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a Weight gain in <t>Redd1</t> −/− mice and their WT littermates fed NC or HFD for 16 weeks ( n = 6 per group). b Mass of eWAT and iWAT in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 8 per group). c Representative images of perilipin (green) and F4/80 (purple) staining in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). Scale bar, 100 μm. d Average adipocyte size in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). e Relative area of F4/80-positive cells in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Relative number of crown-like structures (CLSs) in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). g NF-κB activity in the eWAT from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). h Plasma levels of inflammatory cytokines in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Sh Redd1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation"

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

Journal: Nature Communications

doi: 10.1038/s41467-022-34110-1

a Weight gain in Redd1 −/− mice and their WT littermates fed NC or HFD for 16 weeks ( n = 6 per group). b Mass of eWAT and iWAT in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 8 per group). c Representative images of perilipin (green) and F4/80 (purple) staining in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). Scale bar, 100 μm. d Average adipocyte size in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). e Relative area of F4/80-positive cells in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Relative number of crown-like structures (CLSs) in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). g NF-κB activity in the eWAT from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). h Plasma levels of inflammatory cytokines in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Weight gain in Redd1 −/− mice and their WT littermates fed NC or HFD for 16 weeks ( n = 6 per group). b Mass of eWAT and iWAT in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 8 per group). c Representative images of perilipin (green) and F4/80 (purple) staining in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). Scale bar, 100 μm. d Average adipocyte size in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). e Relative area of F4/80-positive cells in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Relative number of crown-like structures (CLSs) in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). g NF-κB activity in the eWAT from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). h Plasma levels of inflammatory cytokines in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Techniques Used: Staining, Activity Assay, Clinical Proteomics

a Fasting plasma levels of glucose and insulin in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 6 per group). b Representative images of insulin (green)-stained pancreatic islets from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Scale bar, 100 μm. c Quantification of average islet size ( n = 6 per group). d Calculation of the HOMA-IR scores ( n = 6 per group). e Assessment of GTT and ITT in mice fasting for 12 and 6 h, respectively, in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Representative western blots of Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) in eWAT and skeletal muscle from mice injected i.p. with saline or insulin ( n = 3). g Representative western blots of phosphorylated Akt and FOXO1 in the liver of mice injected with saline or insulin ( n = 6). h Quantification of the phosphorylated FOXO1 to total FOXO1 ratio ( n = 6 per group). i Quantification of G6pc , Pck1 , and Fbp1 mRNA levels in the liver ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Fasting plasma levels of glucose and insulin in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 6 per group). b Representative images of insulin (green)-stained pancreatic islets from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Scale bar, 100 μm. c Quantification of average islet size ( n = 6 per group). d Calculation of the HOMA-IR scores ( n = 6 per group). e Assessment of GTT and ITT in mice fasting for 12 and 6 h, respectively, in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Representative western blots of Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) in eWAT and skeletal muscle from mice injected i.p. with saline or insulin ( n = 3). g Representative western blots of phosphorylated Akt and FOXO1 in the liver of mice injected with saline or insulin ( n = 6). h Quantification of the phosphorylated FOXO1 to total FOXO1 ratio ( n = 6 per group). i Quantification of G6pc , Pck1 , and Fbp1 mRNA levels in the liver ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Techniques Used: Clinical Proteomics, Staining, Western Blot, Phospho-proteomics, Membrane, Injection, Saline

a Weight gain over time in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) mice fed HFD for 16 weeks ( n = 6 per group). b Mass measurements for the eWAT and iWAT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of Redd1 fl/fl and Redd1 Δ Adipoq mice fed HFD ( n = 6 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). e , f Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). g Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of phosphorylated IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylated Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after i.p. injection of saline or insulin ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice compared with NC-fed mouse groups ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t-test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Weight gain over time in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) mice fed HFD for 16 weeks ( n = 6 per group). b Mass measurements for the eWAT and iWAT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of Redd1 fl/fl and Redd1 Δ Adipoq mice fed HFD ( n = 6 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). e , f Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). g Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of phosphorylated IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylated Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after i.p. injection of saline or insulin ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice compared with NC-fed mouse groups ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t-test. Source data are provided as a Source Data file.

