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Mutations in specific keratin genes cause improper hair structure in mice due to faulty keratin protein assembly.

Cysteines in wool fibers are accessible and form important disulfide bonds.

Recombinant keratins can form useful structures for medical applications, overcoming natural keratin limitations.

Keratin structure changes during keratinization, but the exact model remains uncertain.

Keratin proteins in epithelial cells are dynamic and crucial for cell processes and disease understanding.

ERK activation spreads between cells in mouse skin, linked to cell division and influenced by TPA and EGF receptors.

Disulfide bonds are crucial for hair structure during keratinization.

Cats with abnormal hair had DSG4 gene changes causing hair problems.

Disrupting β-catenin signaling in certain cells causes anorectal malformations.

CTHRC1 is essential for healing and preventing heart rupture after a heart attack.

Oxidation changes the structure of hair protein filaments, causing them to compact and rearrange.

Lack of Cisd2 disrupts calcium balance in cells, leading to poorly functioning neutrophils.

Calcium signaling in skin cells is crucial for communication and regeneration.

Human hair keratins K85 and K35 create unique filament patterns important for early hair formation.

G2 stem cells control calcium signaling for skin regeneration.

Disrupting the Tsc2 gene in certain cells leads to thicker skin, larger hair, and changes in hair growth signaling, which can be partly reversed with specific treatment.

A woman with a unique syndrome similar to TRPS has a genetic change near the TRPS1 gene, affecting its regulation.

Cross-linked proteins help maintain the structure of hair, feathers, and hagfish teeth.

Quiescent cells have increased mitochondrial activity and ECM gene expression, but reduced glycolysis.

Age-related hair curvature increases due to internal structural changes from grooming.

Folliculin deficiency causes problems with cell division and positioning due to disrupted RhoA signaling and interaction with p0071.

The connective tissue around hair follicles changes structure throughout the hair cycle.

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

Spiny mice have a unique skin structure that helps them heal and regenerate quickly.

Disrupting YAP signaling in skin cells leads to scar-free healing directed by specific cell signals.

The Glu413Lys mutation in keratin affects hair stability, while Glu413Asp does not.

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

Lack of functional CYLD in mice leads to early aging and cancer.

Keratin 17 is crucial for cell growth in wound healing by aiding protein synthesis.