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This study suggests that eruptive vellus hair cysts often have atypical pathological changes and likely originate from the infrainfundibulum and sebaceous duct based on keratin expression analysis.

This study found that a newly identified gene, mK17n, may explain the lack of nail issues in mK17 null mice by compensating for mK17's function in the nail bed.

This study found that ectopic expression of the lymphoid-enhancer factor can induce K17 protein in the skin, suggesting a link between skin development and wound repair processes in mice.

This review discusses the recent advancements in understanding how keratins influence cytoarchitecture, cell dynamics, and disease processes but reports no new clinical results; the authors highlight its roles in development and diseases like cancer.

This study found that mutations in the K17 gene underlie both pachyonychia congenita type 2 and steatocystoma multiplex phenotypes, regardless of the specific mutation involved.

This study found that keratin 17 and TNFα play interdependent roles in regulating hair follicle cycling, with TNFα required for the anagen–catagen transition and its ablation partially rescuing hair cycling defects in K17-null mice.

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 this study, researchers identified the ventral matrix as the primary source of nail plate formation, while the dorsal portion is generated by the apical matrix.

Keratin 17 is important for hair and nail structure and affects pachyonychia congenita symptoms.

This study found that keratin genes in the epidermis of aquatic mammals like cetaceans have evolved to replace stress-inducible keratins K1 and K10 with constitutively expressed K6 and K17, suggesting adaptations to their environment.

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.

This review discusses the mechanisms of keratin 17 regulation in diseases such as psoriasis and cancers but presents no new experimental findings, calling for further exploration of anti-K17 therapies.

This study showed that a 2-kilobase upstream region of the mouse keratin 17 gene enables targeted GFP expression in major epithelial appendages of transgenic mice, indicating sonic hedgehog's involvement in its regulation.

This study demonstrated that hair follicle bulge stem cells can form epidermis in a tissue-engineered skin model, highlighting the significance of K5/K17 filaments in slow-cycling stem cell subsets.

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 serine 44 in the N-terminal head domain of keratin 17 is phosphorylated in response to various stimuli affecting skin keratinocyte growth, linking K17 up-regulation with growth and stress responses in skin epithelium.

This study reports that eccrine sweat glands in mice predominantly develop on the footpads, offering a reference for skin research involving genetically engineered mice.

This study found that in psoriasis patients, the K17 protein probably functions as an autoantigen, with the HLA-Cw*06:02 risk genotype strongly linked to the T cell response size.

This study found that while malignant pilomatricomas maintain some keratin expression patterns seen in benign counterparts, they notably express additional epithelial keratins, potentially influencing tumor calcification.

This study found that in vivo confocal scanning laser microscopy accurately quantifies neogenic hair follicles in mice, producing results similar to histology while avoiding fixation artifacts.

This study found that AIRE, a usually nuclear protein, is expressed in the cytoplasm of human epidermal and follicular keratinocytes and associates with the intermediate filament protein cytokeratin 17, potentially impacting ectodermal abnormalities in APECED syndrome.

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

This study found that hair follicle-specific keratins can form different structural assemblies depending on ionic conditions, with hair cortex keratins requiring physiological salt conditions to form intermediate filaments.

This study found that TRH modulates specific keratins in human scalp tissue, suggesting its potential influence on hair growth and the need for further exploration of neuroendocrine controls in keratin expression.

In this study, injecting chimeric RNA–DNA oligonucleotides into mice skin caused a temporary mutation in keratin 17, altering hair morphology, but the mutation was transient due to genetic compensation or cell replacement.

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

In this study, researchers found that K17−/− mice suffered more severe hair follicle damage but showed reduced epidermal inflammation after ionizing radiation, with K17's absence leading to aberrant cell cycle progression due to altered p53 genome binding and reduced B-Myb degradation.

This study suggests that the expression patterns of keratin and filaggrin indicate milia may originate from the outermost cells of the hair bulge in the outer root sheath.