<博士論文>
FEATは精巣ライディッヒ細胞のINSL3産生を亢進する

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概要 FEAT, the protein encoded by methyltransferase-like 13 (METTL13), is aberrantly upregulated in most human cancers and potently drives tumorigenesis in vivo; however, its role in normal tissues remains... elusive. Immunoblotting has displayed weak FEAT expression in normal human tissues, including the testis. Here, we found that FEAT is expressed in fetal and adult Leydig cells in the testis. FEAT knockdown using siRNA increased primary cilia formation in MA-10 Leydig tumor cells, accompanied by enhanced 5' adenosine monophosphate-activated protein kinase (AMPK) activation. Immunofluorescence analyses of FEAT-silenced MA-10 cells showed diminished insulin-like factor 3 (INSL3) expression. A male Mettl13+/- mouse developed bilateral intraabdominal cryptorchidism, suggesting defective INSL3 production by fetal Leydig cells. Leydig cells from the mouse showed markedly decreased INSL3 protein by immunohistochemistry. Together, these results suggest that FEAT facilitates the INSL3 production in testicular Leydig cells that is essential for transabdominal testis migration.続きを見る

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pdf med3168_abstract pdf 105 KB 271 要旨
pdf med3168_review pdf 167 KB 111 審査結果要旨

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登録日 2019.02.12
更新日 2019.03.08

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