-
Study identified iRHOM2 as a novel regulator of K16 in humans and mice, with important implications for palmoplantar keratodermas, wound healing, inflammatory skin disease and cancers.
-
results suggest a conditional regulation of KRT16 gene by ATF4 that may be inhibited in normal cells, but engaged during cancer progression. Potential roles of KRT16, FAM129A and HKDC1 genes upregulation in adaptive stress responses and pathologies are discussed
-
inflammatory cytokines promoted Nrf2 nuclear translocation in psoriatic epidermis, which led to elevated expression of K6, K16, and K17, thus promoting keratinocyte proliferation and contributing to the pathogenesis of psoriasis.
-
The wider spectrum of KRT16 mutations suggests that changes in codons 125, 127, and 132 are most commonly responsible for PC-1 and that proline substitution mutations at codons 127 or 128 may produce more severe disease
-
analysis of a new p.Leu421Pro (c.1262T>C) mutation in the highly conserved helix termination motif of K16 in a large Spanish family that may have a role in pachyonychia congenita
-
Keratin 16 regulates innate immunity in response to epidermal barrier breach.
-
Data established a seven-gene (AR, ESR2, GATA3, GBX2, KRT16, MMP28 and WNT11) prognostic signature to define a subset of triple-negative breast cancer (TNBC).
-
Genotype-phenotype correlations among PC patients with codon-125 mutation in KRT16 were established, while the phenotypes caused by the IVS8-2A>C mutation in KRT6A need further studies to confirm the rare feature of fissured tongue
-
We found that the KRT16 mutation carriers developed plantar keratoderma at a similar age to KRT6A carriers wheras KRT6B and KRT17 carriers were significantly more likely to report later onset.
-
Phenotypic differences exist between KRT6A and KRT16 mutations support adoption of a new classification system.
-
Patients with p.Asn125Asp and p.Arg127Pro mutations in KRT16 exhibited more severe disease than patients carrying p.Asn125Ser and p.Arg127Cys mutations in terms of age of onset of symptoms, extent of nail involvement, and impact on daily quality of life.
-
Data suggest that an immune response to trichohyalin and K16 may have a role in the pathogenesis of the enigmatic disorder.
-
these data highlight the possibility of a physiological role for K6/K16 heterodimers in keratinocyte cell migration, in addition to the heterodimer's known functions in cell differentiation and mechanical resilience.
-
coinheritance of mutations in KRT16 and filaggrin may aggravate the pachyonychia congenita phenotype
-
disease-associated keratin 16 expression is induced by epidermal growth factor is regulated through cooperation of transcription factors Sp1 and c-Jun
-
K16 expression is observed in non-lesional psoriatic skin and may serve as a marker of preclinical psoriasis.
-
ERK2-mediated C-terminal serine phosphorylation of p300 was a key event in the regulation of EGF-induced keratin 16 expression.
-
Four new missense and five known mutations in K6a, one new deletion and three previously identified missense mutations in K16, plus one known mutation in K17 are reported in pachyonychia congenita.
-
K14 and K16 were detected in the tumour cells, suggesting differentiation towards the outer root sheath beneath the orifice of the sebaceous duct.
-
PC-1 is due to mutations of the KRT16 gene or its expression partner KRT6A, wheres PC-2 is caused by mutations in the KRT17 or KRT6B genes.
