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β-catenin affects hair growth and can lead to tumors, needing more research for better understanding.

In this study, the researchers observed that transfecting hair follicle cells with an amino-terminal truncated beta-catenin gene significantly increased cell proliferation, potentially by enhancing c-myc gene expression.

This review examines beta-catenin's role in stem cell renewal, lineage selection, and tumor formation in the epidermis and reports no new experimental findings.

This study found that in a transgenic mouse model, a modified form of β-catenin inhibited normal hair follicle development and promoted epidermal cyst formation, revealing distinct effects on Wnt signaling.

In this study using transgenic mice, activating P-catenin signaling induced new hair follicle formation and maintained follicle tumors, with implications for understanding skin homeostasis.

This study suggests that β-Catenin and extracellular matrix components interact in a regulatory loop to influence fibroblast behavior and wound repair properties in dermal tissue.

In this study, the researchers observed that inducing and then withdrawing β-catenin expression in a bigenic mouse model caused reversible changes in skin morphology, indicating dependence on β-catenin signaling.

Wnt/β-catenin signaling is crucial for cell fusion in placental development.

This study found that in mice, inactivating beta-catenin in the dermal papilla reduces hair follicle progenitor proliferation and disrupts the hair cycle.

This study found that in fetal skin development, both α- and β-catenins showed similar expression patterns, indicating their related roles in the development of the epidermis and skin appendages.

This study found that activating β-catenin signaling in embryonic epidermis promoted hair follicle characteristics at the expense of normal epidermal differentiation, leading to early pigmentation and innervation.

In this study, the researchers reported that altering β-catenin signaling in a transgenic mouse model led to changes in skin cell fate, notably converting hair follicle cells into epidermal cells and forming cysts instead of follicles.

This study suggests that inactivation of β-catenin is necessary for chick retina regeneration, as it allows cells to enter the cell cycle during injury and promotes regeneration without needing FGF2.

This study reports that inhibition of Wnt/β-catenin signaling disrupts hemidesmosome organization in keratinocytes by altering the localization of components like plectin and collagen XVII.

This study indicated that abnormal Bmp signaling in β-catenin gain-of-function mutants is associated with anorectal malformations, shedding light on potential mechanisms underlying these congenital conditions.

This study demonstrated that β-catenin signaling in CD133+ dermal papilla cells enhances postnatal hair growth by accelerating the proliferation and differentiation of keratinocytes in the murine hair cycle.

In this mouse study, researchers found that dermal Wnt signaling/β-catenin activity is essential for fibroblast proliferation and initiating hair follicle formation by interacting with epidermal Wnt ligands.

This study concluded that Wnt/β-catenin signaling, through Shh and Bmp pathways, is crucial for determining hair follicle fate in embryonic epidermal development.

This study found that loss of the Pten gene in Lgr5+ hair follicle stem cells promoted squamous cell carcinoma formation through the Akt/β-catenin signaling pathway.

In this study, β-catenin overexpression in human hair outer root sheath cells increased the expression of Pitx2, which activated the follicular differentiation pathway, suggesting Pitx2's potential role as a modulator in hair growth control.

This study found that stabilizing β-catenin in a specific mouse model led to temporarily increased hair density but ultimately accelerated hair follicle aging and hair thinning.

This review discusses the role of the CXXC5 protein as a transcription factor and signaling coordinator, noting its involvement in embryonic development, tissue homeostasis, and diseases such as tumorigenesis, but reports no new experimental findings.

This study observed that β-catenin overexpression in human squamous cell carcinoma cells led to increased CREB expression, which significantly enhanced clonogenic activity, suggesting CREB as a β-catenin-regulated factor promoting cancer characteristics.

The authors concluded that the dermal response to epidermal Wnt/β-catenin signaling depends on distinct fibroblast lineages, with each responding to different paracrine signals such as Hedgehog and TGF-β.

The study found that up-regulating β-catenin signaling in CD 133-positive dermal papilla cells enhanced their ability to promote hair follicle regeneration both in vitro and in vivo.

In this study, researchers identified CENPV as a new CYLD interacting partner that localizes to primary cilia and regulates acetylated tubulin levels, offering insights into the pathogenesis of skin appendage tumors.

This study found that stabilized beta-catenin is crucial for activating stem cell transition from quiescence to proliferation in hair follicles by influencing gene expression within the stem cell niche.

This study established a method for selecting human hair follicle stem cells through quick-adherence to collagen, and found that β-catenin plays a role in their proliferation and differentiation.

This study found that different epidermal stem cell populations contribute to the formation of various skin tumors and new hair follicles following β-catenin activation in the adult epidermis.