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This study found that TPA treatment induced expression of keratins K6 and K16 in mouse epidermis, with K6 expressed across all cell layers and K16 only in post-mitotic cells.

This study found that activating cannabinoid receptor 1 reduces the expression of keratins K6 and K16 in human keratinocytes, suggesting potential implications for psoriasis management.

This study found that CB1 activation by a specific agonist led to decreased expression of keratins K6 and K16 in human skin and inhibited keratinocyte proliferation, suggesting potential for cannabinoid receptors in psoriasis management.

This study found that CB1 receptor activation reduced keratin K6 and K16 expression in human keratinocytes in vitro and in situ, suggesting potential relevance for both psoriasis management and wound healing.

This study found that despite strong homology between two K16 genes, only one encoded a functional protein that assembled into keratin filaments in epithelial cells, possibly due to promoter strength differences.

This study identified a new type II cytokeratin, named K6hf, exclusively expressed in the companion layer of the human hair follicle, distinguishing it from other keratins and suggesting a unique biochemical role.

This study found that K17 is crucial for the structural integrity and survival of hair-producing cells, with K17 null mice developing alopecia due to hair fragility and follicular alterations.

In a transgenic mouse model, this study found that overexpression of keratin 16 in skin keratinocytes led to hyperkeratosis and increased EGF receptor signaling, altering skin cell behavior and structure.

This study suggests that an immune response to trichohyalin and keratin 16 may contribute to the pathogenesis of alopecia areata.

This study found that keratin K17 is induced in the suprabasal layer of psoriatic scalp epidermis during epidermal hyperproliferation, suggesting it is not specific to hair follicles.

In this study, expressing human K16 in the epidermis of K14 null mice prevented early skin blistering but led to age-related anomalies, indicating K16 and K14 have distinct roles despite their sequence similarity.

This study suggests that the HCR risk allele within the PSORS1 locus may contribute to psoriasis susceptibility by altering gene expression related to skin structure and differentiation, although these changes alone might not result in clinical symptoms.

Basal cell carcinoma shows keratin patterns similar to undifferentiated hair follicle cells.

This study found that the unique functions of keratin 16 are likely determined by its tail domain, challenging the previous hypothesis about the role of the helix 1B subdomain.

This study found that high levels of human cytokeratin 16 expression in transgenic mice lead to skin lesions and altered keratinocyte structure, suggesting potential implications for human skin disorders and wound healing.

This review discusses recent advances in the genetic understanding of inherited hair and nail disorders and reports no new clinical results.

This study suggests that pilomatricoma can differentiate towards various hair follicle structures, including hair matrix, hair cortex, follicular infundibulum, outer root sheath, and hair bulge.

This study identified various cell types in the canine claw, showing complex mechanisms of cellular differentiation similar to mammalian hair and human nails.

This study suggests that impaired Nrf2 signaling and its relationship with keratin 16 may contribute to follicular hyperkeratinization and occlusion in hidradenitis suppurativa, opening new therapeutic avenues.

This study observed that heavy draft horses with verrucous pastern dermatitis showed significantly increased expression of keratins K6 and K16, suggesting a phylogenetically conserved keratin expression pattern in response to skin inflammation and proliferation.

This study found that keratin expression patterns vary within nail unit structures, with the nail matrix uniquely expressing the acidic hair-type keratin Ha1.

This study found that trichohyalin is expressed in various normal and pathological epithelia beyond hair follicle cells, where it is uniquely associated with filaggrin, suggesting a specific role in aggregating K6/K16-containing intermediate filaments.

This study suggests that onychopapilloma may originate from the nail bed rather than the nail matrix, with nail bed-related keratins and HK31 potentially serving as diagnostic markers.

This study demonstrates that overexpression of K16 in transgenic mice disrupts normal keratinization, leading to hyperkeratosis, acanthosis, and alterations in the skin's epithelial cells.

This study found that among the two highly homologous K16 genes on chromosome 17, only one produced a functional protein due to stronger promoter activity.

Human melanocytes in skin and hair follicles don't express keratin 16 or 6 naturally.

This study found that in mice, deleting the keratin 10 gene enhances sebocyte differentiation and increases secretion of sebum and certain lipids without affecting proliferation-associated keratins.

The compound (NH4)2Mn0.17Cu0.83Cl4.2H₂O has a specific structure, shows weak magnetism at low temperatures, and undergoes phase changes at high temperatures.

Healthy aging can be promoted through physical activity, lifestyle changes, and certain treatments.

This abstract reviews the role of the human KRT 16 wild-type allele in skin and hair development and its association with certain genetic skin disorders, without presenting new findings.