Techniques Used: Staining, Activity Assay, Clinical Proteomics, Western Blot, Injection, Saline, Expressing, Two Tailed Test

a Weight gain in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ LysM ( R Δ LysM ) mice fed HFD for 16 weeks ( n = 5 per group). b Measurement of fat (eWAT + iWAT) mass in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). e Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). f Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). g Calculation of HOMA-IR scores in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of the insulin-responsive phosphorylation of IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylation of Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice compared with NC-fed mouse groups ( n = 5 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Weight gain in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ LysM ( R Δ LysM ) mice fed HFD for 16 weeks ( n = 5 per group). b Measurement of fat (eWAT + iWAT) mass in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). e Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). f Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). g Calculation of HOMA-IR scores in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of the insulin-responsive phosphorylation of IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylation of Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice compared with NC-fed mouse groups ( n = 5 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques Used: Staining, Activity Assay, Clinical Proteomics, Western Blot, Phospho-proteomics, Expressing, Two Tailed Test

a – c Representative oil red-O (ORO)-stained images of WT and Redd1 −/− SVF cells ( a ), shControl (shC)- or sh-Redd1-transfected 3T3-L1 cells ( b ), and WT ( Redd1 fl/f l , R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) SVF cells ( c ) when cultured in differentiation medium (MDI) and quantification of relative ORO intensity ( n = 4). d – f , Expression levels of adipogenic genes ( d ), REDD1 ( e ), and lipogenic genes ( f ) in R fl/fl and R Δ Adipoq SVF cells cultured in MDI medium and quantification of relative ORO intensity ( n = 4). g Assessment of NF-κB–Luc activity in 3T3-L1 cells transfected either with siRNA for control, Ikka , Ikkb , or NF-κB p65 ( p65 ) or with pcDNA3.1/His- Ikba ( n = 5). h , i Representative images and realative quantification of ORO-stained images ( h ) and expression levels of Pparg and Cebpa ( i ) in 3T3-L1 cells infected with control adenovirus (Ad-C) or adenoviral Redd1 (Ad- R ) after transfection with vector alone or pcDNA3.1/His- Ikba ( n = 4). j NF-κB–Luc activity in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 4). k Cytokine production in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 5). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( g , h ) and two-way ANOVA ( a , i ) followed by the Holm–Sidak post hoc test and an unpaired two-tailed t -test ( b – f , j , k ). Source data are provided as a Source Data file.

Figure Legend Snippet: a – c Representative oil red-O (ORO)-stained images of WT and Redd1 −/− SVF cells ( a ), shControl (shC)- or sh-Redd1-transfected 3T3-L1 cells ( b ), and WT ( Redd1 fl/f l , R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) SVF cells ( c ) when cultured in differentiation medium (MDI) and quantification of relative ORO intensity ( n = 4). d – f , Expression levels of adipogenic genes ( d ), REDD1 ( e ), and lipogenic genes ( f ) in R fl/fl and R Δ Adipoq SVF cells cultured in MDI medium and quantification of relative ORO intensity ( n = 4). g Assessment of NF-κB–Luc activity in 3T3-L1 cells transfected either with siRNA for control, Ikka , Ikkb , or NF-κB p65 ( p65 ) or with pcDNA3.1/His- Ikba ( n = 5). h , i Representative images and realative quantification of ORO-stained images ( h ) and expression levels of Pparg and Cebpa ( i ) in 3T3-L1 cells infected with control adenovirus (Ad-C) or adenoviral Redd1 (Ad- R ) after transfection with vector alone or pcDNA3.1/His- Ikba ( n = 4). j NF-κB–Luc activity in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 4). k Cytokine production in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 5). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( g , h ) and two-way ANOVA ( a , i ) followed by the Holm–Sidak post hoc test and an unpaired two-tailed t -test ( b – f , j , k ). Source data are provided as a Source Data file.

Techniques Used: Staining, Transfection, Cell Culture, Expressing, Activity Assay, Control, Infection, Plasmid Preparation, Two Tailed Test

