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This study developed an in vitro model using NTERT keratinocytes expressing AEC-related TP63 mutations, which replicated skin defects observed in AEC patients and offers a valuable tool for understanding the disorder and developing new treatments.

This study created transgenic mouse models with the LMNA gene mutation common in Hutchinson-Gilford progeria syndrome, revealing skin and teeth abnormalities related to transgene expression levels.

This study found that skin organoids derived from iPSCs with an HS-associated NCSTN mutation showed defects in hair follicle stem cell differentiation and increased expression of inflammatory proteins related to hidradenitis suppurativa.

This review provides an overview of the hairless gene in mice and humans, discussing its structure, expression, and implications for understanding skin physiology and human disorders related to gene disruption, but it reports no new empirical findings.

This study showed that a 2-kilobase upstream region of the mouse keratin 17 gene enables targeted GFP expression in major epithelial appendages of transgenic mice, indicating sonic hedgehog's involvement in its regulation.

This study suggests a regulatory model where HOXC13 activates Foxn1, affecting hair and nail differentiation, supported by similarities in Hoxc13(tm1Mrc) and Foxn1(nu) mice phenotypes and gene expression patterns.

In this study, deleting the transcriptional pause factor Nelfb in mouse preadipocyte lineages led to defective dermal fat formation and lethal outcomes, while interventions targeting Pparg could rescue adipocyte differentiation and promote dermal white adipose tissue formation, underscoring Nelfb's critical role in adipogenesis.

This study found that while most mice lacking MK6a and MK6b genes died from tongue epithelium disintegration, about 25% survived and showed no hair or nail defects due to a newly discovered MK6hf gene.

In this study, targeted deletion of the stearoyl-CoA desaturase 1 gene in mice disrupted the epidermal lipid barrier, leading to increased water loss, impaired thermoregulation, and metabolic issues.

This study highlights the role of Orai1 in ameloblast differentiation and maturation, showing that its down-regulation affects cell proliferation and enamel formation during tooth development.

This study suggests that egfl6 expression in the pharyngeal pouches is not essential for craniofacial development in zebrafish.

This study identified histologic lesions and a defect in adhesion molecules causing hair loss in mice with the bal mutation, linked to a mutation in the desmoglein 3 gene.

In this study, researchers found that overexpression of the hairless protein in Hr mutant mice disrupts inner root sheath formation by downregulating Dlx3 and associated keratins in hair follicle development.

This study found that while Eda and Edar proteins interact in vitro, their roles in dental development differ, with downless mutant mice showing distinct tooth defects compared to tabby mutants.

The study found that severe insulin resistance and premature diabetes are common in patients with PCNT genetic defects, primarily affecting those over four years old, while not impacting early insulin signaling in adipocytes.

This study found that, despite the unchanged total level of 18-MEA, deletion of the Sox21 gene disrupts its attachment to the hair cuticle, increases cholesterol sulphate levels, and differentially affects ceramide composition.

In this mouse study, the absence of the Ascl4 gene did not affect the development of hair follicles, teeth, or mammary glands, suggesting it is non-essential for these processes.

This study identified a nonsense mutation in the zinc-finger domain of the hairless gene associated with congenital atrichia in a Japanese family, indicating a potential genetic cause for this rare form of alopecia.

In their mouse study, Oda et al. found that removing the MED1 gene in the skin led to hair loss and changes in epidermal cell differentiation, indicating MED1's significant role in these processes.

This study found that oxidative damage is present in the mitochondria of PolG mice, which exhibit premature aging-like phenotypes due to mitochondrial dysfunction.

The researchers reported finding a recessive nonsense variant in the EGFR gene responsible for perinatal lethality in the "Blonde d'Aquitaine" cattle breed, prompting the development of a screening test to help eradicate this genetic flaw.

This study found that the transcription factor Meis2 is crucial for the maturation and innervation of sensory neurons responsible for light touch in mice, with its absence leading to reduced touch sensitivity.

This study found that the transcription factor Meis2 regulates the maturation and innervation of sensory neurons in mice, affecting their response to light touch.

Mutations in the androgen receptor gene cause androgen insensitivity, leading to female traits in genetically male individuals.

This paper describes the hGRα gene structure and its expression, focusing on the functional properties of the longest GRα isoform, but reports no new results.

This review discusses the role of oxidative stress in hair greying and suggests that understanding melanocyte susceptibility at different follicular locations may help develop therapies for preventing and reversing the process; it reports no new experimental results.

In this study, researchers discovered that the interaction between the hairless protein and the wise protein is crucial for hair-follicle regeneration, helping bald mice regrow fur.

In this study, researchers observed that EGFR deficiency in the epidermis affects gene expression related to cell differentiation and structure, highlighting spatial and temporal roles of EGFR during skin and hair follicle development.

This study found that Origanum vulgare extract improved testicular structure and function in mice against finasteride-induced damage by enhancing antioxidant defense and modulating gene expression related to apoptosis.

This study found that in skin blister healing, hair follicle development is compromised as stem cells repair wounds at the expense of morphogenesis gene expression.