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This study developed microneedles combining insulin-like growth factor-1 and type XVII collagen, showing more effective hair regeneration and reduced inflammation compared to minoxidil in a mouse model of androgenetic alopecia.

This study found that recombinant human type XVII collagen (rhCOL17A1) promotes hair growth by activating the Wnt/β-catenin and SHH/GLI signaling pathways and increasing type XVII collagen expression, with significant effects observed in both cell and mouse models.

This study found that a microneedle patch with recombinant collagen XVII significantly improved hair coverage, follicle density, and angiogenesis in an androgenic alopecia mouse model, showing potential as a novel therapeutic strategy alongside established treatments like minoxidil.

This study found that COL17 plays a key role in regulating epidermal keratinocyte differentiation and proliferation, influencing the expression of differentiation markers and cellular growth in specific conditions.

In this study, researchers identified a recurrent nonsense mutation, c.409C>T (p.Arg137*), in the COL7A1 gene through whole exome sequencing in a family with autosomal recessive dystrophic epidermolysis bullosa, demonstrating the importance of this method for diagnosing genetically complex conditions.

In this study, researchers identified a collagen fragment, sample-1707, expressed in E. coli, which forms nanofibers and promotes blood clotting, osteoblast differentiation, and skin cell regeneration, making it a promising biomaterial for skin care, with a large-scale production yield of 600 mg/L.

This study found that COL17 deficiency in neonatal mice causes abnormal skin cell proliferation due to disrupted Wnt signaling, while replenishing or overexpressing COL17 can reverse this effect in both neonatal and aged skin.

COL17A1 is crucial for preventing hair graying and loss by supporting hair and pigment stem cells.

This study indicates that COL17A1 plays a crucial role in the differentiation process of hair-follicle-associated pluripotent stem cells.

This article discusses junctional epidermolysis bullosa caused by COL17 deficiency, noting a lack of experimental therapies and the impact of nonsense mutations, but it reports no new clinical results.

This letter to the editor presents a case of non-Herlitz junctional epidermolysis bullosa associated with a COL17A1 mutation and reports no new clinical findings.

This review explores the physiological roles of collagen XVII in the epidermis, its involvement in stem cell maintenance, and its connections with signaling pathways, but it reports no new results.

This study reported the creation of isogenic immortalized COL7A1-deficient keratinocyte lines, providing a model for researching Recessive Dystrophic Epidermolysis Bullosa biology and potential therapies.

In this study, Tanimura et al. reported that loss of collagen XVII in mice leads to hair loss and pigmentation defects, potentially due to impaired TGF-beta signaling affecting melanocyte stem cell maintenance.

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.

Loss of COL17A1 causes hair follicle stem cells to age and leads to hair loss.

This study found that mutations in exon 3 of the hr gene are strongly associated with congenital hypotrichosis in Valle del Belice sheep, suggesting a potential genetic link to the disorder.

This study found that apocynin restored COL17A1 expression in human keratinocytes and reduced UVB-induced cellular senescence, DNA damage, and cell cycle arrest.

CRISPR/Cas9 and prime editing can potentially fix skin disorder genes safely and effectively.

This study identified a cluster of genes on chromosome 17 related to hair keratin-associated proteins, including 37 genes forming seven multigene families, localized in the hair shaft's upper cortex.

This study reports the first cases of recessive KRT17-related pachyonychia congenita involving all ectodermal derivatives in seven members of two consanguineous Pakistani families.

This study developed new immortalized keratinocyte cell lines lacking COL7A1 using CRISPR/Cas9 technology, providing a valuable model to explore the biology and treatment options for recessive dystrophic epidermolysis bullosa.

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 found that in mice, type XVII collagen is essential for controlling epidermal cell proliferation through Wnt signaling, with its deficiency or altered distribution leading to skin hyperproliferation and aging-like changes.

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

The researchers investigated a Maine Coon cat with suspected classical Ehlers-Danlos Syndrome and discovered a heterozygous deletion in the COL5A1 gene, underscoring the value of whole-genome sequencing for precise veterinary diagnostics.