a Predictive binding conformation between REDD1 and IκBα using computational protein-protein molecular docking methods. b Co-immunoprecipitation analysis of the interaction between REDD1 and IκBα in HEK293 cells transfected with pcDNA3.1/His- Ikba (His- Ikba ) and either pFlag-CMV-1- Redd1 ( Redd1 ) or Redd1 mutants ( R KKAA and R KKRAAA ) ( n = 3). c Representative confocal images of NF-κB p65 nuclear translocalization in HEK293 cells infected with Ad-C, Ad- Redd1 , or its mutants ( n = 4). Scale bar, 50 μm. d Assessment of NF-κB–Luc activity in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or its mutants ( n = 4). e Representative ORO-stained images of 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA and quantification of relative ORO intensity ( n = 4). f Expression levels of Pparg and Cebpa in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). g Production of MCP-1 and TNF-α in macrophages infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( d , e ) and two-way ANOVA ( f , g ) followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Predictive binding conformation between REDD1 and IκBα using computational protein-protein molecular docking methods. b Co-immunoprecipitation analysis of the interaction between REDD1 and IκBα in HEK293 cells transfected with pcDNA3.1/His- Ikba (His- Ikba ) and either pFlag-CMV-1- Redd1 ( Redd1 ) or Redd1 mutants ( R KKAA and R KKRAAA ) ( n = 3). c Representative confocal images of NF-κB p65 nuclear translocalization in HEK293 cells infected with Ad-C, Ad- Redd1 , or its mutants ( n = 4). Scale bar, 50 μm. d Assessment of NF-κB–Luc activity in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or its mutants ( n = 4). e Representative ORO-stained images of 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA and quantification of relative ORO intensity ( n = 4). f Expression levels of Pparg and Cebpa in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). g Production of MCP-1 and TNF-α in macrophages infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( d , e ) and two-way ANOVA ( f , g ) followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Techniques Used: Binding Assay, Immunoprecipitation, Transfection, Infection, Activity Assay, Control, Staining, Expressing

a Weight gain in WT and Redd1 KKAA mice after being fed HFD for 16 weeks ( n = 10 per group). b eWAT and iWAT mass measurements in HFD-fed Redd1 KKAA mice and their WT littermates ( n = 10 per group). c Expression levels of Pparg and Cebpa in the eWAT of Redd1 KKAA mice and WT littermates fed HFD for 10 weeks ( n = 8 per group). d Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 KKAA mice and WT littermates ( n = 5 per group). Scale bar, 100 μm. e NF-κB activity in the eWAT from HFD-fed Redd1 KKAA mice and WT littermates ( n = 6 per group). f , g Plasma levels of inflammatory cytokines in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). h Fasting plasma levels of glucose and insulin in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). i Assessment of GTT and ITT in HFD-fed Redd1 KKAA mice and WT littermates after fasting for 12 and 6 h, respectively ( n = 6 per group). j , k Representative western blots of insulin-responsive Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) levels in the eWAT and skeletal muscle ( j ) and Akt and FOXO1 phosphorylation in the liver ( k ) of HFD-fed Redd1 KKAA mice and WT littermates ( n = 3). l Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 KKAA mice and WT littermates compared with NC-fed mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Weight gain in WT and Redd1 KKAA mice after being fed HFD for 16 weeks ( n = 10 per group). b eWAT and iWAT mass measurements in HFD-fed Redd1 KKAA mice and their WT littermates ( n = 10 per group). c Expression levels of Pparg and Cebpa in the eWAT of Redd1 KKAA mice and WT littermates fed HFD for 10 weeks ( n = 8 per group). d Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 KKAA mice and WT littermates ( n = 5 per group). Scale bar, 100 μm. e NF-κB activity in the eWAT from HFD-fed Redd1 KKAA mice and WT littermates ( n = 6 per group). f , g Plasma levels of inflammatory cytokines in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). h Fasting plasma levels of glucose and insulin in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). i Assessment of GTT and ITT in HFD-fed Redd1 KKAA mice and WT littermates after fasting for 12 and 6 h, respectively ( n = 6 per group). j , k Representative western blots of insulin-responsive Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) levels in the eWAT and skeletal muscle ( j ) and Akt and FOXO1 phosphorylation in the liver ( k ) of HFD-fed Redd1 KKAA mice and WT littermates ( n = 3). l Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 KKAA mice and WT littermates compared with NC-fed mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques Used: Expressing, Staining, Activity Assay, Clinical Proteomics, Western Blot, Phospho-proteomics, Membrane, Two Tailed Test

a Representative images of H&E-stained liver tissues from HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and control mice, and quantification of hepatic steatosis from H&E-stained liver tissues ( n = 6 per group). Scale bars, 100 μm. b Expression levels of Acc , Fasn , and Scd-1 in the liver of HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and their control mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Figure Legend Snippet: a Representative images of H&E-stained liver tissues from HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and control mice, and quantification of hepatic steatosis from H&E-stained liver tissues ( n = 6 per group). Scale bars, 100 μm. b Expression levels of Acc , Fasn , and Scd-1 in the liver of HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and their control mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques Used: Staining, Control, Expressing, Two Tailed Test

Image Search Results

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Weight gain in Redd1 −/− mice and their WT littermates fed NC or HFD for 16 weeks ( n = 6 per group). b Mass of eWAT and iWAT in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 8 per group). c Representative images of perilipin (green) and F4/80 (purple) staining in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). Scale bar, 100 μm. d Average adipocyte size in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). e Relative area of F4/80-positive cells in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Relative number of crown-like structures (CLSs) in the eWAT of NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). g NF-κB activity in the eWAT from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). h Plasma levels of inflammatory cytokines in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Article Snippet: In addition, mouse adipose SVF cells and 3T3-L1 preadipocytes (5.0 × 10 5 cells/well, American Type Culture Collection) were plated and transfected with sh Redd1 (#sc-45807-SH, Santa Cruz Biotechnology, Santa Cruz, CA.

