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Using ALPK1−/− C57BL/6 mice and primary lens epithelial cells with ALPK1 knockout, the work evaluates lens architecture, apical protein transport, ER stress, apoptosis, and differentiation. ALPK1 loss yields cataracts with disrupted polarity and junctions, enhanced ER stress and apoptosis, while lentiviral ALPK1 re-expression restores transparency and normal ZO-1 localization.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/loss-of-alpha-kinase-1-contributes-to-the-formation-of-congenital-cataracts-in-mice/432621/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/loss-of-alpha-kinase-1-contributes-to-the-formation-of-congenital-cataracts-in-mice/432621.png","ImageObject",300,407,{"name":92,"@type":93},"Mary Man","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":24},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What role does ALPK1 appear to play in lens epithelial cell homeostasis?","Question",{"text":112,"@type":113},"ALPK1 helps maintain lens epithelial cell homeostasis by regulating myosin Ia phosphorylation-dependent apical trafficking and tight junction integrity.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What phenotypes and molecular changes occur in ALPK1−/− mice?",{"text":117,"@type":113},"ALPK1−/− mice develop congenital cataracts with combined Y-suture and cortical opacities, disrupted lens architecture, reduced myosin Ia phosphorylation, mislocalized ZO-1, increased CHOP, and increased apoptosis.",{"name":119,"@type":110,"acceptedAnswer":120},"How does restoring ALPK1 affect congenital cataracts in the study?",{"text":121,"@type":113},"Lentiviral ALPK1 re-expression significantly restores lens transparency and ZO-1 apical localization, reduces CHOP expression, and suppresses apoptosis.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},432621,1790740621,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":24,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":56,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144,"preview_page_count":4},7421720224475,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","Wang et al. Cellular & Molecular Biology Letters (2026) 31:1 [https://doi.org/10.1186/s11658-025-00827-2](https://doi.org/10.1186/s11658-025-00827-2)  \nCellular & Molecular Biology Letters  \nRESEARCH ARTICLE Open Access  \nLoss of alpha-kinase 1 contributes to the formation of congenital cataracts in mice  \nHui-Shan Wang 1†, Yu-Xin Yang 1†, Shang-Shang Duan 1†, Fang-Yi Long2, Ting Wu 1, Nai-Hong Yan 1, Xiao-Hong Li 1* and Jun-Rong Du 1*  \n†Hui-Shan Wang, Yu-Xin Yang and Shang-Shang Duan have contributed equally to this work.  \n*Correspondence:  \nXiao-Hong Li[li_xiaohong@scu.edu.cn](li_xiaohong@scu.edu.cn)  \nJun-Rong Du[dujunrong@scu.edu.cn](dujunrong@scu.edu.cn)  \n1West China School of Pharmacy, West China School of Public Health, Research Laboratory of Ophthalmology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China 2Laboratory Medicine Center, Sichuan Provincial Maternity and Child Health Care Hospital, Chengdu 610032, Sichuan, China  \nAbstract  \nBackground Alpha-kinase 1 (ALPK1), a cytosol ic receptor involved in innate immune activation, promotes apical trafficking in epithelial cells. While its role in autoinflammatory disorders is known, its function in epithelial homeostasis remains unexplored. This study investigates ALPK1’s role in murine lens development and its pathological relevance to congenital cataracts (CCs) .  \nMethods We utilized ALPK1-deficient (ALPK1−/− ) C57BL/6 mice and primary lens epithelial cells (LECs) with ALPK1 knockout (via lentiviral sgRNA) to analyze lens histomorphological alterations and cellular and molecular pathologies, including apical protein transport and localization, endoplasmic reticulum (ER) stress, apoptosis, and LEC differentiation.  \nResults We observed strong ALPK1 immunoreactivity in the LECs of C57BL/6 mice. ALPK1−/− mice developed CCs with combined Y-suture and cortical opacities, disrupted lens cell architecture, and vacuolar degeneration. Molecular dysregulation included reduced phosphorylation of myosin Ia, mislocalization of zonula occludens-1 (ZO-1) from apical tight junctions to cytoplasmic aggregates, upregulation of the endoplasmic reticulum (ER) stress marker C/EBP-homologous protein (CHOP), increased apoptosis (evidenced by TUNEL-positive cells), and disorganized interlocking patterns in lens fiber cells. Lentiviral ALPK1 re-expression in ALPK1−/− mice significantly restored lens transparency and ZO-1 apical localization, reduced CHOP expression, and suppressed apoptosis.  \nConclusions This study first demonstrates that ALPK1 is critical for maintaining LEC homeostasis by regulating myosin Ia phosphorylation-dependent apical trafficking and tight junction integrity. ALPK1 deficiency disrupts these processes, leading to loss of apical polarity, ER stress-induced apoptosis, and ultimately CC formation.  \nKeywords ALPK1, Apical transport, Congenital cataracts, Lens epithelial cells, Myosin Ia  \nBackground  \nCataracts are opacity of the crystalline lens that is caused by various changes to lens cell structure and lens proteins. Congenital cataracts (CCs) are observed at birth or during the first decade of life, caused by the aberrant development of the lens. The opaque lens  \n© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licenc","cbCainCwAIZTuY75","https://ap.wps.com/l/cbCainCwAIZTuY75","pdf",4195327,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusions\n# Background","[{\"question\":\"What role does ALPK1 appear to play in lens epithelial cell homeostasis?\",\"answer\":\"ALPK1 helps maintain lens epithelial cell homeostasis by regulating myosin Ia phosphorylation-dependent apical trafficking and tight junction integrity.\"},{\"question\":\"What phenotypes and molecular changes occur in ALPK1−/− mice?\",\"answer\":\"ALPK1−/− mice develop congenital cataracts with combined Y-suture and cortical opacities, disrupted lens architecture, reduced myosin Ia phosphorylation, mislocalized ZO-1, increased CHOP, and increased apoptosis.\"},{\"question\":\"How does restoring ALPK1 affect congenital cataracts in the study?\",\"answer\":\"Lentiviral ALPK1 re-expression significantly restores lens transparency and ZO-1 apical localization, reduces CHOP expression, and suppresses apoptosis.\"}]","Loss of alpha-kinase 1 contributes to the formation of congenital cataracts in mice | PDF",1790660566,48]