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This study found that active BMP signaling prevents epithelial stem cell activation and expansion in hair follicles, while its inhibition leads to HF stem/progenitor cell overproduction and matricomas.

This review summarizes the roles of bone morphogenetic proteins in the development and regulation of normal and diseased skin, but it does not provide new clinical results.

This review discusses the conserved molecular mechanisms controlling hair follicle development and cycling and suggests they may also apply to other ectodermal derivatives, like teeth and feathers, but it reports no new results.

This study found that dermal Shh signaling regulates specific dermal papilla signatures essential for maintaining hair follicle development, suggesting that the Shh-Noggin signaling loop is crucial for hair morphogenesis.

This study found that laminin-511 is crucial for hair morphogenesis in mice, as it influences primary cilia formation and dermal papilla maintenance through noggin and sonic hedgehog signaling.

This study found that transgenic mice overexpressing the BMP antagonist noggin showed increased hair follicle size and altered hair type, linked to changes in cell proliferation and gene expression.

This study found that BMP-2 activates Dlx3 gene transcription in murine keratinocytes by binding with Smad1/Smad4, suggesting a mechanism for BMP signaling's role in skin and hair follicle regulation.

This study found that BMP signaling influences hair pigmentation in mice by affecting the Agouti protein and interacts with MC-1R pathways to modulate melanin production.

This study found that overexpressing the BMP inhibitor Noggin in transgenic mice led to a significant loss of nontylotrich hair follicles, suggesting a critical role for BMP signaling in hair follicle morphogenesis and cycling.

This study found that penile and clitoral differentiation in mice is influenced by androgen exposure, with penile features developing postnatally requiring prenatal and ongoing androgen presence.

Noggin promotes skin tumors by activating certain cell signaling pathways.

This study found that reducing BMP signaling in mouse nipple epithelia, achieved through Noggin overexpression, can convert them into hairy skin with pilosebaceous units.

This study found that GLI2 plays a key role in activating follistatin, an activin/BMP antagonist, in response to hedgehog signaling in human epidermal cells, with implications for hair follicle development and basal cell carcinoma.

In this mouse study, researchers found that the absence of laminin-511 in skin delays hair follicle development and disrupts hair shaft differentiation, affecting key transcription factors for hair keratins.

This study found that overexpression of R-spondin 3 in a mice model impaired hair morphogenesis and regeneration by reducing hair matrix progenitor cell proliferation, thus disrupting the Wnt pathway's regulation of stem cells.

This study observed that GREM2 was specifically and robustly expressed in the dermal sheath cup of hair follicles during various hair cycle phases, suggesting its significant role in regulating hair cycling processes through BMP signaling.

In this study, the anti-wrinkle effect of bone morphogenetic protein receptor 1a extracellular domain was significantly greater than that of retinoic acid in a mouse model, suggesting potential for BMP antagonists in skin or hair treatments.

This study found that Ishige sinicola extract stimulated osteoblast differentiation and bone formation in MC3T3-E1 cells, suggesting potential use for osteoporosis prevention and treatment.

This study found that transplanting genetically modified dermal fibroblasts into full-thickness skin defects in rats led to the formation of hair follicles with mature pilosebaceous systems by 16 weeks.

The article concludes that studying how skin forms is key to understanding skin diseases and improving regenerative medicine.

This study found that manipulating Wnt/β-catenin signaling in embryonic mammary glands impacted their development, with high activity levels hindering branching and potentially redirecting cells toward hair follicle identity instead of mammary tissue.

This chapter discusses stem cell activity in feather and hair follicles, emphasizing how stem cells maintain their population by cycling between quiescence and activation in specialized niches but reports no new results.

This study observed that the loss of H3K9me3, via the ablation of Suv39h1, Suv39h2, and Setdb1 in embryonic mouse epidermis, disrupts skin development processes such as keratinocyte differentiation and hair follicle formation, highlighting H3K9me3's crucial role in epidermal morphogenesis.

This study found that rete ridge morphogenesis in mammalian skin is directed by a BMP-dependent developmental program, which is evolutionarily distinct from other known pathways controlling the development of hair follicles, sweat glands, and fingerprint ridges.

Skin organoids can regenerate hair by forming specific cell units with certain signals.

In this study, transgenic mice with active BMPR1A signaling in the epidermis had impaired hair follicle morphogenesis and showed age-related hair loss, implicating BMP signaling in hair follicle development and homeostasis.

This study found that in keratin 14-targeted transgenic mice, BMP antagonism via noggin led to the development of hair follicle tumors, mediated through alterations in Wnt and Shh signaling pathways.

The study observed that the tumor suppressor activity of bone morphogenetic proteins in mouse skin epithelium depends on Noggin levels, inhibiting Wnt and Shh signaling pathways to prevent tumor initiation and progression.

This study concluded that bone morphogenetic proteins are crucial for hair follicle stem cell differentiation and that their downregulation by androgens may contribute to the development of androgenetic alopecia.