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This study identifies NFAT5 as a crucial transcription factor necessary for triggering innate immune responses in the blood vessel lining that lead to atherosclerosis under hypertonic stress conditions.

This study found that overexpression of PKCepsilon in mouse epidermis was associated with increased susceptibility to metastatic squamous cell carcinoma, potentially through a mechanism involving tumor necrosis factor-alpha.

This study found that in mice, knockout of Rac1 and Rac3 in keratinocytes led to reduced white adipose tissue and revealed Rac-dependent paracrine pathways affecting pre-adipocyte differentiation.

This study reported that ELL is crucial for maintaining the proliferative capacity of the basal layer in human epidermal keratinocytes by stabilizing RNA polymerase II at the transcription start site.

This study concluded that heterozygous NFKB2 mutations lead to a distinct and severe form of primary immunodeficiency with early onset, primarily T cell-mediated autoimmunity, and impaired B-cell differentiation.

In this study, researchers found that K17−/− mice suffered more severe hair follicle damage but showed reduced epidermal inflammation after ionizing radiation, with K17's absence leading to aberrant cell cycle progression due to altered p53 genome binding and reduced B-Myb degradation.

This study found that a truncated region of the K5 promoter directs expression in stratified epithelia, particularly in epidermis, hair follicles, and tongue, potentially involving specific keratinocyte nuclear proteins in regulation.

This review discusses the mechanisms of keratin 17 regulation in diseases such as psoriasis and cancers but presents no new experimental findings, calling for further exploration of anti-K17 therapies.

This study found that overexpression of PKCɛ in mouse epidermis increased sensitivity to metastatic squamous cell carcinoma, suggesting that a PKCɛ-mediated microenvironment may promote cancer development through specific cytokines like TNFα.

This study found that inhibiting NF-κB Essential Modulator (NEMO) in senescent murine dermal fibroblasts successfully reduced key factors associated with the senescence associated secretory phenotype (SASP), highlighting its potential as a therapeutic target for aging-related diseases.

This study found that activating cannabinoid receptor 1 reduces the expression of keratins K6 and K16 in human keratinocytes, suggesting potential implications for psoriasis management.

In this transgenic mouse study, preliminary findings suggest that overt melanocyte hyperplasia may require prior keratinocyte hyperplasia, indicating a potential role for keratinocyte mutation in early melanoma development.

This research identified that the constitutive and inducible expression of the Keratin 6 gene in transgenic mice skin is controlled by multiple regulatory elements spread throughout its 5' flanking region.

This study found that ILK/ELMO2 complexes in epidermal keratinocytes are selectively activated by epidermal growth factor to induce cell migration, unlike with other growth factors.

In this study, researchers found that AP-2α and AP-2β are critical for maintaining epidermal homeostasis in adult skin, with their combined loss leading to severe skin and hair abnormalities and early skin inflammation due to impaired keratinocyte differentiation.

This study identified CD201+ fibroblast progenitors in mouse skin that regulate wound healing through differentiation into specialized cell types, with retinoic acid and hypoxia influencing this process.

This study found that CB1 receptor activation reduced keratin K6 and K16 expression in human keratinocytes in vitro and in situ, suggesting potential relevance for both psoriasis management and wound healing.

This review reports that KRT80 is overexpressed in various cancers, enhancing cancer cell proliferation, invasiveness, and migration, suggesting it as a potential therapeutic target, though more clinical studies are needed to fully understand its role in cancer prognosis.

This research observed that removing RNase L in mice enhances regenerative capacity through increased IL-36 and wound-induced hair neogenesis, highlighting RNase L as a gene that represses regeneration by moderating immune responses during viral infections.

This study found that mrp/plf-mRNA expression in murine skin increases in response to different tumor promoters, suggesting its potential as a short-term biomarker for chemical carcinogenesis.

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.

In this study, researchers found that the absence of type I or type II keratins in mice leads to severe skin barrier defects, highlighting keratins' crucial role in epidermal structure and function.

This study observed that targeted expression of the neu oncogene in transgenic mice led to significant epidermal hyperplasia and a carcinoma-like appearance, suggesting a crucial role for erbB2 signaling in epidermal proliferation and carcinogenesis.

This study found that RNase L acts as a regeneration repressor gene in mammals, as seen in Rnasel-/- mice which showed increased regenerative capacity and elevated Wound Induced Hair Neogenesis through enhanced IL-36α signaling, suggesting a tradeoff between regeneration and immune regulation.

This study found that rapamycin effectively inhibits TPA-induced keratinocyte proliferation and skin tumor promotion by targeting mTORC1 signaling in both wild-type and transgenic mice.

This study highlighted Keratin 17's critical role in cancer therapy resistance across several malignancies, involving various signaling pathways, and identified it as a significant biomarker and potential therapeutic target, particularly in reversing resistance.

This study found that systemic treatment with DS77754007, a KLK5 inhibitor, improved skin symptoms in a mouse model of Netherton Syndrome more effectively than certain antibody treatments, suggesting KLK5 inhibition as a promising therapeutic approach for this condition.

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.