Techniques: Staining, Activity Assay, Clinical Proteomics

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Fasting plasma levels of glucose and insulin in NC- or HFD-fed Redd1 −/− mice and their WT littermates ( n = 6 per group). b Representative images of insulin (green)-stained pancreatic islets from NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 6 per group). Scale bar, 100 μm. c Quantification of average islet size ( n = 6 per group). d Calculation of the HOMA-IR scores ( n = 6 per group). e Assessment of GTT and ITT in mice fasting for 12 and 6 h, respectively, in NC- or HFD-fed Redd1 −/− mice and WT littermates ( n = 8 per group). f Representative western blots of Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) in eWAT and skeletal muscle from mice injected i.p. with saline or insulin ( n = 3). g Representative western blots of phosphorylated Akt and FOXO1 in the liver of mice injected with saline or insulin ( n = 6). h Quantification of the phosphorylated FOXO1 to total FOXO1 ratio ( n = 6 per group). i Quantification of G6pc , Pck1 , and Fbp1 mRNA levels in the liver ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using two-way ANOVA followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Techniques: Clinical Proteomics, Staining, Western Blot, Phospho-proteomics, Membrane, Injection, Saline

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Weight gain over time in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) mice fed HFD for 16 weeks ( n = 6 per group). b Mass measurements for the eWAT and iWAT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of Redd1 fl/fl and Redd1 Δ Adipoq mice fed HFD ( n = 6 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). e , f Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). g Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice ( n = 6 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of phosphorylated IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylated Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice after i.p. injection of saline or insulin ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ Adipoq mice compared with NC-fed mouse groups ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t-test. Source data are provided as a Source Data file.

Techniques: Staining, Activity Assay, Clinical Proteomics, Western Blot, Injection, Saline, Expressing, Two Tailed Test

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Weight gain in Redd1 fl/fl ( R fl/fl ) and Redd1 Δ LysM ( R Δ LysM ) mice fed HFD for 16 weeks ( n = 5 per group). b Measurement of fat (eWAT + iWAT) mass in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). c Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). Scale bar, 100 μm. d NF-κB activity in the eWAT from HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). e Plasma levels of inflammatory cytokines in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). f Fasting plasma levels of glucose and insulin in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). g Calculation of HOMA-IR scores in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 5 per group). h Assessment of GTT and ITT in HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice fasting for 12 and 6 h, respectively ( n = 5 per group). i , j Representative western blots of the insulin-responsive phosphorylation of IRS-1 and Akt in the eWAT and skeletal muscle ( i ) and phosphorylation of Akt and FOXO1 in the liver ( j ) of NC- or HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice ( n = 3). k Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 fl/fl and Redd1 Δ LysM mice compared with NC-fed mouse groups ( n = 5 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques: Staining, Activity Assay, Clinical Proteomics, Western Blot, Phospho-proteomics, Expressing, Two Tailed Test

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a – c Representative oil red-O (ORO)-stained images of WT and Redd1 −/− SVF cells ( a ), shControl (shC)- or sh-Redd1-transfected 3T3-L1 cells ( b ), and WT ( Redd1 fl/f l , R fl/fl ) and Redd1 Δ Adipoq ( R Δ Adipoq ) SVF cells ( c ) when cultured in differentiation medium (MDI) and quantification of relative ORO intensity ( n = 4). d – f , Expression levels of adipogenic genes ( d ), REDD1 ( e ), and lipogenic genes ( f ) in R fl/fl and R Δ Adipoq SVF cells cultured in MDI medium and quantification of relative ORO intensity ( n = 4). g Assessment of NF-κB–Luc activity in 3T3-L1 cells transfected either with siRNA for control, Ikka , Ikkb , or NF-κB p65 ( p65 ) or with pcDNA3.1/His- Ikba ( n = 5). h , i Representative images and realative quantification of ORO-stained images ( h ) and expression levels of Pparg and Cebpa ( i ) in 3T3-L1 cells infected with control adenovirus (Ad-C) or adenoviral Redd1 (Ad- R ) after transfection with vector alone or pcDNA3.1/His- Ikba ( n = 4). j NF-κB–Luc activity in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 4). k Cytokine production in mouse peritoneal macrophages infected with Ad-C or Ad- Redd1 ( n = 5). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( g , h ) and two-way ANOVA ( a , i ) followed by the Holm–Sidak post hoc test and an unpaired two-tailed t -test ( b – f , j , k ). Source data are provided as a Source Data file.

