Journal: The Journal of Biological Chemistry

Article Title: An N-terminal di-proline motif is essential for fatty acid–dependent degradation of Δ9-desaturase in Drosophila

doi: 10.1074/jbc.M117.801936

Figure Lengend Snippet: Role of the di-proline motif in degradation of Δ9-desaturase. N-terminal amino acid sequences of Δ9-desaturases were compared (D. melanogaster DESAT1 (NP_652731), Mus musculus SCD1 (NP_033153), M. musculus SCD3 (NP_077770), Homo sapiens SCD1 (NP_005054), Danio rerio stearoyl-CoA desaturase (AAO25582), and S. cerevisiae Ole1 (CAA96757)) (A). Schematic illustration of DESAT1, mouse SCD1, and constructed mutants is shown (B). S2 cells expressing mouse SCD1-FLAGC, chimera-FLAGC, chimera (AA)-FLAGC, and SCD1 (di-Pro)-FLAGC were treated with C18:1 (100 μm) for 6 h (C) or DESAT1 inhibitor 37c (1 μm) for 16 h (D), and the amounts of endogenous DESAT1, FLAG-tagged exogenous Δ9-desaturases, and α-tubulin protein were detected with anti-DESAT1 antibody, anti-FLAG antibody, and anti-α-tubulin antibody, respectively. Band intensities were determined by ImageJ software, and levels of SCD1 proteins are shown relative to the amount of SCD1 protein in vehicle-treated cells (C and D). Mean ± S.D. (n = 3). *, p < 0.05; ***, p < 0.001; n.s., not significant.

Article Snippet: DESAT1 coding sequence was isolated from a cDNA library of strain Canton-S. cDNA encoding mouse SCD1 was purchased from ORIGENE.

Techniques: Construct, Expressing, Software

Journal: Cell Death and Differentiation

Article Title: SIRT3 promotes lipophagy and chaperon-mediated autophagy to protect hepatocytes against lipotoxicity

doi: 10.1038/s41418-019-0356-z

Figure Lengend Snippet: SIRT3 suppresses lipogenesis in lipotoxic hepatocytes. a SCD1 protein level in vector and SIRT3OE hepatocytes treated with or without P/O mixture for 24 h. b SIRT3 and SCD1 protein levels in SIRT3 and SCD1 double overexpressed hepatocytes. The lipid content c and the cellular TG content d in SIRT3 and SCD1 double overexpressed hepatocytes. White: blank, vector; gray: blank, SIRT3OE; light gray: P/O, vector; black: P/O, SIRT3OE. Data are shown as mean ± S.D., n = 6, * p < 0.05, and *** p < 0.001, vector vs. SIRT3OE, ### p < 0.001 blank vs. P/O treatment. && p < 0.01, &&& p < 0.001, SCD1OE vs. vector. One-way ANOVA was used to calculate the p -values

Article Snippet: The plasmid of pCMV3-SCD1-N-Myc was purchased from Sino Biological (MG51311-NM, Wayne, PA, USA).

Techniques: Plasmid Preparation

Journal: Cell Death and Differentiation

Article Title: SIRT3 promotes lipophagy and chaperon-mediated autophagy to protect hepatocytes against lipotoxicity

doi: 10.1038/s41418-019-0356-z

Figure Lengend Snippet: Schematic of the role of SIRT3 in protecting hepatocytes against lipotoxicity. SIRT3 activates AMPK to enhance macroautophagy and CMA on LDs and promote LDs dispersion on detyrosinated MTs, inhibits SCD1 expression to suppress lipogenesis, and deacetylates LCAD to increase fatty acid oxidation in mitochondria, resulting in attenuation of lipotoxicity in hepatocytes

Article Snippet: The plasmid of pCMV3-SCD1-N-Myc was purchased from Sino Biological (MG51311-NM, Wayne, PA, USA).

Techniques: Expressing