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Gene Review

Krt16  -  keratin 16

Mus musculus

Synonyms: AI324768, CK-16, Cytokeratin-16, K16, Keratin, type I cytoskeletal 16, ...
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Disease relevance of Krt16

  • In hypertrophic scars the mRNA distribution corroborated the abnormal K16 protein distribution [1].
  • Analysis of the lesional keratins of psoriasis patients showed that etretinate caused a reduction in keratin 16 and an increase in the keratin 14:keratin 16 ratio, although the magnitude of these changes and their correlation with clinical improvement was variable [2].
  • The availability of K16 in a purified recombinant form will allow us to study how its properties may relate to its function during wound healing and in skin diseases [3].
  • The acetylation pattern of histone H4 in mouse lymphosarcoma cells induced by TSA was established in which acetylation initially occurred at K16 followed by K12 and then K8 and/or K5 [4].

High impact information on Krt16

  • Absence of a hair phenotype correlates with a genetic strain-dependent compensation by related keratins, including K16 [5].
  • The inability of K16 to form urea-stable tetramers in vitro correlates with an increase in its turnover rate in vivo [6].
  • While a structural function has been clearly defined for K14, we have proposed that a function of K16 may be to play a role in the process of keratinocyte activation that occurs after acute injury to stratified epithelia [7].
  • In fact, tyrosine phosphorylation of the EGF receptor is increased in the newborn skin of K16 transgenic mice [8].
  • 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 [9].

Biological context of Krt16

  • The functional diversity of epidermal keratins revealed by the partial rescue of the keratin 14 null phenotype by keratin 16 [7].
  • Rather, these data implicate the tail domain of K16 as the more likely protein domain that determines the unique functions [10].
  • We therefore used the skin of heterozygous and homozygous mice to create a cDNA library, and we report here the successful cloning and sequencing of mouse K16 [10].
  • These remarkable changes were accompanied by the induction of c-Myc, cyclin D1, 14-3-3sigma and of wound healing keratins K6 and K16 [11].
  • In this study, we analyzed the distribution of mouse type I keratin 16 during skin morphogenesis, in the adult hair cycle, and in challenged epidermis [12].

Anatomical context of Krt16


Associations of Krt16 with chemical compounds


Other interactions of Krt16

  • Our results suggest that the expression of K6 and K16 is less restricted by cellular replication than the normally occurring K1 and K10 keratins [13].
  • Exposure of cultures to a variety of different retinoids produced both dose-dependent decreases in keratin 16 with consequent increases in the keratin 14: keratin 16 ratio, and a decrease in envelope formation [2].
  • A conserved aspect of this response is a rapid switch in gene expression whereby the type II keratin 6 (K6) and type I keratins 16 and 17 (K16, K17) are induced in epithelial cells at the wound edge [18].

Analytical, diagnostic and therapeutic context of Krt16

  • K16 mRNA was localized by in situ hybridization using a highly specific cRNA probe [1].
  • Keratin 6, keratin 16, and keratin 17, which are known to be upregulated during keratinocyte activation and in hyperproliferative epidermis, were highly expressed in cultured skin substitutes in vitro [19].
  • By real-time PCR, TH replete cell expression of K6a, K16, and K17 was greater than in deficient cells: 18- (P < 0.001), 10- (P < 0.001), and 4-fold (P < 0.005), respectively [20].
  • By RT-PCR, keratin 6a (K6a) and 16 (K16) gene expression in TH replete cells was 3.8- (P < 0.005) and 1.9-fold (P < 0.05) greater, respectively, than expression in TH-deficient cells [20].


