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Loss of lipin 1 function results in activation of Notch signaling in zebrafish and mammalian cells. (A) Dual luciferase reporter assay to quantify the Notch signaling activity as her1 was coinjected with lpin1 morpholino into zebrafish embryos. (B) Lpin1-deficient zebrafish embryos showed upregulated gene expressions of Notch signaling components, which can be partially rescued by Notch inhibitor DAPT. (C) Dual luciferase reporter assay to quantify the Notch signaling activity as HES1 was coexpressed with the indicated LPIN1 cDNA in HEK293T cells. (D) Western blot and quantification analysis of LPIN1 wild type and mutant proteins. (E)LPIN1 siRNA in HEK293T cells achieved 65% knockdown with upregulated gene expressions of NOTCH signaling components. The abnormal upregulation of NOTCH signaling can be rescued by NOTCH inhibitor DAPT. Values in (A-E) represent means ± SE of data from three independent experiments, *p< 0.05, **p< 0.01, and ***p< 0.001 (Student's t-test).
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