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This study found that JunB, a transcription factor, is crucial for maintaining epidermal-pilosebaceous stem cell homeostasis by regulating progenitor cell behavior and preventing sebaceous gland dysfunction.

This study found that JUNB enhances hair regeneration in mice by promoting dermal papilla cell proliferation through the Wnt signaling pathway, suggesting JUNB as a potential molecular target for improving cashmere quality and breeding in cashmere goats.

This study found that deletion of c-Jun and JunB in mouse bulge hair follicle stem cells was sufficient to trigger psoriasis-like skin disease through thymic stromal lymphopoietin signaling.

This study found that selectively targeting HDAC4 and HDAC7 in mice can reduce Th17 cell-mediated intestinal inflammation, suggesting a potential treatment approach for Th17-related inflammatory diseases like ulcerative colitis.

This study discusses how redox imbalance, specifically through reduced Insulin-like Growth Factor-1 mediated by the transcription factor JunB and sphingolipid metabolism changes, contributes to skin aging by depleting stem cell pools and altering the extracellular matrix, ultimately impacting skin integrity and function.