{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LCE1B is a member of the Late Cornified Envelope family that encodes structural proteins integrated into the cornified cell envelope—a critical component of the epidermal barrier. Its product participates in the terminal differentiation of keratinocytes, thereby contributing to the mechanical resilience and proper barrier function of the stratum corneum. Studies have demonstrated that LCE1B expression is modulated by several signaling pathways. For example, one study showed that p53 can directly transactivate LCE1 cluster genes, suggesting that LCE1B might contribute to tumor‐suppressive mechanisms through interactions with factors such as protein arginine methyltransferase 5 (PRMT5)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In addition, genetic association analyses in distinct populations have revealed that single nucleotide polymorphisms in LCE1B and neighboring genes are significantly associated with psoriasis vulgaris, underlining the gene’s importance in maintaining epidermal integrity and its potential role in inflammatory skin diseases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Moreover, experimental work using a three-dimensional epidermis model demonstrated that the inflammatory cytokine interleukin-17A directly downregulates keratinocyte differentiation-related and cornified envelope-related genes—including LCE1B—thereby perturbing epidermal differentiation in psoriatic conditions."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Collectively, these findings indicate that LCE1B plays a multifaceted role in epidermal differentiation, skin barrier formation, and the modulation of inflammatory responses, making it an attractive candidate for further investigation as a potential therapeutic target in skin disorders.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhenzhong Deng, Koichi Matsuda, Chizu Tanikawa, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Late Cornified Envelope Group I, a novel target of p53, regulates PRMT5 activity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neoplasia (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.neo.2014.07.008"}], "href": "https://doi.org/10.1016/j.neo.2014.07.008"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25220593"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25220593"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Li Sun, Yuting Cao, Nagonbilig He, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Association between LCE gene polymorphisms and psoriasis vulgaris among Mongolians from Inner Mongolia."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Arch Dermatol Res (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00403-018-1813-0"}], "href": "https://doi.org/10.1007/s00403-018-1813-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29397434"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29397434"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Emi Sato, Narumi Yano, Yuka Fujita, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Interleukin-17A suppresses granular layer formation in a 3-D human epidermis model through regulation of terminal differentiation genes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Dermatol (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/1346-8138.15250"}], "href": "https://doi.org/10.1111/1346-8138.15250"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32020672"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32020672"}]}]}]}