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This article reviews phenotypic variability linked to WNT10A nonsense mutations and does not present new research findings.

This study explains that while trichothiodystrophy and xeroderma pigmentosum share genetic defects, TTD patients primarily exhibit issues in transcription initiation, not the increased skin cancer risk seen in XP.

In this study, the presence of the HPV11-E2 protein in transgenic mice was found to increase and vary the expression of a reporter gene in hair follicle bulge regions.

This study found that Wnt10b promotes melanocyte maturation and pigmentation in the hair bulbs of mice by activating canonical Wnt signaling.

This study developed a DPC cell line by introducing mutant CDK4, Cyclin D1, and TERT, making it a promising tool to study downstream signaling pathways activated by testosterone in androgenetic alopecia.

This study found that the K6/ODC transgenic mouse model is highly sensitive to identifying genotoxic carcinogens, showing 100% concordance with traditional rodent bioassays.

Wnt-10b helps skin cells and hair grow.

This study found that in AGA, the risk allele at locus 2q35 alters WNT10A expression through EBF1, suggesting a potential androgen-dependent regulatory mechanism.

This study indicates that MAGE-11 modulates androgen receptor transcriptional activity through F-box interactions, independent of the activation function 2 pathway, revealing a novel mechanism for androgen receptor regulation.

This study found that disrupting Adam10 in the epidermis led to severe skin and multi-organ abnormalities, implicating Adam10 as crucial for proper Notch signaling and skin maintenance.

In this study, TCDD administered to male rats down-regulated EGF receptor in liver plasma membranes and increased protein kinase activity, suggesting EGF receptor–mediated toxicological effects.

TCDD changes skin gene expression and may harm skin health.

This study found that dimethylarsinic acid significantly accelerates skin tumor development in hair follicle-targeted K6/ODC transgenic mice.

In this study, researchers identified a new dominant mutation in Hairless mice, called Pied, resulting from a deletion in the Adam10 gene, which causes freckle-like skin pigmentation by inhibiting melanocyte expansion.

Wnt-10b helps skin cells develop into hair-related structures.

In this study, dutasteride treatment in retinitis pigmentosa mice increased photoreceptor survival and reduced glial activation, suggesting it may offer a neuroprotective effect.

This review discusses the association between WNT10A gene variants and various ectodermal disorders, highlighting their clinical relevance in dermatology and dentistry, but reports no new findings.

This study found that the 11R-No. 10 peptide, delivered transdermally, significantly inhibited melanogenesis and produced a whitening effect in a UV-induced sun-tanning guinea pig model without cytotoxicity.

Stimulating OR10J1 can promote hair growth and may help treat hair loss.

This review highlights the role of the glycoprotein WNT10A in human tissue and organ development, exploring its genetic structure, expression, and association with disorders like ectodermal dysplasia and pathological conditions such as fibrosis and cancer.

In this study, researchers found that TCDD exposure accelerated differentiation and altered gene expression in human epidermal cells, indicating the epidermal barrier as a target of TCDD-activated AHR.

This study identified a heterozygous de novo mutation in the ODC1 gene causing a new disorder characterized by overgrowth and developmental delay, and suggests that DFMO treatment may help manage elevated ODC activity and putrescine levels.

A new change in the WNT10A gene caused a condition leading to short hair growth in a Chinese family.

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.

This study found that TCDD significantly reduced EGF receptor binding in various animal models, linked to toxic symptoms like weight loss and developmental delays, with receptor phosphorylation persisting several days.

This article reviews the genetic and phenotypic characteristics of Trichothiodystrophy and discusses the associated DNA repair defects, but does not report new clinical findings.

In this study, engineered mice with a mutation similar to that in Olmsted syndrome showed progressive hair loss due to impaired inner root sheath keratinocyte differentiation and stem cell exhaustion.

This study identified several genes regulated by dihydrotestosterone in an SV40T-transformed human dermal papilla cell line, which may play a role in androgen-mediated hair growth regulation.