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This study found that mice lacking the vitamin D receptor showed disrupted hair follicle cycling and balance between cell proliferation and differentiation, highlighting VDR's role in hair cycling regulation.

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 WISP-1 plays a key role in ligamentum flavum fibrosis through the Hedgehog-Gli1 pathway, with cyclopamine showing potential to reduce fibrosis effects in a rabbit model.

This study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.

This study found that lymphatic vessels promote hair follicle growth in mice, suggesting new therapeutic strategies for hair loss treatments.

This study found that altering CDK4 expression in mice affects the population of keratinocyte stem cells, suggesting a correlation with susceptibility to skin papillomas.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

This review examines the role of Hairless, a nuclear receptor corepressor, in regulating Wnt signaling during hair cycling and reports no new clinical results.

This study found that the protein CCN2 in dermal papilla cells is a physiologically relevant suppressor of hair follicle formation by destabilizing β-catenin, which may help maintain stem cell quiescence.

In this study using a mouse model of Pemphigus vulgaris, researchers found that loss of desmoglein 3 adhesion in hair follicle stem cells triggers a regenerative program restoring stem cell function, requiring Hedgehog pathway suppression.

This study found that downregulation of Sonic hedgehog signaling may promote HPV replication and wart formation by inducing cell cycle arrest in keratinocytes.

In this study, the authors concluded that the TS-associated polyomavirus may disrupt Wnt/β-catenin signaling, likely contributing to abnormal hair follicle formation in trichodysplasia spinulosa.

This review discusses the roles of epithelial-mesenchymal interactions and dermal papilla in hair follicle growth and cycling, but it reports no new clinical results.

In this study, deleting the -catenin gene in vitamin D receptor-null mice did not prevent tumor development, suggesting -catenin's predicted protective role was not observed.

Using a combination of specific cell cycle regulators is better for safely keeping hair root cells alive indefinitely compared to cancer-related methods.

This study found that conditional knockout of N-WASP in keratinocytes of mice led to skin barrier defects, increased immune cell infiltration, and hyperproliferation of keratinocytes, indicating its crucial role in skin homeostasis.

This study concluded that the hairless protein interacts with the vitamin D receptor to repress transcription crucial for hair cycling, employing multiple protein interfaces and modulating chromatin structure.

This study reviews the role of the zinc finger protein CXXC5 in cellular signaling and its implications for cancer, discussing how its dysregulation is linked to various physiological and pathological processes, as well as potential therapies targeting CXXC5.

This study found that Wnt ligands from CD133-positive dermal papilla cells are essential for maintaining hair growth by supporting cell signaling between different hair follicle structures.

In this study, Msx2-deficient mice showed progressive hair loss due to shortened anagen phase and prolonged catagen and telogen phases, resulting in cyclic alopecia with structurally abnormal hair shafts.

This study found that Gsdma3 mutation in mice allows hair follicles to bypass a typical telogen phase and directly enter the anagen phase, suggesting Gsdma3's role in hair cycle transitions by regulating Wnt signaling.

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 reported that an HS-associated NCSTN mutation in iPSC-derived skin organoids led to altered hair follicle stem cell differentiation and increased expression of proteins linked to HS inflammation.

This study investigated the effects of Wnt-3a, Wnt-5a, Wnt11, and Wnt-10b on the hair induction-ability of cultured dermal papilla cells.

This study suggests that vitamin D and calcium signaling play a crucial role in wound healing by regulating stem cell activation through enhanced β-catenin transcriptional activity in mice.

This study identified a splicing-site deletion in the DCAF17 gene associated with Woodhouse-Sakati syndrome in a large consanguineous pedigree, leading to typical phenotypic features.

In this study, ectopic Wnt10b-mediated β-catenin activation in hair follicles resulted in larger regenerating anagen hair structures, an effect modulated by the Wnt inhibitor DKK1.

This study found that the E3 ligases NEDD4 and NEDD4L regulate intestinal stem cell priming by degrading the LGR5 receptor, and their loss leads to increased Wnt activation and crypt proliferation, which in turn accelerates intestinal tumor progression in mice.

This study found that Wnt10b induces hair follicle regeneration in mice, likely by activating the canonical Wnt signaling pathway in stem cells and their daughter cells.