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Targeting the PIEZO1 and MLCK axis may offer a new treatment for hair loss.

Mice with too much Claudin-6 have skin barrier problems and abnormal hair growth.

Blocking CXXC5 speeds up diabetic wound healing by improving blood vessel growth and skin repair.

Studying rare genetic disorders can help us understand and treat common diseases better.

Scientists created a cell model to study and find treatments for a skin disease called RDEB.

The Wave complex controls skin growth by suppressing certain signals.

Phospholipase C-δ1 is crucial for normal hair development.

Desmosomal adhesion is essential for healthy skin structure and function.

Certain proteins help nerve cells branch, and other findings relate to cancer, stem cell behavior, and cell division.

Basonuclin is crucial for hair follicle development and cycling in mice.

Type VII collagen absence helps skin development by allowing tissue remodeling.

Cantú syndrome is caused by mutations in the ABCC9 gene.

Collagen XVII and CD151 affect cell movement, with CD151 inhibiting migration when bound to integrins.

A girl with excessive hair growth had a genetic change on chromosome 17 that reduced the activity of two genes linked to hair growth.

Basonuclin helps identify and track hair follicle development and cycling in mice.

Weak cell junctions disrupt hair follicle stem cell rest.

Mutations at Val-889 and Arg-752 disrupt key interactions in androgen receptor dimerization.

PolyQ repeats in neural proteins evolve together, affecting brain function and disease.

SCUBE3 is a potential target for cancer and alopecia treatment but is challenging to target due to its varied roles.

Blocking CISD1 reduces hearing loss from cisplatin in mice.

Sox13 is a new marker for early hair follicle development and differentiation.

Targeting SOX proteins may improve cancer treatment by restoring immune function.

The protein FLCN is involved in cellular cleanup and is regulated by ULK1.

KIF18B is important for correctly positioning cell division machinery in skin cells, affecting hair follicle development.

Noggin overexpression delays eyelid opening by affecting cell death and skin cell development.