KERATIN 10 gum salon LEAVE IN MIRACLE TREATMENT 300ml RSP £19.99

Product Information

Higashiyama, M., Hashimoto, K., Matsumoto, K. & Yoshikawa, K. Differential expression of transforming growth factor-alpha (TGF-alpha) and EGF receptor in transitional area of psoriatic epidermis. J. Dermatol. Sci. 7, 45–53 (1994). In a 3-year-old Turkish girl with mild EHK, born of first-cousin parents, Tsubota et al. (2008) identified homozygosity for a nonsense mutation in the KRT10 gene (C427X; 148080.0020). Immunohistochemical labeling of suprabasal epidermal layers by antibodies to KRT5 ( 148040), KRT6, and KRT14 ( 148066) suggested compensatory expression of 1 or more of these keratins by suprabasal keratinocytes. Polkoff KM et al. LGR5 is a conserved marker of hair follicle stem cells in multiple species and is present early and throughout follicle morphogenesis. Sci Rep 12:9104 (2022). KID ( keratitis-ichthyosis-deafness) syndrome — mutation in gap junction gene GJB2 encoding connexin 26 Darmon MY, Sémat A, Darmon MC, Vasseur M (1988). "Sequence of a cDNA encoding human keratin No 10 selected according to structural homologies of keratins and their tissue-specific expression". Mol. Biol. Rep. 12 (4): 277–83. doi: 10.1007/BF00444680. PMID 2448602. S2CID 4322605.

Ben-Bassat, H. et al. Inhibitors of epidermal growth factor receptor kinase and of cyclin-dependent kinase 2 activation induce growth arrest, differentiation, and apoptosis of human papilloma virus 16-immortalized human keratinocytes. Cancer Res. 57, 3741–3750 (1997).a b "Entrez Gene: KRT10 keratin 10 (epidermolytic hyperkeratosis; keratosis palmaris et plantaris)". In 2 unrelated patients with IWC, who both died from aggressive squamous cell carcinomas, Burger et al. (2020) identified heterozygosity for KRT10 mutations: the woman had the recurrent splicing mutation in intron 6 (148080.0023), and the man had an indel mutation in exon 7 (148080.0025). Truong, A. B. & Khavari, P. A. Control of keratinocyte proliferation and differentiation by p63. Cell Cycle 6, 295–299 (2007). Histological features of epidermolytic ichthyosis include hyperkeratosis, vacuolar degeneration in cells of the stratum spinosum/granulosum, coarse irregular keratohyaline granules, dyskeratosis, and acantholysis. [see Epidermolytic hyperkeratosis pathology] Burger, B., Ghosh, A., Ng, C. K. Y., Piscuoglio, S., Spoerri, I., Itin, P. H., Greer, K., Elbaum, D.

Zhou XM, Idler WW, Steven AC, etal. (1988). "The complete sequence of the human intermediate filament chain keratin 10. Subdomainal divisions and model for folding of end domain sequences". J. Biol. Chem. 263 (30): 15584–9. doi: 10.1016/S0021-9258(19)37628-8. PMID 2459124. Ichthyosis with confetti (IWC) [MIM: 609165]: An autosomal dominant, rare skin condition characterized by slowly enlarging islands of normal skin surrounded by erythematous ichthyotic patches in a reticulated pattern. The condition starts in infancy as a lamellar ichthyosis, with small islands of normal skin resembling confetti appearing in late childhood and at puberty. Histopathologic findings include band-like parakeratosis, psoriasiform acanthosis, and vacuolization of keratinocytes with binucleated cells in the upper epidermis, sometimes associated with amyloid deposition in the dermis. Ultrastructural abnormalities include perinuclear shells formed from a network of fine filaments in the upper epidermis. { ECO:0000269 PubMed: 20798280}. Note=The disease is caused by variants affecting the gene represented in this entry.A height below that which is expected according to age and gender norms. Although there is no universally accepted definition of short stature, many refer to \"short stature\" as height more than 2 standard deviations below the mean for age and gender (or below the 3rd percentile for age and gender dependent norms). Sequence of a cDNA encoding human keratin no. 10 selected according to structural homologies of keratins and their tissue-specific expression.

Extensive size polymorphism of the human keratin 10 chain resides in the C-terminal V2 subdomain due to variable numbers and sizes of glycine loops. Renz et al. (2019) noted that the genodermatosis IWC is caused by dominant-negative variants that result in aberrant KRT10 proteins that localize to the nucleus rather than the cytoplasm. The mislocalization is associated with a C terminus that is altered from a polyglycine tail to either a polyarginine or polyalanine tail. Renz et al. (2019) demonstrated that only K10 with an arginine-rich C terminus (K10arg) translocates to the nucleus, whereas wildtype K10, K10ala, and truncated K10 remain in the cytoplasm. The authors also showed that the presence of K10arg enables cotranslocation of non-K10arg proteins into the nucleus. They concluded that arginine-rich K10 tails are responsible for the pathogenic nuclear localization of K10 in patients with IWC. Mild recessive bullous congenital ichthyosiform erythroderma due to a previously unidentified homozygous keratin 10 nonsense mutation. Rothnagel JA, Fisher MP, Axtell SM, etal. (1994). "A mutational hot spot in keratin 10 (KRT 10) in patients with epidermolytic hyperkeratosis" (PDF). Hum. Mol. Genet. 2 (12): 2147–50. doi: 10.1093/hmg/2.12.2147. PMID 7509230.Choate, K. A., Lu, Y., Zhou, J., Choi, M., Elias, P. M., Farhi, A., Nelson-Williams, C., Crumrine, D., Williams, M. L., Nopper, A. J., Bree, A., Milstone, L. M., Lifton, R. P. Hsieh, S.-L. & Lin, W.-W. Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions. J. Biomed. Sci. 24, 39 (2017). There is no cure for epidermolytic ichthyosis, and treatments are limited to management of symptoms depending on the age and sex of the patient, severity of the disease, and location of the skin lesions [2,3]. These include: Identification of the genetic locus for keratosis palmaris et plantaris on chromosome 17 near the RARA and keratin type I genes.