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This study suggests that dermal Vδ1+ T-cells in human skin can promote alopecia areata by interacting with stressed hair follicles, potentially providing a target for new treatments.

This study identified complex regulatory elements and interactions involving the Hr gene and HR protein that are crucial for hair follicle formation and cycling in mammals.

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.

TRH in hair follicles can influence hair color by increasing melanin.

This study found that CTHRC1 is crucial for sweat gland function and vascular network integrity in mice, and its administration improved sweat gland performance by reconstructing nearby blood vessels.

TGF-β1 increases androgen receptor activity in hair loss, but Hic-5/ARA55 can counter this effect.

This study on mice found that activating TRPML channels with MLSA1 promoted hair regeneration, accelerated hair cycle transition, and influenced human dermal papilla cells to secrete hair growth promoting factors while reducing hair growth inhibitors and oxidative damage.

Trichohyalin in hair can trigger immune attacks in alopecia areata.

Hhip-Cre effectively targets dermal papilla cells for gene manipulation in hair biology.

This study identified a distinct gene near the hairless locus on chromosome 8p that is responsible for hereditary Marie Unna type hypotrichosis in a German family.

This study suggests that abnormal hair cycles in Hr mutant mice may be caused by HR protein overexpression, which down-regulates miR-31 and increases Tgf-β2 expression.

This study identified genetic variants in the Trichohyalin gene that account for approximately 6% of the variance in hair morphology among Australians of European descent.

In this study, TLR1 gene polymorphism rs4833095 was significantly associated with increased susceptibility to alopecia areata in the Korean population.

This study found a novel nonsynonymous genetic variant in the hHb1 gene of a family with monilethrix, which differs from ten previously reported pathogenic mutations.

In this study, the CYP 21A2 gene p.V281L mutation was associated with an increased susceptibility to familial frontal fibrosing alopecia, suggesting an antigen-driven mechanism linked to certain human leukocyte antigen haplotypes.

This study found that TRPV1 activation in human scalp hair follicles inhibited hair shaft elongation, suppressed proliferation, and induced apoptosis, suggesting TRPV1 as a potential target for managing hair growth and epithelial disorders.

This study found that hHbl gene expression is localized in the cortical cells of the human hair shaft and is notably high in pilomatricoma cells transitioning to hair shaft keratinocytes.

TCHHL1 is a protein important for hair growth, found in hair follicles.

This case report highlights that a patient with resistance to thyroid hormone was misdiagnosed as having Graves’ disease, leading to unnecessary radioactive iodine treatment.

This study identified a specific genetic variant in the CCHCR1 gene that may contribute to alopecia areata through impaired keratinization, suggesting an alternative mechanism beyond autoimmune causes.

This study found that transfecting hair follicle stem cells with a PEI-DNA complex expressing hTERT stimulated hair growth in rats by inducing follicle neogenesis and promoting the anagen phase.

This study found that mutant cells in hair follicles can be tolerated or eliminated by surrounding normal tissue, suggesting the potential for wild-type cells to counteract oncogenic mutations.

This study suggests that a position effect disrupting TRPS1 expression may be linked to hypertrichosis in both Ambras syndrome in humans and a similar phenotype in Koa mice.

TR3 is mainly found in hair follicle stem cells and may be involved in hair loss.

Researchers found a new mutation in the HR gene causing hair loss and skin bumps in a Pakistani family.

This study found that normal human epidermis expresses TSH and may be an indirect target of TSH signaling, with expression regulated by endocrine controls of the hypothalamic-pituitary-thyroid axis.

This study identified molecular elements controlling the expression and stabilization of THH protein in hair follicle cells, revealing key mechanisms that support hair shaft development in mice.

This study reports a mutation in the U2HR gene causing Marie Unna hereditary hypotrichosis in a Turkish family and notes eyebrow loss as a diagnostic clue.

Thyroid-stimulating hormone affects hair follicles but doesn't change hair growth or color.