  1. Activated keratinocytes in the epidermis of hypertrophic scars. Machesney, M., Tidman, N., Waseem, A., Kirby, L., Leigh, I. Am. J. Pathol. (1998) [Pubmed]
  2. Simple assays of retinoid activity as potential screens for compounds that may be useful in treatment of psoriasis. West, M.R., Page, J.M., Turner, D.M., Wood, E.J., Holland, D.B., Cunliffe, W.J., Rupniak, H.T. J. Invest. Dermatol. (1992) [Pubmed]
  3. cDNA cloning and bacterial expression of the human type I keratin 16. Paladini, R.D., Takahashi, K., Gant, T.M., Coulombe, P.A. Biochem. Biophys. Res. Commun. (1995) [Pubmed]
  4. Peptide mass mapping of acetylated isoforms of histone H4 from mouse lymphosarcoma cells treated with histone deacetylase (HDACs) inhibitors. Ren, C., Zhang, L., Freitas, M.A., Ghoshal, K., Parthun, M.R., Jacob, S.T. J. Am. Soc. Mass Spectrom. (2005) [Pubmed]
  5. Keratin 17 null mice exhibit age- and strain-dependent alopecia. McGowan, K.M., Tong, X., Colucci-Guyon, E., Langa, F., Babinet, C., Coulombe, P.A. Genes Dev. (2002) [Pubmed]
  6. A small surface hydrophobic stripe in the coiled-coil domain of type I keratins mediates tetramer stability. Bernot, K.M., Lee, C.H., Coulombe, P.A. J. Cell Biol. (2005) [Pubmed]
  7. The functional diversity of epidermal keratins revealed by the partial rescue of the keratin 14 null phenotype by keratin 16. Paladini, R.D., Coulombe, P.A. J. Cell Biol. (1999) [Pubmed]
  8. Directed expression of keratin 16 to the progenitor basal cells of transgenic mouse skin delays skin maturation. Paladini, R.D., Coulombe, P.A. J. Cell Biol. (1998) [Pubmed]
  9. 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]
  10. cDNA cloning, expression, and assembly characteristics of mouse keratin 16. Porter, R.M., Hutcheson, A.M., Rugg, E.L., Quinlan, R.A., Lane, E.B. J. Biol. Chem. (1998) [Pubmed]
  11. 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]
  12. Keratin 16 expression defines a subset of epithelial cells during skin morphogenesis and the hair cycle. Bernot, K.M., Coulombe, P.A., McGowan, K.M. J. Invest. Dermatol. (2002) [Pubmed]
  13. Expression of keratins K6 and K16 in regenerating mouse epidermis is less restricted by cell replication than the expression of K1 and K10. Heyden, A., Lützow-Holm, C., Clausen, O.P., Brandtzaeg, P., Huitfeldt, H.S. Epithelial cell biology. (1994) [Pubmed]
  14. Characterization of the cytokeratins of human colonic, pancreatic, and gastric adenocarcinoma cell lines. Rafiee, P., Ho, S.B., Bresalier, R.S., Bloom, E.J., Kim, J.H., Kim, Y.S. Pancreas (1992) [Pubmed]
  15. Overexpression of human keratin 16 produces a distinct skin phenotype in transgenic mouse skin. Coulombe, P.A., Bravo, N.S., Paladini, R.D., Nguyen, D., Takahashi, K. Biochem. Cell Biol. (1995) [Pubmed]
  16. Effects of topical retinoids on cytoskeletal proteins: implications for retinoid effects on epidermal differentiation. Eichner, R., Kahn, M., Capetola, R.J., Gendimenico, G.J., Mezick, J.A. J. Invest. Dermatol. (1992) [Pubmed]
  17. Striate palmoplantar keratoderma arising from desmoplakin and desmoglein 1 mutations is associated with contrasting perturbations of desmosomes and the keratin filament network. Wan, H., Dopping-Hepenstal, P.J., Gratian, M.J., Stone, M.G., Zhu, G., Purkis, P.E., South, A.P., Keane, F., Armstrong, D.K., Buxton, R.S., McGrath, J.A., Eady, R.A. Br. J. Dermatol. (2004) [Pubmed]
  18. Role for keratins 6 and 17 during wound closure in embryonic mouse skin. Mazzalupo, S., Wong, P., Martin, P., Coulombe, P.A. Dev. Dyn. (2003) [Pubmed]
  19. Keratin expression in cultured skin substitutes suggests that the hyperproliferative phenotype observed in vitro is normalized after grafting. Smiley, A.K., Klingenberg, J.M., Boyce, S.T., Supp, D.M. Burns : journal of the International Society for Burn Injuries. (2006) [Pubmed]
  20. A role for thyroid hormone in wound healing through keratin gene expression. Safer, J.D., Crawford, T.M., Holick, M.F. Endocrinology (2004) [Pubmed]
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