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In this study, researchers analyzed skin tumors from patients with CYLD cutaneous syndrome and found that loss of CYLD function is linked to changes in cellular signaling pathways, particularly NF-κB signaling, and leads to increased secretion of specific extracellular matrix proteins.

This study developed a culture method to expand and differentiate primary mammary basal cells, identifying key transcription factors like EGR1 and ELF3 that influence Claudin expression and actin organization, offering insights into epithelial cell biology and potential applications in related research fields.

In this study using mice, simultaneous deficiencies in claudin-1 and claudin-3 were associated with hair loss and altered hair follicle architecture during the telogen phase, suggesting a role in hair retention.

The researchers reported that mesenchymal stem cells promote wound healing by using Cx43 hemichannels to mediate ATP secretion, which supports macrophage polarization, angiogenesis, and fibroblast migration, suggesting a potential therapeutic strategy for improving tissue repair.

In this study, CTCF was found to play essential roles in epidermal differentiation and skin barrier formation, simultaneously acting as a suppressor of epithelial inflammatory responses in mouse skin.

This study suggests that CTHRC1, a protein expressed in cardiac fibroblasts, may improve wound repair and prevent cardiac rupture after myocardial infarction by activating a specific signaling pathway.

This study found that exposure to 12-O-tetradecanoyl-phorbol-13-acetate in mouse skin caused changes in claudin expression and localization, indicating disruption and eventual recovery of the epidermal barrier.

This study found that misexpression of Hoxc8 in mice led to ectopic mammary development and suggests Hox genes may play crucial roles in the regional specification and initiation of cutaneous accessory organs.

This study found that CTCF is crucial for proper skin and hair follicle development in mice, affecting keratinocyte differentiation and gene expression in keratin loci.

In this study, researchers found that mouse hair follicles recruit Langerhans cells by secreting chemokines, acting as key portals for these cells in both mice and humans.

This study found that the TLR3 L412F genetic variant is associated with severe viral infections, especially CMV, and immune dysfunction in a subgroup of chronic mucocutaneous candidiasis patients.

This study reported no Cx30 expression in normal interfollicular human epidermis and minimal expression in some skin structures, with faint detection in porokeratosis of Mibelli patient skin.

This study found that the CXXC5 protein is overexpressed in diabetic foot ulcer tissues, suppressing wound healing, and that the small molecule KY19334 accelerated healing in diabetic mice by activating the Wnt/β-catenin pathway.

This study found that inhibiting the interaction between CXXC5 and Dishevelled could stimulate hair regrowth in mouse models by enhancing WNT/β-catenin signaling, suggesting a potential therapeutic strategy for hair loss involving compounds that block this interaction, such as interfering short peptides.

This study found that Bcl-xL deficiency in mice increased apoptosis and resistance to skin tumor development, highlighting Bcl-xL's role in early skin carcinogenesis through anti-apoptotic functions.

This study found that mice lacking CD61 had significantly shorter lower incisors compared to wild-type mice, suggesting CD61 is crucial for proper tooth growth and pre-ameloblast proliferation.

This study found that IL18 signaling plays a crucial role in the homing and retention of mature regulatory T cells in the mouse thymus, primarily by upregulating the chemokine receptor CCR6.

This study found that mutant Cx43 impairs fibroblast function during wound healing and reduces hair follicle cell proliferation, likely contributing to hair growth defects in ODDD patients.

This study found that estrogen, through estrogen receptors, can regulate the expression of the HOXC13 gene involved in hair follicle development, with MLL3 histone methylase playing a collaborative role.

This study found that the transcription factor Lhx2 regulates Sonic Hedgehog signaling in mouse retinal progenitor cells, mainly by controlling the expression of co-receptors essential for effective pathway activation during early retinal neurogenesis.

In this study, researchers found that the pCLCA2 protein is expressed in specific areas of pig skin, but its role in skin structure or function remains unclear.

This study suggests that Mcl-1 has a non-apoptotic role in promoting keratinocyte proliferation and Wnt/β-catenin signaling, potentially indicating a novel oncogenic activity.

This study found that sulfated CCK octapeptide reduces psoriasis-like skin inflammation in mice, suggesting a new pathophysiological role for CCK in regulating epidermal inflammation.

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 found that disrupting Sdf1-Cxcr4 signaling promoted tissue regeneration in wild-type mice, hinting at potential strategies to induce such regeneration in mammals.

This study found that overexpression of the intercellular adhesion protein Necl2 in hair follicle stem cells was associated with reduced cell proliferation and delayed wound healing in both cultured cells and transgenic mice.

This study established a murine chronic graft-versus-host disease model with scleroderma features, showing typical skin changes and cellular infiltrates associated with the condition.

This study found that the protein CCN2 in dermal papilla cells is a physiologically relevant suppressor of hair follicle formation by destabilizing β-catenin, which may help maintain stem cell quiescence.

This study found that LGR5 is uniquely expressed in human corneal endothelial cells and maintains endothelial cell phenotypes while inhibiting mesenchymal transformation through the Wnt pathway.