Techniques: Staining, Transfection, Cell Culture, Expressing, Activity Assay, Control, Infection, Plasmid Preparation, Two Tailed Test

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Predictive binding conformation between REDD1 and IκBα using computational protein-protein molecular docking methods. b Co-immunoprecipitation analysis of the interaction between REDD1 and IκBα in HEK293 cells transfected with pcDNA3.1/His- Ikba (His- Ikba ) and either pFlag-CMV-1- Redd1 ( Redd1 ) or Redd1 mutants ( R KKAA and R KKRAAA ) ( n = 3). c Representative confocal images of NF-κB p65 nuclear translocalization in HEK293 cells infected with Ad-C, Ad- Redd1 , or its mutants ( n = 4). Scale bar, 50 μm. d Assessment of NF-κB–Luc activity in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or its mutants ( n = 4). e Representative ORO-stained images of 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA and quantification of relative ORO intensity ( n = 4). f Expression levels of Pparg and Cebpa in 3T3-L1 cells infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). g Production of MCP-1 and TNF-α in macrophages infected with Ad-control, Ad- Redd1 , or Ad- Redd1 KKAA ( n = 4). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using one-way ANOVA ( d , e ) and two-way ANOVA ( f , g ) followed by the Holm–Sidak post hoc test. Source data are provided as a Source Data file.

Techniques: Binding Assay, Immunoprecipitation, Transfection, Infection, Activity Assay, Control, Staining, Expressing

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Weight gain in WT and Redd1 KKAA mice after being fed HFD for 16 weeks ( n = 10 per group). b eWAT and iWAT mass measurements in HFD-fed Redd1 KKAA mice and their WT littermates ( n = 10 per group). c Expression levels of Pparg and Cebpa in the eWAT of Redd1 KKAA mice and WT littermates fed HFD for 10 weeks ( n = 8 per group). d Representative images showing perilipin (green) and F4/80 (purple) staining in the eWAT of HFD-fed Redd1 KKAA mice and WT littermates ( n = 5 per group). Scale bar, 100 μm. e NF-κB activity in the eWAT from HFD-fed Redd1 KKAA mice and WT littermates ( n = 6 per group). f , g Plasma levels of inflammatory cytokines in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). h Fasting plasma levels of glucose and insulin in HFD-fed Redd1 KKAA mice and WT littermates ( n = 8 per group). i Assessment of GTT and ITT in HFD-fed Redd1 KKAA mice and WT littermates after fasting for 12 and 6 h, respectively ( n = 6 per group). j , k Representative western blots of insulin-responsive Akt phosphorylation and plasma membrane-associated GLUT4 (PM-GLUT4) levels in the eWAT and skeletal muscle ( j ) and Akt and FOXO1 phosphorylation in the liver ( k ) of HFD-fed Redd1 KKAA mice and WT littermates ( n = 3). l Relative expression levels of G6pc , Pck1 , and Fbp1 in the liver of HFD-fed Redd1 KKAA mice and WT littermates compared with NC-fed mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques: Expressing, Staining, Activity Assay, Clinical Proteomics, Western Blot, Phospho-proteomics, Membrane, Two Tailed Test

Journal: Nature Communications

Article Title: REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation

doi: 10.1038/s41467-022-34110-1

Figure Lengend Snippet: a Representative images of H&E-stained liver tissues from HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and control mice, and quantification of hepatic steatosis from H&E-stained liver tissues ( n = 6 per group). Scale bars, 100 μm. b Expression levels of Acc , Fasn , and Scd-1 in the liver of HFD-fed Redd1 −/− , Redd1 ΔAdipoq , Redd1 Δ LysM , Redd1 KKAA , and their control mice ( n = 6 per group). Bar graphs represent mean ± s.e.m. Statistical significance was calculated using an unpaired two-tailed t -test. Source data are provided as a Source Data file.

