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This study found that transgenic mice overexpressing the SSAT gene under a metallothionein promoter suffered delayed hair loss and were highly sensitive to polyamine analogues, which led to significant liver changes and mortality.

In this study, acute restraint stress increased Y1 receptor gene expression in the amygdala and PVN of transgenic mice, but this effect was not due to elevated neuroactive steroid concentrations, indicating a potential ligand-induced mechanism.

In this study, transgenic mice overexpressing the SSAT gene were highly sensitive to polyamine analogues, leading to severe liver changes and high mortality rates after treatment.

This study found that changes in the brain concentrations of neuroactive steroids during pregnancy are linked to increased Y 1 receptor gene expression in the medial amygdala of transgenic mice.

This study found that benign tumors with a high risk of malignant progression primarily arise from hair follicle cells when a mutant ras gene is expressed in a specific population of epidermal cells in mice.

This study found that overexpression of PKCα in mouse epidermis increases expression of specific proinflammatory mediators and induces inflammation but does not significantly affect epidermal differentiation, proliferation, or tumor promotion with TPA.

In this study, ethanol discontinuation in Y 1 R / LacZ transgenic mice significantly decreased neuropeptide Y immunoreactivity and increased Y 1 receptor gene expression in the amygdala, with evidence suggesting an important role for the progesterone metabolite 3α,5α‐TH PROG in these changes.

This study found that overexpression of NSD3 in the mammary gland of transgenic mice led to mammary hyperplasia, dysplasia, and invasive ductal carcinoma, mirroring patterns seen in human breast cancer.

This study found that altering cyclin-dependent kinase 4 (CDK4) levels in the bulge region of hair follicles affects the balance of stem cell numbers, potentially influencing hair follicle self-renewal and proliferation.

This study found that transgenic expression of Endothelin 3 in mice can maintain a dark pigmentation phenotype independently of Mc1r signaling by regulating melanogenic genes.

This study found that restoring vitamin D receptor expression specifically in the keratinocytes of VDR null mice prevented alopecia and enhanced hair follicle response during anagen initiation.

This study found that conserved DNA motifs and expression patterns in keratin genes suggest functional regulatory similarities in hair follicle differentiation across different mammalian species.

This study found that the vitamin D receptor is crucial for initiating the postnatal hair follicular cycle in mice, preventing alopecia associated with its inactivation.

This study suggests that the HCR risk allele within the PSORS1 locus may contribute to psoriasis susceptibility by altering gene expression related to skin structure and differentiation, although these changes alone might not result in clinical symptoms.

This study found that restoring vitamin D receptor expression in keratinocytes of VDR null mice prevents alopecia by enhancing the hair follicle's proliferative response during anagen initiation.

This research explored methods to obtain transgenic sheep embryos expressing synthetic spider silk genes in hair follicles using somatic cell nuclear transfer, with successful in-vitro development observed.

This study found that the promoter region of the sheep KRTAP11-1 gene drives specific transcriptional activity in wool follicles, suggesting it may regulate hair keratinocyte specificity.

This study found that ectopic expression of FGF5s in transgenic Chinese Merino sheep increased wool length and greasy fleece weight compared to non-transgenic controls.

This study demonstrated that the large molecule versican plays a critical role in hair induction in dermal papilla cells, with potential implications for developing new hair growth treatments.

This study suggests that inducible transgenic mice showing hair follicle changes similar to telogen effluvium in humans might serve as a useful model for understanding this type of hair loss.

This study found that in transgenic mice overexpressing a mutant hairless gene, changes in its expression affected hair loss and regrowth, implicating the gene's role in hair follicle biology.

This study successfully established a transgenic sheep fibroblast cell line expressing the spider dragline silk protein gene, laying groundwork for developing transgenic sheep with this capability in hair follicles.

This study provides genetic evidence that desmoglein-1 can compensate for the loss of desmoglein-3 in hair adhesion, supporting the desmoglein compensation hypothesis.

This article reviews the genetic and protein interactions involved in hair growth, highlighting regulatory sequences, expression patterns, and potential genetic modifications, but presents no new experimental findings.

This study found that KLF4 expression in mouse hair follicle stem cells is important for effective cutaneous wound healing, with its knockdown leading to reduced stem cell populations and delayed healing.

This study found that the MsPG3-GFP fusion protein accumulates at the growing root hair tips in Medicago plants, suggesting its role in tip growth during symbiosis.

In this study, researchers found that dentin sialoprotein and phosphophoryn are present in rat and mouse hair follicles, suggesting these proteins may play a role in hair follicle development, similar to their role in dentin mineralization.

This study found that transgenic safflower oil bodies expressing oleosin-rhFGF9 promoted significant hair regrowth and wound healing in mice compared to control groups.

This study found that ectopic expression of the lymphoid-enhancer factor can induce K17 protein in the skin, suggesting a link between skin development and wound repair processes in mice.

This study found that nestin-driven GFP labels blood vessels originating from hair follicles in mice, which could be used to study early events in skin angiogenesis and for antiangiogenesis drug screening.