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Overexpression of sPLA2-IIA in mouse skin reduces hair stem cells and increases cell differentiation through JNK/c-Jun pathway activation.

Human cells in plasma-derived gels can potentially mimic hair follicle environments, improving hair regeneration therapies.

The Ovol2-Zeb1 circuit is crucial for skin healing and hair growth by guiding cell movement and growth.

Changes in keratin affect skin health and can lead to skin disorders like blistering diseases and psoriasis.

Blocking both main energy pathways can stop hair follicle stem cell-induced skin cancer growth.

The Sonic hedgehog pathway is crucial for new hair growth during mouse skin healing.

Skin can heal wounds without hair follicle stem cells, but it takes a bit longer.

Plet-1 protein helps hair follicle cells move and stick to tissues.

Skin cells and certain hair follicle areas produce hemoglobin, which may help protect against oxidative stress like UV damage.

Loss of a specific protein in skin cells causes symptoms similar to psoriasis.

Notch signaling is essential for healthy skin and hair follicle maintenance.

Human skin xenografting could improve our understanding of skin development, renewal, and healing.

Gab1 protein is crucial for hair growth and stem cell renewal, and Mapk signaling helps maintain these processes.

Mice without certain skin proteins had abnormal skin and hair development.

New treatments targeting specific genes show promise for treating keratin disorders.

The 190-kbp domain contains all human type I hair keratin genes, showing their organization and evolution.

Overexpressing the mineralocorticoid receptor in mouse skin causes skin thinning, early skin barrier development, eye issues, and hair loss.

BMP6 and Wnt10b control whether hair follicles are resting or growing.

GasderminA3 is important for normal hair cycle transitions by controlling Wnt signaling.

Increasing ABC transporters in hair follicles may prevent chemotherapy-induced hair loss.

New treatments for hair loss are being developed using molecular biology.

The telogen phase of hair growth is active and important for preparing hair follicles for regeneration, not just a resting stage.

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

The document concludes that mouse models are crucial for studying hair biology and that all mutant mice may have hair growth abnormalities that require detailed analysis to identify.

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

Lower SMAD2/3 activation predicts more severe skin cancer.

Intermediate filaments are crucial for cell differentiation and stem cell function.

The conclusion is that accurately replicating the complexity of the extracellular matrix in the lab is crucial for creating realistic human tissue models.

Only a few hair-specific keratins are linked to inherited hair disorders.

Neuregulin3 affects cell development in the skin and mammary glands.