Techniques: Staining, Control, Expressing, Two Tailed Test

Carboplatin caused C2C12 myotube atrophy and increased REDD1 expression. C2C12 myotubes were treated with carboplatin for 24 or 48 h. ( A ) C2C12 myotube diameter was decreased after carboplatin treatment compared with vehicle in C2C12 cells differentiated for either 4 or 6 days. Scale bar = 50 μm. ( B ) REDD1 mRNA expression was increased in C2C12 myotubes differentiation for 4 days and treated with carboplatin for either 24 or 48 h. ( C ) REDD1 protein expression was increased in C2C12 myotubes differentiation for 4 days and treated with carboplatin for either 24 or 48 h. ( A ) One‐way ANOVA with Tukey's post‐hoc test for multiple comparisons, or Student's t ‐test. ( B–C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. * P < .05 ** P < 0.01, *** P < 0.001, **** P < 0.0001. ( A ) Approximately 100 myotubes assessed, n = 3 biological replicates for all groups. ( B–C ) n = 3 biological replicates for all groups.

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Carboplatin caused C2C12 myotube atrophy and increased REDD1 expression. C2C12 myotubes were treated with carboplatin for 24 or 48 h. ( A ) C2C12 myotube diameter was decreased after carboplatin treatment compared with vehicle in C2C12 cells differentiated for either 4 or 6 days. Scale bar = 50 μm. ( B ) REDD1 mRNA expression was increased in C2C12 myotubes differentiation for 4 days and treated with carboplatin for either 24 or 48 h. ( C ) REDD1 protein expression was increased in C2C12 myotubes differentiation for 4 days and treated with carboplatin for either 24 or 48 h. ( A ) One‐way ANOVA with Tukey's post‐hoc test for multiple comparisons, or Student's t ‐test. ( B–C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. * P < .05 ** P < 0.01, *** P < 0.001, **** P < 0.0001. ( A ) Approximately 100 myotubes assessed, n = 3 biological replicates for all groups. ( B–C ) n = 3 biological replicates for all groups.

Article Snippet: pLKO.1 (Addgene plasmid #10878 ) (shControl), pcDNA3‐EGFP (Addgene plasmid #13031), and REDD1 shRNA (shREDD1) construct TRCN0000176020 (Sigma, Darmstadt, Germany) were used for in vivo electroporation.

Techniques: Expressing

Loss of REDD1 in vivo attenuates carboplatin‐induced cachexia. ( A ) REDD1 mRNA expression in the TA muscle of wild‐type or REDD1 knockout (REDD1 KO) mice treated with carboplatin. ( B ) Whole animal body weight of mice treated with vehicle or carboplatin. ( C ) Weight of the TA, gastrocnemius, EDL and soleus muscles of mice treated with vehicle or carboplatin. ( A ) Student's t ‐test * P < 0.05. ( B–C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ( B ) * P < 0.05, ** P < 0.01 wild‐type + vehicle compared with wild‐type + carboplatin; ‡ P < 0.05 wild‐type + carboplatin compared with REDD1 KO + carboplatin. ( C )* P < 0.05, ** P < 0.01, **** P < 0.0001. n = 8 biological replicates for each group ( A–C ).

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Loss of REDD1 in vivo attenuates carboplatin‐induced cachexia. ( A ) REDD1 mRNA expression in the TA muscle of wild‐type or REDD1 knockout (REDD1 KO) mice treated with carboplatin. ( B ) Whole animal body weight of mice treated with vehicle or carboplatin. ( C ) Weight of the TA, gastrocnemius, EDL and soleus muscles of mice treated with vehicle or carboplatin. ( A ) Student's t ‐test * P < 0.05. ( B–C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ( B ) * P < 0.05, ** P < 0.01 wild‐type + vehicle compared with wild‐type + carboplatin; ‡ P < 0.05 wild‐type + carboplatin compared with REDD1 KO + carboplatin. ( C )* P < 0.05, ** P < 0.01, **** P < 0.0001. n = 8 biological replicates for each group ( A–C ).

Techniques: In Vivo, Expressing, Knock-Out

Loss of REDD1 prevents carboplatin‐induced myofibre atrophy. ( A ) Representative cross sections and CSA quantification from the TA muscle of mice treated with vehicle or carboplatin. Scale bar = 50 μm. ( B ) Myofibre distribution frequency from the TA muscle of mice treated with vehicle or carboplatin. ( C ) Representative cross sections and quantification of MyHC fibre type from the TA muscle of mice treated with vehicle or carboplatin. ( A , C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ** P < 0.01. n = 3 biological replicates for ( A–C ). Average CSA from ~200 fibres per replicate for ( A–B ) and fibre‐type quantitation ( C ).

