Journal: Diabetes

Article Title: Maternal Exercise-Induced SOD3 Reverses the Deleterious Effects of Maternal High-Fat Diet on Offspring Metabolism Through Stabilization of H3K4me3 and Protection Against WDR82 Carbonylation.

doi: 10.2337/db21-0706

Figure Lengend Snippet: Figure 4—Beneficial effects of maternal exercise on glucose metabolism and WDR82 carbonylation in offspring of HFD-fed dams were blocked by placenta-specific Sod3 knockout. A and B: Glucose tolerance measured at 24 weeks in Sod3f/f or Sod3/ offspring of dams that were sedentary or trained and fed chow or the HFD. Glucose area under the curve (AUC) of male (A) and female (B) offspring is shown. GTT, glucose tolerance test. Data are means ± SEM (n = 5–7/group). **P < 0.01 vs. Chow-Sod3f/f-Sed; §P < 0.01 effect of genotype; ¶P < 0.01 effect of diet. Glucose production in hepatocytes of 16-week-old male (C) and female (D) Sod3f/f or Sod3/ offspring of dams that were sedentary (Sed) or trained and fed the HFD. Data are means ± SEM (n = 3). **P < 0.01 vs. Sod3f/f-HFD-Sedentary, §P < 0.01

Article Snippet: Human SOD3 (hSOD3) cDNA was obtained from Origene (RC204156) and was cloned into p3xFLAG-CMV8 vector (E9908, Sigma-Aldrich).

Techniques: Knock-Out

Journal: Diabetes

Article Title: Maternal Exercise-Induced SOD3 Reverses the Deleterious Effects of Maternal High-Fat Diet on Offspring Metabolism Through Stabilization of H3K4me3 and Protection Against WDR82 Carbonylation.

doi: 10.2337/db21-0706

Figure Lengend Snippet: Figure 5—Effects of SOD3 on offspring glucose metabolism are distinct from NAC. A and D: Developmental system used to treat off- spring livers with recombinant SOD3 or NAC exo utero. Offspring livers were collected at 4 weeks (A) or at E13.5 (D). Glucose production in primary hepatocytes of 4-week-old male (B) and female (C) offspring of HFD-fed, saline-, SOD3-, or diethyldithiocarbamate (DETCA)- treated dams (n = 3). **P < 0.01 vs. pCPT-saline. Effects of SOD3 or NAC treatment in utero on ROS levels (E), carbonylated protein con- tent (F), WDR82 carbonylation levels (G), mRNA expression of glucose metabolism genes (H), AMPKa phosphorylation (pAMPKa) levels (I), and mRNA expression of Tet and Idh (J) in livers of E13.5 offspring of HFD-fed dams (n = 3). IP, immunoprecipitation. All data are reported as means ± SEM. **P < 0.01 vs. pCPT-saline; ***P < 0.01 vs. pCPT-saline; ****P < 0.01 vs. pCPT-saline. Statistical signifi- cance was determined by one- or two-way ANOVA, with Tukey and Bonferroni post hoc analysis.

Article Snippet: Human SOD3 (hSOD3) cDNA was obtained from Origene (RC204156) and was cloned into p3xFLAG-CMV8 vector (E9908, Sigma-Aldrich).

Techniques: Recombinant, Saline, In Utero, Expressing, Phospho-proteomics, Immunoprecipitation

Journal: eLife

Article Title: CPT1A mediates radiation sensitivity in colorectal cancer

doi: 10.7554/eLife.97827

Figure Lengend Snippet: ( A ) The protein level of FOXM1, CPT1A, catalase (CAT), SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( B ) The mRNA level of FOXM1, CAT, SOD1, SOD2, SOD3 after knockout and overexpression of CPT1A. ( C ) Venn diagram showing the potential transcription factor of SOD1, SOD2, and CAT. ( D ) The protein level of FOXM1, CPT1A, CAT, SOD1, SOD2 after overexpression of FOXM1 in HCT116-CPT1AKO cells. ( E ) Schematic diagram summarising our working model, namely, decreased CPT1A promotes the transcription factor activity of FOXM1, increasing the mRNA and protein level of CAT, SOD1, and SOD2, followed by increasing ROS scavenge after irradiation and therefore colorectal cancer (CRC) cells become radioresistance. ***p<0.001, **p<0.01, *p<0.05. Figure 6—source data 1. Original files for western blot analysis displayed in . Figure 6—source data 2. PDF file containing original western blots for .

Article Snippet: Antibody , SOD3 Rabbit Polyclonal antibody , Proteintech (China) , 14316-1-AP , .

Techniques: Knock-Out, Over Expression, Activity Assay, Irradiation, Western Blot

Journal: eLife

Article Title: CPT1A mediates radiation sensitivity in colorectal cancer

doi: 10.7554/eLife.97827

Figure Lengend Snippet:

Article Snippet: Antibody , SOD3 Rabbit Polyclonal antibody , Proteintech (China) , 14316-1-AP , .

