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Spiny mice regenerate skin better than laboratory mice due to larger hair bulges, more stem cells, and different collagen ratios.

Overexpressing ovine β-catenin in mice skin increases hair follicle density and growth.

Removing β-catenin in certain stem cells causes hair whitening and pigmentation issues.

Damaged hair follicles make mice more prone to skin inflammation and skin cancer after UV exposure.

Mouse and human keratin 16 can both form filaments, with differences likely due to the tail domain, not the helical domain.

Researchers developed a mouse model that successfully mimics the bladder damage seen in humans after radiation therapy.

Alopecia areata in these mice is inherited, more common in young females, and can be treated with triamcinolone acetonide.

A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.

Krt15+ cells in mice can resist radiation, regenerate tissue, and start tumors, suggesting new cancer treatment targets.

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

Male-to-female skin grafts in mice are rejected due to sex-linked antigens.

Deleting the Hoxc13 gene in frogs shows its crucial role in developing skin structures similar to hair.

HT-scCAT-seq helps understand gene regulation in embryonic skin development.

The African spiny mouse can fully regenerate its muscle without scarring, unlike the common house mouse.

Keratin 16 delays skin maturation and affects skin and hair development in mice.

Ovariectomy in mice affects hair growth and skin thickness, suggesting potential for obesity treatment research.

Adult spiny mice recover better from heart attacks than common lab mice.

Human basal cell carcinomas and squamous cell carcinomas have unique gene expression patterns not fully mirrored in mouse models.

The research cloned keratin 7 genes from humans, mice, and marsupials, found similarities between human and mouse genes, and discovered new areas of K7 expression in mice.

EPI-NCSCs from hair follicles may help treat brain development issues in mice.

A specific gene region can control targeted and responsive gene expression in mice, useful for skin disorder treatments.

MRL/MpJ mice's skin wounds heal with scars, unlike their ear wounds which can regenerate.

The transgene likely activated an oncogene or interrupted a tumor suppressor gene, causing melanoma in mice.

Hair follicles in C57BL/6 mice develop rapidly from late embryonic stages to shortly after birth, with key growth and regeneration phases identified.

Rabbits lacking the Hoxc13 gene show similar hair and skin issues to humans with ECTD-9, making them good for research on this condition.

Oncogenic melanocyte stem cells can develop into melanoma similar to human cases.

The method effectively induces skin cancer in mice for studying tumor development.

Over-expression of Sp2 can lead to cancer by preventing proper stem cell differentiation.

Hairless mice lose hair by 3-4 weeks, develop thicker, folded skin, and show pigmentation differences.

A new method can detect mutations in mice by observing changes in hair follicle cells.