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Loss of REDD1 prevents carboplatin‐induced myofibre atrophy. ( A ) Representative cross sections and CSA quantification from the TA muscle of mice treated with vehicle or carboplatin. Scale bar = 50 μm. ( B ) Myofibre distribution frequency from the TA muscle of mice treated with vehicle or carboplatin. ( C ) Representative cross sections and quantification of MyHC fibre type from the TA muscle of mice treated with vehicle or carboplatin. ( A , C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ** P < 0.01. n = 3 biological replicates for ( A–C ). Average CSA from ~200 fibres per replicate for ( A–B ) and fibre‐type quantitation ( C ).

Techniques: Quantitation Assay

Loss of REDD1 attenuates carboplatin‐induced protein synthesis. Puromycin incorporation in vivo from the TA muscle of mice treated with vehicle or carboplatin. Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons * P < 0.05. n = 3 biological replicates for each group.

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Loss of REDD1 attenuates carboplatin‐induced protein synthesis. Puromycin incorporation in vivo from the TA muscle of mice treated with vehicle or carboplatin. Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons * P < 0.05. n = 3 biological replicates for each group.

Techniques: In Vivo

Knockdown of REDD1 expression both in vitro and in vivo attenuates carboplatin‐induced myofibre atrophy. ( A ) Representative images of carboplatin‐treated C2C12 myotubes electroporated with REDD1 shRNA or control shRNA and quantification of GFP positive myotube diameter. ( B ) REDD1 mRNA expression from C2C12 treated with carboplatin. ( C ) Representative cross sections and CSA quantification of GFP positive fibres. ( D ) REDD1 mRNA expression from the TA of carboplatin‐treated mice electroporated with shControl or shREDD1. ( A – D ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ** P < 0.01, *** P < 0.001. n = 3 biological replicates for ( A – D ). Average myotube diameter from ~75 GFP positive myotubes per replicate ( A ). Average CSA from ~100 GFP positive fibres per replicate for ( C ). ( A , C ) Scale bar = 50 μm. n = 3 biological replicates for ( A – D ).

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Knockdown of REDD1 expression both in vitro and in vivo attenuates carboplatin‐induced myofibre atrophy. ( A ) Representative images of carboplatin‐treated C2C12 myotubes electroporated with REDD1 shRNA or control shRNA and quantification of GFP positive myotube diameter. ( B ) REDD1 mRNA expression from C2C12 treated with carboplatin. ( C ) Representative cross sections and CSA quantification of GFP positive fibres. ( D ) REDD1 mRNA expression from the TA of carboplatin‐treated mice electroporated with shControl or shREDD1. ( A – D ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. ** P < 0.01, *** P < 0.001. n = 3 biological replicates for ( A – D ). Average myotube diameter from ~75 GFP positive myotubes per replicate ( A ). Average CSA from ~100 GFP positive fibres per replicate for ( C ). ( A , C ) Scale bar = 50 μm. n = 3 biological replicates for ( A – D ).

Techniques: Expressing, In Vitro, In Vivo, shRNA

Loss of REDD1 prevents carboplatin‐induced muscle weakness. ( A ) Deletion of REDD1 prevents carboplatin‐induced forelimb grip strength reduction in vivo . ( B ) Absolute force generated from the EDL muscle of mice treated with vehicle or carboplatin. ( C ) Specific force of the EDL muscle of mice treated with vehicle or carboplatin. ( A – C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. (A) *** P < 0.001, compared with wild‐type + vehicle. (B) * P < 0.05, ** P < 0.01 all groups compared with wild‐type + carboplatin. ( C ) * P < 0.05, ** P < 0.01 wild‐type + vehicle compared with wild‐type + carboplatin n = 8 biological replicates for all groups.

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Loss of REDD1 prevents chemotherapy‐induced muscle atrophy and weakness in mice

doi: 10.1002/jcsm.12795

Figure Lengend Snippet: Loss of REDD1 prevents carboplatin‐induced muscle weakness. ( A ) Deletion of REDD1 prevents carboplatin‐induced forelimb grip strength reduction in vivo . ( B ) Absolute force generated from the EDL muscle of mice treated with vehicle or carboplatin. ( C ) Specific force of the EDL muscle of mice treated with vehicle or carboplatin. ( A – C ) Two‐way ANOVA with Tukey's post‐hoc test for multiple comparisons. (A) *** P < 0.001, compared with wild‐type + vehicle. (B) * P < 0.05, ** P < 0.01 all groups compared with wild‐type + carboplatin. ( C ) * P < 0.05, ** P < 0.01 wild‐type + vehicle compared with wild‐type + carboplatin n = 8 biological replicates for all groups.

