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Scientists made a mouse that shows how a specific protein in the skin changes and affects hair growth and shape.

M-CSF-stimulated myeloid cells can cause alopecia areata in mice.

BRG1 is essential for skin cells to move and heal wounds properly.

Some children in Malaysia with symptoms have either profound or partial biotinidase deficiency, and early testing and treatment are important.

MILL molecules are unique immune proteins in mice that don't need TAP to appear on cell surfaces.

Children with alopecia areata, especially with Down syndrome or thyroid issues, should be screened for thyroid disease.

Both HLA-B and MICA are independently linked to alopecia areata.

BcFLA1 protein is crucial for root hair growth in response to low phosphate in Brassica carinata.

HtrA2 activity is crucial for normal hair growth by regulating fat cell development.

The we/we wal/wal mice have defects in hair growth and skin layer formation, causing hair loss, useful for understanding alopecia.

Higher CRBP1 levels are linked to more severe alopecia areata.

Mutations in the ACTB gene cause Becker’s nevi and may lead to muscle issues in Becker’s nevus syndrome.

Non-coding RNA boosts retinoic acid production and signaling, aiding regeneration.

A man with alopecia universalis regrew hair temporarily after a bone treatment.

Tmem30b is essential for hearing by maintaining hair cell structure in the ear.

BST2 is a key marker for hair loss disease alopecia areata.

BST2 is highly expressed in certain immune cells in alopecia areata, suggesting a role in the disease.

Alkaline ceramidase 1 is crucial for healthy skin and energy balance.

Brg1 is crucial for keeping hair follicle stem cells and repairing skin, working with the Sonic Hedgehog pathway to promote hair growth.

Dicer is crucial for hair growth in mice.

LTBP1 is a key regulator in diseases and a potential target for new treatments.

AP-1 and TGFß work together to drive resistance in basal cell carcinoma, suggesting new treatment options.

Four new cases of Bachmann-Bupp syndrome suggest potential for targeted treatment.

Deleting the MAD2L1 gene is tolerated in certain mouse cancer models.

High BMP signaling disrupts hair growth and balance in skin cells.

Genetic mutation and carcinogen treatment are both needed for skin cancer to develop in these specific mice.

ATP-dependent chromatin remodeling is crucial for skin development and stem cell function.

Targeting NMMHC IIA may help treat blood-brain barrier damage.

Sex steroids affect the MafB gene differently in male and female hamsters.

BIK1 gene helps plants resist some pathogens but makes them more vulnerable to others.