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COL17A1, also known as collagen type XVII alpha 1 chain, is a protein anchored in cell membranes, crucial for many biological functions. It forms part of structures called hemidesmosomes, essential for anchoring skin cells to the underlying basement membrane [1][2][3]. COL17A1 helps skin cells called keratinocytes stick to the basement membrane, keeping the skin intact [4]. It's also vital for creating a suitable environment for special skin cells called melanocyte stem cells, important for skin cell renewal, aging, and the development of skin cancer [5][6]. When COL17A1 levels drop, it affects skin balance and can accelerate aging, especially with exposure to sunlight [4][7]. In cancer, COL17A1 is often overproduced, promoting the growth, spread, and resistance to cell death [8]. On the flip side, changes in how the COL17A1 gene is controlled can increase cancer cell invasion [9]. Removing a specific part of the COL17A1 gene can trigger skin inflammation linked to certain immune responses [10]. Mutations in COL17A1 are associated with skin disorders, both inherited and acquired, like junctional epidermolysis bullosa and corneal dystrophies [11]. Scientists are investigating ways to target COL17A1 for therapy in these conditions, such as correcting gene defects to restore normal protein levels.
References:
[1] F. Jönsson, B. Byström, A. Davidson, L. Backman, T. Kellgren, S. Tuftet al., "Mutations in collagen, type xvii, alpha 1 (col17a1) cause epithelial recurrent erosion dystrophy (ered)", Human Mutation, vol. 36, no. 4, p. 463-473, 2015. https://doi.org/10.1002/humu.22764
[2] Y. Xiang, Y. Liu, Y. Yang, Y. Yan, A. Kim, C. Guoet al., "Reduced expression of collagen 17a1 in naturally aged, photoaged, and uv-irradiated human skin in vivo: potential links to epidermal aging", Journal of Cell Communication and Signaling, vol. 16, no. 3, p. 421-432, 2022. https://doi.org/10.1007/s12079-021-00654-y
[3] S. Tanimura, Y. Tadokoro, K. Inomata, N. Bình, W. Nishie, S. Yamazakiet al., "Hair follicle stem cells provide a functional niche for melanocyte stem cells", Cell Stem Cell, vol. 8, no. 2, p. 177-187, 2011. https://doi.org/10.1016/j.stem.2010.11.029
[4] D. Tong, M. Tanaka, H. Eguchi, Y. Okazaki, M. Muramatsu, & T. Arai, "Col17a1 germline variant p.ser1029ala and mucosal malignant melanoma: an autopsy study", Molecular and Clinical Oncology, vol. 16, no. 2, 2021. https://doi.org/10.3892/mco.2021.2465
[5] Z. Xu, "Bazi bushen alleviates skin senescence by orchestrating skin homeostasis in samp6 mice", Journal of Cellular and Molecular Medicine, vol. 27, no. 18, p. 2651-2660, 2023. https://doi.org/10.1111/jcmm.17833
[6] F. Mao, D. Li, Z. Xin, Y. Du, X. Wang, P. Xuet al., "High expression of col17a1 predicts poor prognosis and promotes the tumor progression via nf-κb pathway in pancreatic adenocarcinoma", Journal of Oncology, vol. 2020, p. 1-12, 2020. https://doi.org/10.1155/2020/8868245
[7] P. Thangavelu, T. Krenács, E. Dray, & P. Duijf, "In epithelial cancers, aberrant col17a1 promoter methylation predicts its misexpression and increased invasion", Clinical Epigenetics, vol. 8, no. 1, 2016. https://doi.org/10.1186/s13148-016-0290-6
[8] C. Fu, L. Chen, Y. Cheng, W. Yang, H. Zhu, X. Wuet al., "Identification of immune biomarkers associated with basement membranes in idiopathic pulmonary fibrosis and their pan-cancer analysis", Frontiers in Genetics, vol. 14, 2023. https://doi.org/10.3389/fgene.2023.1114601
[9] K. Tasanen, L. Tunggal, G. Chometon, L. Bruckner‐Tuderman, & M. Aumailley, "Keratinocytes from patients lacking collagen xvii display a migratory phenotype", American Journal of Pathology, vol. 164, no. 6, p. 2027-2038, 2004. https://doi.org/10.1016/s0002-9440(10)63762-5
[10] M. Nomura, Y. Hamasaki, I. Katayama, K. Abe, N. Niikawa, & K. Yoshiura, "Eosinophil infiltration in three patients with generalized atrophic benign epidermolysis bullosa from a japanese family: molecular genetic and immunohistochemical studies", Journal of Human Genetics, vol. 50, no. 9, p. 483-489, 2005. https://doi.org/10.1007/s10038-005-0282-4
[11] M. Ablinger, T. Lettner, N. Friedl, H. Potocki, T. Palmetzhofer, U. Kolleret al., "Personalized development of antisense oligonucleotides for exon skipping restores type xvii collagen expression in junctional epidermolysis bullosa", International Journal of Molecular Sciences, vol. 22, no. 7, p. 3326, 2021. https://doi.org/10.3390/ijms22073326
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