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miR-22, a type of microRNA, controls hair growth and its overproduction can cause hair loss, while its absence can speed up hair growth.

Runx1 controls fat-related genes important for normal and cancer cell growth, affecting skin and hair cell behavior.

Laminin 332 is essential for normal skin cell behavior and structure.

Lipocalin-Type Prostaglandin D2 Synthase (L-PGDS) is a protein that plays many roles in the body, including sleep regulation, pain management, food intake, and protection against harmful substances. It also affects fat metabolism, glucose intolerance, cell maturation, and is involved in various diseases like diabetes, cancer, and arthritis. It can influence sex organ development and embryonic cell differentiation, and its levels can be used as a diagnostic marker for certain conditions.

The right amount of retinoic acid is essential for normal hair growth and development.

Mutant mice help researchers understand hair growth and related genetic factors.

Aging mice have slower hair regeneration due to changes in signal balance, but the environment, not stem cell loss, controls this, suggesting treatments could focus on environmental factors.

Human hair follicles can regenerate and recover after severe injury by going through a brief abnormal resting phase before growing again.

Mice lacking a key DNA methylation enzyme in skin cells have a lower chance of activating stem cells necessary for hair growth, leading to progressive hair loss.

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

Blocking Wnt signaling in young mice causes thymus shrinkage and cell loss, but recovery is possible when the block is removed.

Blocking CRF-R1 can reduce alcohol intake in stressed mice.

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

Eating grape powder may reduce the severity of skin allergy symptoms.

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

Deleting the CRIF1 gene in mice disrupts skin and hair formation, certain proteins affect hair growth, a new compound may improve skin and hair health, blood cell-derived stem cells can create skin-like structures, and hair follicle stem cells come from embryonic cells needing specific signals for development.

A protein from certain immune cells is key for new hair growth after skin injury in mice.

Mice can correct hair follicle orientation without certain genes, but proper overall alignment needs those genes.

Mice with more Flightless I protein grew back their claws better after amputation.

The Itpr3 gene causes a specific hair pattern in mice.

Dermal EZH2 controls skin cell growth and differentiation in mice.

Disrupting Notch signaling in blood vessels increases scarring during wound healing in mice.

Mitochondrial problems in tooth cells lead to bad enamel and dentin development in mice.

Some wound-healing cells can turn into fat cells around new hair growth in mice.

Deleting the p63 gene in certain cells causes problems in thymus development and severe hair loss in mice.

Mutations in the HEPHL1 gene cause abnormal hair and cognitive issues.

Epithelial stem cells are crucial for tissue renewal and repair, and understanding them could improve treatments for damage and cancer.

The Gsdma3 gene is essential for normal hair development in mice.

A special environment is needed to fully activate sleeping stem cells.

The method quickly analyzes hair growth genes and shows that blocking Smo in skin cells stops hair growth.