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Mice with extra PKCδ resist chemical-induced skin cancer but not UV-induced.

XEDAR triggers a specific signaling pathway in cells.

Super-enhancers control CD25 expression in specific cell types, affecting immune function.

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

TCDD speeds up skin barrier formation by increasing certain gene expressions.

PI3Kδ inhibition may effectively treat cutaneous chronic graft-versus-host disease.

Activating PKCα in skin causes cell death and inflammation through different pathways.

The DMI3 gene is essential for nodule development and symbiosis in certain plants.

CD271 is crucial for maintaining healthy skin and preventing inflammation.

Activating c-Myc in skin causes rapid cell growth and changes, but these effects are reversible.

Late diagnosis of congenital adrenal hyperplasia can greatly affect physical development, gender identity, and sexual health.

The ID2 gene can help distinguish between sensitizers and irritants in skin cells.

CENPV, a new partner of CYLD, helps regulate ciliary acetylated tubulin and is overexpressed in certain skin tumors.

The CD44-CD49d complex boosts T cell activation and survival in autoimmune disease.

Toluene diisocyanate exposure can cause immune sensitization by interacting with proteins in hair follicles and sebaceous glands.

TCDD reduces EGF receptors in the liver, affecting growth and development.

Cyclic ADP-ribose helps regulate calcium and signals that promote hair growth in hair follicle cells.

Activating β-catenin in certain skin cells speeds up hair growth in mice.

TPA strongly increases ODC activity in certain skin cells, potentially aiding tumor growth.

TCDD changes skin cell growth and keratin production in mice.

CaM7 and CNGC14 interaction controls root hair growth in Arabidopsis.

CCDC22 and CCDC93 are essential for root and root hair growth in Arabidopsis.

CREB, a protein that can promote cancer traits, is controlled by β-catenin in skin cancer cells.

Blocking certain immune signals can reduce skin damage from radiation therapy.

Skin tumors with CYLD cutaneous syndrome show more NF-κB activity and less organized collagen.

Certain interactions help prepare the androgen receptor for pairing and activation, which is important for its role in development and disease.

The vitamin D receptor can work without its usual activating molecule.

Boosting β-catenin signaling in certain skin cells can enhance hair growth.