Techniques: Transfection, Construct, SYBR Green Assay, Protein Extraction, Single Cell Gel Electrophoresis, Activity Assay

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 1. SOD3 is expressed at high levels in adipose tissue and adipocytes. Adult

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques:

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 2. SOD3 expression is increased in adipose tissue from HFD-fed obese mice. Adult

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques: Expressing

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 3. SOD3 expression and secretion are increased in adipocytes differentiated from

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques: Expressing

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 4. SOD3 expression and secretion are increased in differentiated human

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques: Expressing

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 5. Human differentiating adipocytes treated with SOD3 shRNA lentivirus increased

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques: shRNA

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 6. SOD3 knockout (KO) mice are more obese and insulin resistant than WT mice.

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques: Knock-Out

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 7. SOD3 KO mice show higher level of adipose tissue hypertrophy than WT mice.

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques:

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 8. SOD3 KO mice show enhanced adipose tissue inflammation compared to WT

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques:

Journal: Antioxidants & redox signaling

Article Title: SOD3 Is Secreted by Adipocytes and Mitigates High-Fat Diet-Induced Obesity, Inflammation, and Insulin Resistance.

doi: 10.1089/ars.2018.7628

Figure Lengend Snippet: Figure 9. SOD3 KO mice show higher level of serum lipids and inflammatory cytokines

Article Snippet: Generation of global SOD3 knockout mice Heterozygous SOD3 knockout (SOD3+/-) mice were generated by CRISPR / cas9 technology by targeting on the exon 2 of mouse SOD3 gene (Cyagen, Biosciences, Suzhou, China).

Techniques:

Journal: Cancer Research

Article Title: MicroRNA-21 Modulates the Levels of Reactive Oxygen Species by Targeting SOD3 and TNFα

doi: 10.1158/0008-5472.can-12-0639

Figure Lengend Snippet: Figure 2. miR-21 directly targets SOD3. A, SOD levels were measured in cells with or without stable miR-21 overexpression at different times after 0.5 Gy low- or high-LET IR by Western blot analysis. b-Actin was used as an internal loading control. B, potential miR-21 binding site in the 30-UTR of SOD3 and the effects of the binding site on luciferase activity. 293T cells were transfected with a firefly luciferase reporter plasmid containing a partial 30-UTR of SOD3 with the putative miR-21 binding site (WT) or without the binding site or deleted mutation (DM). Luciferase activity was assayed 48 hours after transfection with miR-21 mimic (miR-21) or control RNA (mock) and are standardized by b-galactosidase activity. , P < 0.01. C, SOD3 levels were measured in cells with up- or downregulation of SOD3 expression in cells overexpressing miR-21 or a vector by Western blot analysis. b-Actin was used as an internal loading control. D, ROS levels (left, O2 ; right, H2O2) were measured in cells with up- or downregulation of SOD3 at 3 hours after 0.5 Gy low-LET ionizing radiation. The data are an average of three separate experiments. : P < 0.05.

Article Snippet: The siRNA against SOD2, SOD3, TNFa, the control RNA and the antibody against SOD1, SOD2, or b-actin was purchased from Santa Cruz Biotech Inc.

Techniques: Over Expression, Western Blot, Control, Binding Assay, Luciferase, Activity Assay, Transfection, Plasmid Preparation, Mutagenesis, Expressing

Journal: Cancer Research

Article Title: MicroRNA-21 Modulates the Levels of Reactive Oxygen Species by Targeting SOD3 and TNFα

doi: 10.1158/0008-5472.can-12-0639

Figure Lengend Snippet: Figure 4. miR-21 increases IR-induced cell transformation partially via targeting SOD3 and TNFa. A, the data reflect the number of colonies that were grown from cells with or without miR-21 overexpression in soft agar for 3 weeks. The results were obtained from 2 separate experiments with triple dishes per sample in each experiment. , P < 0.01; , P < 0.001. B, similar experiments were carried out as described in A, but with the cells upregulated either by SOD3 or TNFa cDNAs. The results were confirmed in 2 separate experiments with triple dishes per sample in each experiment. , P < 0.001. C, a model proposed to explain how miR-21 could stimulate cell transformation partially through increasing superoxide, thereby contributing to the role of miR-21 in carcinogenesis. miR-21–increased IR-induced superoxide levels through targeting SOD3 and TNFa (a transcriptional activator of SOD2), which contributes to IR- induced cell transformation and carcinogenesis.

Article Snippet: The siRNA against SOD2, SOD3, TNFa, the control RNA and the antibody against SOD1, SOD2, or b-actin was purchased from Santa Cruz Biotech Inc.

Techniques: Transformation Assay, Over Expression