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This study found that TRF1 plays a crucial role in maintaining pluripotency and stem cell compartments, but it is not a suitable in vivo telomere length marker.

This study reported that IL-6/STAT3 signaling influences p63 isoform expression in keratinocytes and is involved in wound-induced hair follicle neogenesis, highlighting the interplay between immune and developmental pathways.

In a conditional knockout mouse model, this study found that loss of the transcription elongation factor SPT6 in basal keratinocytes led to psoriasis-like skin inflammation and delayed wound healing, suggesting SPT6 plays a crucial role in maintaining epidermal immune quiescence by suppressing proinflammatory NF-κB signaling.

This study found that Plakophilin 1 regulates innate immune responses in keratinocytes by controlling RNA helicase activity, balancing inflammation during epidermal immune challenges.

This study found that HPV8-induced actinic keratoses may mechanistically involve Lrig1+ hair follicle keratinocyte stem cells, with the E6 gene promoting downstream STAT3 activity in a mouse model.

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.

This study found that a mutation causing Stormorken syndrome in mice led to skeletal abnormalities and unusual hair growth, showcasing the STIM1 R304W protein’s role in bone development and cell fate.

This research reexamined transcriptomic data to study stem and progenitor cell proliferation in psoriasis, finding that the number of committed progenitor cells increased eight-fold in psoriatic skin without altering stem cell numbers, potentially identifying new therapeutic targets.

This study found that CLK1 is necessary for epidermal differentiation but does not affect sebocyte differentiation in a telogen skin stem cell line.

This study found that the K19 promoter is active in certain gastrointestinal cancer cells and its activity is influenced by the interaction between GKLF and Sp1 transcription factors.

This study found that cutaneous squamous cell carcinomas in mice infected with murine papillomavirus preferentially arise from Lgr5+ progenitor cells, while squamous cell dysplasia does not.

In this study, Meis1 was found to regulate epidermal homeostasis and act as a proto-oncogenic factor in skin tissues, with differences in expression patterns between normal and tumor cells.

This study suggests that the NCSTN knockout mouse could serve as an HS animal model, with tamoxifen potentially used for gene deletion in mice.

This study found that Cutl1 mutant mice experienced retarded lung differentiation and abnormal hair follicle morphogenesis, indicating the vital role of CDP in lung development and hair follicle cell-lineage specification.

In this study, the deletion of NIPP1 in keratinocytes led to chronic skin inflammation and epidermal changes in mice, with early cell-cycle arrest and premature senescence observed, potentially contributing to reduced mutagen sensitivity.

In this study, PINCH-1 gene loss in mouse epidermis led to detachment from the basement membrane, thickened skin, and hair loss, with findings suggesting PINCH-1 plays a role in keratinocyte adhesion through both ILK and EPLIN pathways.

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.

This study found that Foxp1, a transcriptional factor, plays a key role in regulating hair follicle stem cell proliferation by modulating oxidative stress and the cell cycle during hair growth phases.

This study found that BBS7 is crucial for maintaining Sonic hedgehog signaling activity and periodontal ligament homeostasis, with changes in gene expression observed in occlusal hypofunctional PDL.

This study observed that aberrant DNA methylation in murine and human cutaneous squamous cell carcinoma likely contributes to the silencing of tumor suppressor genes, notably affecting the FILIP1L gene.

In this study, researchers reported that hair follicle stem cells maintain quiescence through a PIEZO1-dependent mechanism that senses mechanical forces and translates them into localized calcium influx, involving a transcriptional network that regulates cell adhesion and cytoskeleton-related genes.

In this study, the researchers identified CEP135 as a biomarker linked to poor sarcoma survival and suggested PLK1 as a potential therapeutic target for sarcoma patients with high CEP135 expression.

This study identified a 14,883 bp genomic deletion affecting the Plcd1 and Vill genes as likely responsible for the abnormal phenotype observed in snthr-1Bao mice.

This study found that overexpression of the transcription factor NFIC may enhance the proliferation and differentiation of stem cells from the apical papilla, suggesting its potential role in dentin/root regeneration.

This study found that PBX1 overexpression reduces hair follicle-derived mesenchymal stem cell senescence and apoptosis by alleviating ROS-mediated DNA damage, rather than enhancing DNA repair.

This study found that inhibiting PI3 kinase in epidermal stem cells reduces YBX1 phosphorylation, thereby decreasing cellular senescence and enhancing wound healing and regeneration in adult-derived skin models.