Schonemann, M.D., Flynn, S.E., Pearse, R.V., Singh, H., Rosenfeld, M.G. Science (1993) [Pubmed]
  7. Suprabasal expression of a dominant-negative RXR alpha mutant in transgenic mouse epidermis impairs regulation of gene transcription and basal keratinocyte proliferation by RAR-selective retinoids. Feng, X., Peng, Z.H., Di, W., Li, X.Y., Rochette-Egly, C., Chambon, P., Voorhees, J.J., Xiao, J.H. Genes Dev. (1997) [Pubmed]
  8. Concerted action of TGF-beta 1 and its type II receptor in control of epidermal homeostasis in transgenic mice. Cui, W., Fowlis, D.J., Cousins, F.M., Duffie, E., Bryson, S., Balmain, A., Akhurst, R.J. Genes Dev. (1995) [Pubmed]
  9. Focal activation of a mutant allele defines the role of stem cells in mosaic skin disorders. Arin, M.J., Longley, M.A., Wang, X.J., Roop, D.R. J. Cell Biol. (2001) [Pubmed]
  10. Overexpression of bone morphogenetic protein-6 (BMP-6) in the epidermis of transgenic mice: inhibition or stimulation of proliferation depending on the pattern of transgene expression and formation of psoriatic lesions. Blessing, M., Schirmacher, P., Kaiser, S. J. Cell Biol. (1996) [Pubmed]
  11. 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]
  12. 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]
  13. Hyperproliferation, induction of c-Myc and 14-3-3sigma, but no cell fragility in keratin-10-null mice. Reichelt, J., Magin, T.M. J. Cell. Sci. (2002) [Pubmed]
  14. Loss of keratin 10 is accompanied by increased sebocyte proliferation and differentiation. Reichelt, J., Breiden, B., Sandhoff, K., Magin, T.M. Eur. J. Cell Biol. (2004) [Pubmed]
  15. The expression of keratin k10 in the basal layer of the epidermis inhibits cell proliferation and prevents skin tumorigenesis. Santos, M., Paramio, J.M., Bravo, A., Ramirez, A., Jorcano, J.L. J. Biol. Chem. (2002) [Pubmed]
  16. Regulated expression of differentiation-associated keratins in cultured epidermal cells detected by monospecific antibodies to unique peptides of mouse epidermal keratins. Roop, D.R., Huitfeldt, H., Kilkenny, A., Yuspa, S.H. Differentiation (1987) [Pubmed]
  17. 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]
  18. The two-chain coiled-coil molecule of native epidermal keratin intermediate filaments is a type I-type II heterodimer. Steinert, P.M. J. Biol. Chem. (1990) [Pubmed]
  19. Inverse relationship between human papillomavirus (HPV) type 16 early gene expression and cell differentiation in nude mouse epithelial cysts and tumors induced by HPV-positive human cell lines. Dürst, M., Bosch, F.X., Glitz, D., Schneider, A., zur Hausen, H. J. Virol. (1991) [Pubmed]
  20. Normal ultrastructure, but altered stratum corneum lipid and protein composition in a mouse model for epidermolytic hyperkeratosis. Reichelt, J., Doering, T., Schnetz, E., Fartasch, M., Sandhoff, K., Magin, A.M. J. Invest. Dermatol. (1999) [Pubmed]
  21. Attenuated type II TGF-beta receptor signalling in human malignant oral keratinocytes induces a less differentiated and more aggressive phenotype that is associated with metastatic dissemination. Huntley, S.P., Davies, M., Matthews, J.B., Thomas, G., Marshall, J., Robinson, C.M., Eveson, J.W., Paterson, I.C., Prime, S.S. Int. J. Cancer (2004) [Pubmed]
  22. 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]
  23. Loss of keratin 10 leads to mitogen-activated protein kinase (MAPK) activation, increased keratinocyte turnover, and decreased tumor formation in mice. Reichelt, J., Furstenberger, G., Magin, T.M. J. Invest. Dermatol. (2004) [Pubmed]
  24. Abnormal expression and processing of keratins in pupoid fetus (pf/pf) and repeated epilation (Er/Er) mutant mice. Fisher, C., Jones, A., Roop, D.R. J. Cell Biol. (1987) [Pubmed]
  25. Out of balance: consequences of a partial keratin 10 knockout. Reichelt, J., Bauer, C., Porter, R., Lane, E., Magin, V. J. Cell. Sci. (1997) [Pubmed]
  26. Binding of keratin intermediate filaments (K10) to the cornified envelope in mouse epidermis: implications for barrier function. Ming, M.E., Daryanani, H.A., Roberts, L.P., Baden, H.P., Kvedar, J.C. J. Invest. Dermatol. (1994) [Pubmed]
  27. Topical application of 12-O-tetradecanoylphorbol-13-acetate induces dyssynchronous expression of keratins K1 and K10 in mouse epidermis. Heyden, A., Lützow-Holm, C., Clausen, O.P., Brandtzaeg, P., Huitfeldt, H.S. Cytometry. (1995) [Pubmed]
  28. Role for SUMO modification in facilitating transcriptional repression by BKLF. Perdomo, J., Verger, A., Turner, J., Crossley, M. Mol. Cell. Biol. (2005) [Pubmed]
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