Dot1l deficiency leads to increased intercalated cells and upregulation of V-ATPase B1 in mice
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- 作者：Zhou Xiaoa ; b ; Lihe Chenc ; Qiaoling Zhoua ; Wenzheng Zhangb ; c ; 1 ; Wenzheng.zhang@uth.tmc.edu" class="auth_mail" title="E-mail the corresponding author ; zhangw1@mail.amc.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：V-ATPase ; Histone methyltransferase Dot1l ; Conditional knockout ; Principal cells ; Intercalated cells
- 刊名：Experimental Cell Research
- 出版年：2016
- 出版时间：10 June 2016
- 年：2016
- 卷：344
- 期：2
- 页码：167-175
- 全文大小：3069 K
文摘
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Dot1lAC vs. Dot1lf/f mice have significantly reduced PCs and increased ICs.
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Both α- and β-ICs are significantly increased in Dot1lAC vs. Dot1lf/f mice.
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Dot1l downregulates expression of V-ATPase B1.
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Dot1l and H3m2K79 bind the promoter of Atp6v1b1.
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Atp6v1b1 is a new Dot1a target gene for transcriptional regulation.