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To evaluate the role of\n                    <jats:italic>Ucp4<\/jats:italic>\n                    in the cerebellar Purkinje cells (PCs), we generated the conditional knockdown of\n                    <jats:italic>Ucp4<\/jats:italic>\n                    in PCs (\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice) by breeding\n                    <jats:italic>Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice with\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Series results by Western blot, immunofluorescent staining, and triple RNAscope in situ hybridization confirmed the specific ablation of\n                    <jats:italic>Ucp4<\/jats:italic>\n                    in PCs in\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice, but did not affect the expression of\n                    <jats:italic>Ucp2<\/jats:italic>\n                    , the analog of\n                    <jats:italic>Ucp4<\/jats:italic>\n                    . Combined behavioral tests showed that\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice displayed a characteristic bradykinesia in the spontaneous movements. The electromyogram recordings detection excluded the possibility of hypotonia in\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice. And the electrical patch clamp recordings showed the altered properties of PCs in\n                    <jats:italic>Pcp2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>cre<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Ucp4<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Moreover, transmission electron microscope (TEM) results showed the increased mitochondrial circularity in PCs; ROS probe imaging showed the increased ROS generation in molecular layer; and finally, microplate reader assay showed the significant changes of mitochondrial functions, including ROS, ATP, and MMP in the isolated cerebellum tissue. The results suggested that the specific knockdown of mitochondrial protein\n                    <jats:italic>Ucp4<\/jats:italic>\n                    could damage PCs possibly by attacking their mitochondrial function. The present study is the first to report a close relationship between UCP4 deletion with PCs impairment, and suggests the importance of UCP4 in the substantial support of mitochondrial function homeostasis in bradykinesia. UCP4 might be a therapeutic target for the cerebellar-related movement disorder.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Graphical Abstract<\/jats:bold>\n                  <\/jats:p>","DOI":"10.1007\/s12035-023-03607-1","type":"journal-article","created":{"date-parts":[[2023,9,9]],"date-time":"2023-09-09T08:01:56Z","timestamp":1694246516000},"page":"1119-1139","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Ucp4 Knockdown of Cerebellar Purkinje Cells Induces Bradykinesia"],"prefix":"10.1007","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3578-467X","authenticated-orcid":false,"given":"Ya-Yun","family":"Wang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5577-4690","authenticated-orcid":false,"given":"Shu-Jiao","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ban","family":"Feng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yun-Qiang","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shui-Bing","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8246-1756","authenticated-orcid":false,"given":"Yan-Ling","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2023,9,9]]},"reference":[{"key":"3607_CR1","doi-asserted-by":"publisher","unstructured":"Kumar, R.. et al. 2022 Uncoupling proteins as a therapeutic target for the development of new era drugs against neurodegenerative disorder. 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