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This study demonstrated that multipotent stem cells in adult mice whisker follicles migrate to produce whisker growth, and that this process requires precise control of stem cell trafficking.

NFATc1 controls hair stem cell activity, affecting hair growth and could be a target for hair loss treatments.

This study found that transient activation of c-Myc in transgenic mice stimulates keratinocyte proliferation and sebocyte differentiation, affecting normal epidermal and hair follicle development.

Inhibiting Bmp signaling disrupts hair growth and differentiation.

This study found that mitochondrial reactive oxygen species are crucial for normal epidermal differentiation and hair follicle growth, as demonstrated by impaired development in mice lacking these signals due to a keratinocyte-specific TFAM deficiency.

This study found that in the absence of hair follicles, cutaneous wounds in mice showed delayed reepithelialization but eventually achieved normal wound closure after expanding the activated epidermis region.

In this study, researchers found that quiescent stem cells resist immune attack due to downregulated antigen presentation, which may help explain the immune evasion of early cancer-initiating cells.

This study found that COL17 deficiency in neonatal mice causes abnormal skin cell proliferation due to disrupted Wnt signaling, while replenishing or overexpressing COL17 can reverse this effect in both neonatal and aged skin.

Phospholipase Cδ1 is crucial for normal skin and hair development.

This study found that prolonged Nrf2 activation in mouse keratinocytes led to enlarged sebaceous glands, hair loss, and cysts, suggesting a role for Nrf2 in conditions like MADISH.

In this study, researchers found that Notch signaling is crucial for late-stage epidermal differentiation and postnatal hair cycle homeostasis by regulating hair follicle stem cell proliferation and differentiation.

Cathepsin L deficiency causes hair and skin issues in mice.

This study found that the absence of Sostdc1 in mice alters mammary gland and hair follicle development, particularly by increasing vibrissae numbers and causing unusual nipple-like structures.

This study found that inactivating CerS4 in mice led to hair follicle stem cell exhaustion and hair loss, indicating its role in regulating hair regeneration through ceramide composition and signaling pathways.

This study found that the absence of Ctip2 in epidermal keratinocytes led to impaired wound healing in mice, affecting cell migration, proliferation, and hair follicle stem cell maintenance.

In this study, transgenic mice expressing Msx-2 developed flaky skin with hyperproliferation and misalignment in epidermal cells, suggesting Msx-2 plays a role in skin and appendage growth control.

This study reports that the autotaxin–LPA–LPA3 signaling pathway at the embryo-epithelial boundary plays a critical role in decidualization by up-regulating HB-EGF and COX-2 in the uterine epithelium.

This study demonstrated that cultured epidermal stem cells and skin-derived precursors can regenerate functional hair follicles and sebaceous glands in both mice and adult humans, suggesting potential for bioengineered skin substitutes.

In this study, researchers found that contrary to expectations, keratin 10 domains did not reduce cell proliferation and instead increased tumor development in genetically modified mice.

In this study, transgenic mice expressing a truncated form of latent transforming growth factor-β-binding protein exhibited altered hair cycles due to increased active transforming growth factor-β, impacting keratinocyte proliferation and hair cycle phases.

This study found that in neonatal mice, the absence of the NG2 proteoglycan leads to reduced epidermal thickness and delayed subcutis thickening due to impaired proliferation and adipocyte deficiencies.

This study found that extracellular vesicles from stimulated human dermal fibroblasts enhanced hair follicle growth ex vivo by activating dermal papilla cells and involving the Norrin and β-catenin pathways.

This study found that canine bulge-derived keratinocytes are highly proliferative and can reconstitute pilosebaceous structures, indicating their potential utility in studying human stem cell biology and hair disorders.

This study found that knocking out the transactivation domain of Miz1 in mouse keratinocytes disrupted hair follicle orientation, caused irregular pigmentation, and increased keratinocyte proliferation, indicating Miz1's role in hair follicle development and morphogenesis.

In this study, knockout of B-raf and C-raf genes in mice showed they are not needed for early melanocyte development, but are crucial for maintaining melanocyte stem cells, as evidenced by hair graying due to stem cell depletion.

This study observed that epidermal-specific deletion of aPKCλ in mice disrupts hair follicle stem cell quiescence, leading to altered hair follicle cycling and skin anomalies.

This study suggests that impaired VDR signaling in mice leads to dysregulated Ddit4 expression, impacting hair cycle progression and wound healing.

This study found that the loss of Msx2 in knockout mice led to phenotypes similar to Peters anomaly and microphthalmia, suggesting that MSX2 plays a critical role in anterior segment development of the eye.

This study found that MYC and FGF pathways are crucial for hair cell regeneration in chick and zebrafish models, suggesting potential targets for promoting hair cell regeneration in mammals.

This study found that transgenic mice expressing a mutant CYLD protein lacking deubiquitinase function showed signs of premature aging and spontaneous tumor development, likely due to over-activation of specific molecular pathways and chronic inflammation.