{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T14:12:21Z","timestamp":1789135941137,"version":"build-2803163510"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"abstract":"<jats:p>\n                    The progressive decline in sperm motility is a major contributor to male infertility. The cation channel of sperm (CatSper) complex is a sperm-specific calcium (Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ) channel that plays a crucial role in regulating sperm motility. However, the molecular mechanisms governing CatSper regulation remain incompletely understood. This study found that the expression level of transmembrane protein 196 (TMEM196) positively influences human sperm quality and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration.\n                    <jats:italic toggle=\"yes\">TMEM196<\/jats:italic>\n                    -null male mice showed reduced fertility, characterized by fewer offspring and decreased sperm Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration. Sperm quality analysis revealed that\n                    <jats:italic toggle=\"yes\">TMEM196<\/jats:italic>\n                    deficiency led to reduced sperm concentration, impaired hyperactivation, and decreased motility in male mice. Further investigations demonstrated that the reduction in sperm motility in\n                    <jats:italic toggle=\"yes\">TMEM196<\/jats:italic>\n                    -null mice was associated with decreased sperm Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration and was independent of hormone levels. Considering the essential role of CatSper in regulating sperm Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis, we examined the expression of CatSper subunits and observed significantly reduced protein levels of CatSper1\u20134 in the testes of\n                    <jats:italic toggle=\"yes\">TMEM196<\/jats:italic>\n                    -null mice.\n                    <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                    , overexpression of\n                    <jats:italic toggle=\"yes\">TMEM196<\/jats:italic>\n                    in GC2 cells enhanced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling and upregulated\n                    <jats:italic toggle=\"yes\">CatSper<\/jats:italic>\n                    -related protein expression. Mechanistically, TMEM196 promoted the transcription of\n                    <jats:italic toggle=\"yes\">CatSper<\/jats:italic>\n                    -related genes by enhancing the phosphorylation of signal transducer and activator of transcription 3 (STAT3). Collectively, these results identify TMEM196 as a novel regulator of the sperm-specific CatSper Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel and demonstrate its critical role in modulating sperm motility.\n                  <\/jats:p>","DOI":"10.4103\/aja202610","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T14:01:14Z","timestamp":1789135274000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Transmembrane protein 196-mediated regulation of CatSper channel through STAT3 phosphorylation influences sperm motility in mammals"],"prefix":"10.4103","author":[{"given":"Kang-Le","family":"Liu","sequence":"first","affiliation":[{"name":"Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing 400038, China"},{"name":"State Key Lab of Trauma and Chemical Poisoning, and Key Lab of Medical Protection for 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Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610054, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-Jiao","family":"Chen","sequence":"additional","affiliation":[{"name":"The Chinese University of Hong Kong, Faculty of Medicine, Department of Anaesthesia and Intensive Care, Hong Kong SAR, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu-Qi","family":"Tang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Bioelectronics, Jiangsu Key Laboratory for Biomaterials and Devices, School of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Chen","sequence":"additional","affiliation":[{"name":"Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing 400038, China"},{"name":"State Key Lab of 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