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This study suggests that hairlessness in nude mice may be due to insufficient expression of phospholipase C-δ1, a molecule essential for normal hair development downstream of the Foxn1 gene.

This study observed that Trps1 gene expression in mice is precisely regulated in skin development, particularly during hair follicle morphogenesis, with distinct localization patterns in different cell types.

This study suggests that FGF18 may enhance radioresistance in telogen hair follicles by inducing cell cycle arrest, potentially serving as a radioprotector against radiation-induced hair follicle damage.

This study found that conditional deletion of Mof in mice resulted in severe defects in skin development, including compromised epidermal differentiation and hair growth, leading to perinatal lethality.

This study found that the Lim-homeodomain transcription factor Lhx2 regulates Sonic Hedgehog signaling during early retinal neurogenesis in mice by controlling the expression of pathway genes in retinal progenitor cells.

This study suggests that Foxn1 acts as a brake on PKC signaling in keratinocytes, thereby modulating the stages of differentiation by controlling PKC activity.

This study found that PLDζ2 and NPC4 enzymes play distinct roles in lipid remodeling and root hair growth in Arabidopsis under phosphate deficiency, influencing root hair density and length in a tissue- and time-specific manner.

In this study of mouse embryos, the researchers found that the expression of the Lhx2 gene plays a significant role in wound healing and may promote scar formation in later stages of development.

In this study, researchers found that WNT activation influenced FGF expression in human scalp-derived fibroblasts, with mouse model results showing FGF9 increased hair follicle number and diameter, while FGF7 reduced diameter.

This study found that upregulation of NFIC may enhance proliferation and osteogenic/cementogenic differentiation in rat dental follicle cells.

In this study on Drosophila embryos, researchers observed that the Slit/Robo signaling pathway is crucial for the collective migration and proper positioning of Posterior Signaling Center cells within the hematopoietic niche, highlighting its role in niche assembly and cellular organization.

This study found that Prdm1 is crucial for whisker development in mice, affecting multiple signaling pathways and possibly playing a role in primates' evolutionary loss of vibrissae.

In a laboratory setting, this study found that overexpression of the FGF5 short form in cultured keratinocytes increased hepatic growth factor gene expression, suggesting a potential role in hair growth.

This study reports that Wise is expressed in specific patterns during the morphogenesis of chick embryos, particularly in regions associated with known signaling molecules like Wnt, Bmp, and Shh.

In this study, androgen was found to increase VEGF expression, but not VEGFR-2, in rat corpus cavernous, with DHT likely playing a key role.

In this study, treatment with recombinant DKK2 was shown to significantly stimulate hair progenitor cell growth and enhance hair shaft elongation in ex vivo human hair follicle cultures by activating the Wnt/ẞ-catenin signaling pathway, suggesting a potential role for DKK2 in promoting hair growth.

This study reports that the loss of the protein Memo in mice leads to a reduced lifespan and suggests that Memo is a key regulator of FGFR signaling and vitamin D production.

This study found that the protein Foxn1 is crucial for the development and fat-storing capacity of dermal white adipose tissue in mice, influencing both lipid metabolism and adipogenesis in the skin through Bmp2 and Igf2 signaling pathways.

This study found that low temperatures and nitrogen deficiency trigger root hair elongation through a molecular mechanism involving the receptor kinase FERONIA and the TOR Complex 1.

A protein called FGF9 helps regenerate hair follicles in mice after skin damage, and increasing FGF9 could potentially help human hair growth.

This study used scRNA-Seq to map the transcriptional changes during zebrafish hair cell regeneration, revealing distinct phases including injury response, transient regeneration gene activation, and reactivation of developmental programs.

This study found that FGF18 signaling helps protect hair follicles from radiation damage by maintaining the resting phase and supporting stem cell survival, potentially reducing radiation-induced hair loss.

This study found that the absence of Hif-p4h-2 in specific mouse skin cells disrupted hair follicle development, leading to hair loss due to irregular keratin formation and pathway signaling.

This study found that recombinant human ADM2 treatment inhibited cell proliferation and induced apoptosis in human hair follicles, contrasting with the previously documented pro-proliferative and anti-apoptotic functions of ADM2.

This study found that Foxn1-like genes in fish and mice are functionally equivalent in activating hair keratin genes, whereas changes in the cephalochordate Foxn1-like gene result in inactivity.

This study found that MPZL3 plays a crucial role in regulating the hair cycle clock in mice, with its absence leading to accelerated hair follicle cycling and suggesting potential therapeutic pathways for alopecia treatment.

This study found that Dkk4-knockout mice exhibited disrupted hair follicle patterning, including a lack of the first wave of hair follicles in the lateral back skin.

This study identified that disrupting Mef2c in dermal papilla cells delays the early stages of hair cycle catagen in mice, revealing potential interactions with Sox18 in regulating hair growth.

This study observed that chemically-induced intersex frogs displayed altered brain mRNA profiles, with finasteride increasing certain hormone-related gene expressions and fadrozole reducing aromatase activity without affecting gene transcript levels.

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.