The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Krt17  -  keratin 17

Mus musculus

Synonyms: CK-17, Cytokeratin-17, K17, Keratin, type I cytoskeletal 17, Keratin-17, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Krt17


High impact information on Krt17

  • Keratin 17 modulates hair follicle cycling in a TNFalpha-dependent fashion [2].
  • Of the proapoptotic challenges tested, K17-null skin keratinocytes in primary culture are selectively more sensitive to TNFalpha [2].
  • Keratin 17 (K17)-null mice develop alopecia in the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair bulb [2].
  • Onset of type I keratin 17 (K17) synthesis marks the adoption of an appendageal fate within embryonic ectoderm, and its expression persists in specific cell types within mature hair, glands, and nail [3].
  • We report that K17 null mice develop severe alopecia during the first week postbirth, correlating with hair fragility, alterations in follicular histology, and apoptosis in matrix cells [3].

Biological context of Krt17

  • The pattern of K17 gene expression during development has direct implications for the morphogenesis of skin epithelia, and points to the existence of a molecular relationship between development and wound repair [4].
  • Due to its high sequence homology to human keratin 17 cDNA, one full-length cDNA is most likely to be mouse keratin 17 (Krt1-17) cDNA [5].
  • These are the major sites for the occurrence of the pili torti (twisted hair) phenotype in the type 2 (Jackson-Lawler) form of pachyonychia congenita, previously shown to arise from inherited K17 mutations [6].
  • At the end of the rodent type I gene cluster, a novel gene related to K14 and K17 was identified, which is converted to a pseudogene in humans [7].
  • Here we review studies focused on a subset of keratin genes, K6, K16 and K17, showing a complex regulation in vivo, including a widely known upregulation during wound repair and in diseased skin [8].

Anatomical context of Krt17

  • The type I keratin 17 (K17) shows a peculiar localization in human epithelial appendages including hair follicles, which undergo a growth cycle throughout adult life [4].
  • Synthesis of K17 protein first occurs in a subset of epithelial cells within the single-layered, undifferentiated ectoderm of embryonic day 10.5 mouse fetuses [4].
  • In vitro characteristics of early epidermal progenitors isolated from keratin 14 (K14)-deficient mice: insights into the role of keratin 17 in mouse keratinocytes [9].
  • We show that newborn mice null for K6alpha, K6beta, and K17 exhibit severe lysis restricted to the nail bed epithelium, where all three genes are robustly expressed, providing strong evidence that this region of the nail unit is initially targeted in PC [10].
  • All three keratins are abundantly expressed within the nail bed epithelium, whereas K17 protein is expressed in the nail matrix, which contains the epithelial cell precursors for the nail plate [6].

Associations of Krt17 with chemical compounds

  • As one possible approach to further explore K17 functions, we have studied the differential patterns of mouse K17 (MK17) transcription during the murine hair cycle by means of in situ hybridization, using a digoxigenin-labeled riboprobe [11].
  • Both K17A-RDO and -ssODN contained a single base mismatch (CGC to CCC) to alter the normal K17 sequence to cause an amino acid substitution (R94P) [12].

Other interactions of Krt17

  • K17 expression was increased approximately 40% in the K14-/- cells [9].
  • Yet null alleles obliterating the function of both K6 genes (K6alpha and K6beta) or the K17 gene, as well as the targeted expression of a dominant-negative K6alpha mutant, elicit only a subset of PC-specific epithelial lesions (excluding that of the nail in mice) [10].
  • 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 [13].
  • Still, detailed studies of the phenotype exhibited by K6 and K17 null mice yielded novel insight into the properties and function of keratin IFs in vivo [8].
  • Suprabasal beta1 integrin expression and induction of keratin 17 in interfollicular epidermis provided evidence of perturbed differentiation [14].

Analytical, diagnostic and therapeutic context of Krt17

  • Western blot analysis of hair extracts prepared from a number of mouse strains confirms this observation and suggests that K17 expression in the hair shaft is a general trait in this species [6].
  • By RT-PCR, K6a and K17 gene expression from control mouse skin was greater than from hypothyroid mouse skin: 5- (P < 0.001) and 1.7-fold (P < 0.05), respectively [15].
  • 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 [15].
  • In vivo alteration of the keratin 17 gene in hair follicles by oligonucleotide-directed gene targeting [12].
  • Although intradermal injection of K17A-RDO or K17-ssODN caused a dominant mutation in K17 affecting hair growth and morphology, these phenotypic changes were transient either due to the compensation of K17 by other keratins or the replacement of the mutated cells by normal surrounding cells during hair growth [12].


  1. A novel mouse type I intermediate filament gene, keratin 17n (K17n), exhibits preferred expression in nail tissue. Tong, X., Coulombe, P.A. J. Invest. Dermatol. (2004) [Pubmed]
  2. Keratin 17 modulates hair follicle cycling in a TNFalpha-dependent fashion. Tong, X., Coulombe, P.A. Genes Dev. (2006) [Pubmed]
  3. 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]
  4. Onset of keratin 17 expression coincides with the definition of major epithelial lineages during skin development. McGowan, K.M., Coulombe, P.A. J. Cell Biol. (1998) [Pubmed]
  5. The genomic organization of type I keratin genes in mice. Sato, H., Koide, T., Sagai, T., Ishiguro, S.I., Tamai, M., Saitou, N., Shiroishi, T. Genomics (1999) [Pubmed]
  6. Keratin 17 expression in the hard epithelial context of the hair and nail, and its relevance for the pachyonychia congenita phenotype. McGowan, K.M., Coulombe, P.A. J. Invest. Dermatol. (2000) [Pubmed]
  7. Comprehensive analysis of keratin gene clusters in humans and rodents. Hesse, M., Zimek, A., Weber, K., Magin, T.M. Eur. J. Cell Biol. (2004) [Pubmed]
  8. Great promises yet to be fulfilled: defining keratin intermediate filament function in vivo. Coulombe, P.A., Tong, X., Mazzalupo, S., Wang, Z., Wong, P. Eur. J. Cell Biol. (2004) [Pubmed]
  9. 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]
  10. Overcoming functional redundancy to elicit pachyonychia congenita-like nail lesions in transgenic mice. Wong, P., Domergue, R., Coulombe, P.A. Mol. Cell. Biol. (2005) [Pubmed]
  11. Keratin 17 gene expression during the murine hair cycle. Panteleyev, A.A., Paus, R., Wanner, R., Nürnberg, W., Eichmüller, S., Thiel, R., Zhang, J., Henz, B.M., Rosenbach, T. J. Invest. Dermatol. (1997) [Pubmed]
  12. In vivo alteration of the keratin 17 gene in hair follicles by oligonucleotide-directed gene targeting. Fan, W., Yoon, K. Exp. Dermatol. (2003) [Pubmed]
  13. 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]
  14. Transgenic mice expressing IFN-gamma in the epidermis have eczema, hair hypopigmentation, and hair loss. Carroll, J.M., Crompton, T., Seery, J.P., Watt, F.M. J. Invest. Dermatol. (1997) [Pubmed]
  15. A role for thyroid hormone in wound healing through keratin gene expression. Safer, J.D., Crawford, T.M., Holick, M.F. Endocrinology (2004) [Pubmed]
WikiGenes - Universities