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This study suggests that Lrig1-positive cells form a previously unknown reservoir of interfollicular epidermal stem cells in adult mouse skin, influencing epidermal proliferation and hair follicle development.

This study found that in a transgenic mouse model, β-HPV infection led to increased skin thickness and proliferation of specific keratinocyte stem cells, which may contribute to squamous cell carcinoma development.

In this study, researchers found that the cell surface protein Lrig1 plays a crucial role in regulating the suppressive function of regulatory T cells, suggesting it as a potential target for treating autoimmune diseases, as evidenced by experiments in mouse models.

This study found that the expression of LRIG1 in Merkel cell carcinoma tumors was associated with improved overall and cancer-specific survival.

The researchers reported that Lrig1 overexpression was observed in 100% of sebaceous carcinoma cases, suggesting it may serve as a potential marker for poorly differentiated sebaceous carcinoma.

This study suggests that with aging, mouse corneal renewal increasingly relies on Lrig1+ stem cells as CD44 expression and Wnt activity decline.

LRIG1 protein affects hair growth by regulating skin receptors, leading to hair loss when overexpressed.

This study found that Lrig1-positive cells in mouse epidermis are a previously unidentified source of adult interfollicular epidermal stem cells, which can contribute to sebaceous gland and epidermal lineage formation.

In this study, Lrig1-positive stem cells in mouse hair follicles were found to be essential for sebaceous gland formation and maintenance, with their depletion causing a temporary loss of these glands and changes in cellular differentiation.

This study found that the E6 gene, but not E7, was responsible for HPV8-induced expansion of keratinocyte stem cells in hair follicle junctional zones in mice.

This study presents evidence that hair matrix progenitors and the enzyme Stearoyl CoA Desaturase 1 may play a role in maintaining the dermal papilla niche via autocrine Wnt and paracrine Hedgehog signaling in mice.

The authors concluded that Lrig1-positive stem cells are essential for sebaceous gland formation in mice, as their ablation led to temporary sebaceous gland disappearance without affecting hair growth.

This dissertation reports that Lrig1 and Lgr6 mark distinct stem cell populations in mouse hair follicles, playing roles in tissue regeneration and tumor development, with Lgr6 regulating Wnt signaling and restraining epidermal lineage commitment.

In this study, researchers overexpressed Lrig3 in mouse skin and observed hair loss linked to changes in skin protein profiles and signaling pathways, suggesting a potential role for Lrig3 in maintaining skin homeostasis.

This article discusses the coordinated roles of different epidermal stem cells and other cell types in the skin's wound healing process and reports no new experimental results.

This review discusses epidermal stem cell diversity, revealing previously unrecognized differences in stem cell populations, but reports no new experimental results; it highlights the need for further exploration of stem cell interactions and quiescence.

This study found that hair follicle stem cells initially contribute to wound re-epithelialization, but long-lasting epidermal cells are primarily derived from a stem cell population in the isthmus portion of hair follicles.

This study found that the creation of hair follicle lumens in mice is driven by the outward migration of keratin 79-positive cells, suggesting a novel mechanism for generating hollow cores in hair follicles.

This study found that different epidermal stem cell populations contribute to the formation of various skin tumors and new hair follicles following β-catenin activation in the adult epidermis.

This review revisits mechanisms underlying acne lesion formation and suggests that preventing comedone development requires controlling critical factors in the pilosebaceous follicle before acne involvement.

This study found that EGFR-targeted cancer therapy can cause skin toxicities by disrupting epidermal signaling, allowing microbiota invasion and inflammation, but identified a potential treatment approach using FGF7 or SOS expression to restore barrier integrity.

This study found that Ng2+ perivascular cells in mouse skin are a diverse lineage-restricted population primarily recruited from papillary or reticular fibroblast lineages during wound healing, maintaining heterogeneity in both wounded and non-wounded skin.

This study observed that epidermal-specific deletion of aPKCλ in mice disrupts hair follicle stem cell quiescence, leading to altered hair follicle cycling and skin anomalies.

This study found that K79+ keratinocytes migrate outward to help form the hair follicle lumen both during development and adult regeneration, revealing a novel mechanism of hair follicle formation in mice.

This study found that abnormal Wnt signalling in stem cells may contribute to blackhead formation in acne by inhibiting cell differentiation and causing cell accumulation in the junctional zone.

This study found that chemically induced skin tumors in mice predominantly originated from Lgr6 + and/or Lrig1 + stem cells of the upper hair follicle rather than from other stem cell populations.

Hair follicle stem cells help maintain skin health after injury.

In this study, researchers observed that abdominal wounds in laboratory rats healed faster, completing epithelialization in 20 days versus 30 days for back wounds, possibly due to a higher expression of skin stem cell marker genes in the abdominal area.

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.