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In this study, researchers found that correcting the HGPS mutation with Adenine base editing partially rescued accelerated skin cell differentiation and reduced cell death in patient-derived stem cells.

In this case report, a three-generation family with Gorlin-Goltz syndrome showed a heterozygous PTCH1 splice-donor variant associated with the disease, and two affected relatives benefited from individualized, side-effect-guided dosing of the drug sonidegib, experiencing regression of basal cell carcinoma lesions.

This review discusses the molecular mechanisms of Hutchinson-Gilford progeria syndrome and evaluates current research trends, available mouse models, and prospects for developing therapies, but reports no new clinical findings.

This study explored the effects of a common Hutchinson-Gilford progeria syndrome mutation in an inducible mouse model, revealing skin abnormalities similar to those in affected patients.

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 report details two patients with Hutchinson-Gilford Progeria syndrome who exhibited generalized shiny skin in infancy and had a novel mutation in the LMNA gene.

This study developed a mouse model to mimic PHGDH gene copy number gain, finding that increased PHGDH expression leads to abnormal melanin production, which may offer insights into its role in melanoma.

This review discusses genetic mutations associated with Hutchinson-Gilford progeria syndrome and reports no clinical results; the authors emphasize the importance of cardiovascular monitoring in management.

This article reviews current understanding of Hutchinson–Gilford Progeria Syndrome and suggests RNA-based treatments show promise, but no new clinical findings are reported.

This study found that the absence of Hes1 in hair follicles delays secondary hair germ activation and shortens the anagen phase, impacting HFSC self-renewal and long-term hair regeneration.

In this study, Gsdma1/2/3 knockout mice showed reduced epidermal hyperplasia and inflammation when induced by PMA, which was attributed to decreased EGFR-Stat3/Akt signaling due to a decrease in related ligands.

This review covers the history, symptoms, and treatment progress for Hutchinson-Gilford Progeria Syndrome, noting that while no cure exists, understanding its molecular mechanism may improve future treatment strategies.

This study found that HMGB1 enhanced hair growth by stimulating PGE2 production in human dermal papilla cells, suggesting a potential therapeutic target for alopecia treatment.

In this study, HPH-15, a newly synthesized compound, demonstrated potential in reducing skin fibrosis in a mouse model by targeting underlying pathogenic mechanisms and exhibited a good safety profile, warranting further clinical trials for fibrotic skin disorders like systemic sclerosis.

This review discusses Hutchinson-Gilford Progeria Syndrome, its symptomatology, and the progress in developing treatment strategies, emphasizing that while a cure remains elusive, advances in understanding the disease's molecular mechanisms show promise for future approaches.

This study identified the genes for pyochelin siderophore biosynthesis as a novel target regulated by the heme-responsive PrrH sRNA in Pseudomonas aeruginosa.

This study found that the PSEN1-P242LfsX11 mutation in hidradenitis suppurativa influences cytokine and chemokine expression in macrophages, potentially affecting inflammatory responses.

This study reports that the transgenic expression of Dsg1 in mice rescued the severe B6-Dsg3−/− phenotype and created a syngeneic mouse model of pemphigus vulgaris, which may aid in understanding autoimmunity mechanisms.

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.

In this study, the gene SlPHL1 was identified as a transcription factor in tomatoes that enhances phosphate starvation responses by upregulating specific genes.

This study reveals that CSPG4-positive basal cell keratinocytes show distinct global gene expression from CSPG4-negative cells, despite similar colony-forming efficiency.

This study reports that compound heterozygous loss-of-function mutations in the HEPHL1 gene in a child were associated with abnormal hair and cognitive issues, linking altered ferroxidase activity to hair disorders.

This study found that patient-derived HGF significantly accelerates wound healing in diabetic mice, particularly improving skin structure and flexibility, and rHGF plays a key role in boosting hair growth.

This study found that notch1 signaling is severely impaired in hidradenitis suppurativa patients with or without NCSTN or other gamma-secretase gene mutations, highlighting a canonical defect at the lesional tissue level.

This study identified several genes highly expressed in germ-line stem cells that are also common in hematopoietic stem cells, potentially aiding the exploration of fundamental stem cell commonalities.

This study found that nitrate, rather than ammonium, significantly enhances phosphate starvation responses in plants through a regulatory cascade involving NIGT1, SPX, and PHR1 proteins.

This case study reports that a heterozygous missense GJA1 mutation, p.Gly138Ser, in a 2-year-old boy with oculodentodigital syndrome primarily resulted in syndactyly, fifth finger hypoplasia, and hypotrichosis, without neurological or craniofacial abnormalities.

This study found that although progerin expression in mouse skin causes significant nuclear shape changes in keratinocytes, it does not result in alopecia or common skin abnormalities seen in human Hutchinson–Gilford progeria syndrome.

This study found that the mammalian Hr protein can interact with the p53 pathway by binding to a specific p53 response element, influencing the regulation of genes involved in cell cycle control.