Techniques: In Vivo, Generated

Amyloid β (Aβ) increased regulated in development and DNA damage response 1 (REDD1) protein levels in the hippocampus. ( A ) Aβ-induced REDD1 upregulation. Hippocampal slices were incubated with Aβ for 4 h. ( B ) Aβ-induced REDD1 upregulation in the hippocampus. Aβ was injected into the fissure layer of the hippocampal CA1 region. Bar = 50 μm. Data represented as mean ± SD with raw data. * p < 0.05 vs. vehicle-treated group.

Journal: International Journal of Molecular Sciences

Article Title: REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment

doi: 10.3390/ijms21249482

Figure Lengend Snippet: Amyloid β (Aβ) increased regulated in development and DNA damage response 1 (REDD1) protein levels in the hippocampus. ( A ) Aβ-induced REDD1 upregulation. Hippocampal slices were incubated with Aβ for 4 h. ( B ) Aβ-induced REDD1 upregulation in the hippocampus. Aβ was injected into the fissure layer of the hippocampal CA1 region. Bar = 50 μm. Data represented as mean ± SD with raw data. * p < 0.05 vs. vehicle-treated group.

Article Snippet: REDD1 shRNA (m) lentiviral particles were purchased from Santa Cruz Biotechnology (sc-45807-V, Santa Cruz, CA, USA).

Techniques: Incubation, Injection

Fyn/ERK/S6 signaling is involved in Aβ-induced REDD1 translation. ( A , B ) Aβ increased REDD1 with translational modulation. Hippocampal slices were incubated with Aβ for 4 h with or without anisomycin (40 μM) or actinomycin D (50 μM). ( C , D ) Aβ activated Fyn/ERK/S6 signaling. Hippocampal slices were incubated with Aβ for 4 h. ( E , F ) Fyn/ERK/S6 signaling is required for Aβ-increased REDD1. Hippocampal slices were incubated with Aβ for 4 h with or without PP1 (10 μM), U0126 (50 μM), SL0101-1 (50 μM), or MPEP (10 μM). Data represented as mean ± SD with raw data. * p < 0.05 vs. vehicle-treated group. # p < 0.05 vs. Aβ-treated group.

Journal: International Journal of Molecular Sciences

Article Title: REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment

doi: 10.3390/ijms21249482

Figure Lengend Snippet: Fyn/ERK/S6 signaling is involved in Aβ-induced REDD1 translation. ( A , B ) Aβ increased REDD1 with translational modulation. Hippocampal slices were incubated with Aβ for 4 h with or without anisomycin (40 μM) or actinomycin D (50 μM). ( C , D ) Aβ activated Fyn/ERK/S6 signaling. Hippocampal slices were incubated with Aβ for 4 h. ( E , F ) Fyn/ERK/S6 signaling is required for Aβ-increased REDD1. Hippocampal slices were incubated with Aβ for 4 h with or without PP1 (10 μM), U0126 (50 μM), SL0101-1 (50 μM), or MPEP (10 μM). Data represented as mean ± SD with raw data. * p < 0.05 vs. vehicle-treated group. # p < 0.05 vs. Aβ-treated group.

Article Snippet: REDD1 shRNA (m) lentiviral particles were purchased from Santa Cruz Biotechnology (sc-45807-V, Santa Cruz, CA, USA).

Techniques: Incubation

REDD1 is required for Aβ-induced synaptic dysfunction. ( A ) REDD1 inducer suppressed hippocampal long-term potentiation (LTP). Hippocampal slices incubated with REDD1 inducer (50 μM) for 4 h. Data represented as mean ± SD. ( B ) REDD1 inducer suppressed mTOR signaling in the hippocampus. Data represented as mean ± SD with raw data. ( C ) Aβ suppressed hippocampal LTP. Hippocampal slices incubated with Aβ (1 μM) for 4 h. Data represented as mean ± SD. ( D ) REDD1 knockdown blocked Aβ-induced LTP impairment. REDD1 shRNA (m) lentiviral particle or scramble lentiviral particle was bilaterally injected into hippocampal fissure layer. Hippocampal slices prepared and incubated with Aβ for 4 h, 7 d after lentiviral injection. Data represented as mean ± SD.

Journal: International Journal of Molecular Sciences

Article Title: REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment

doi: 10.3390/ijms21249482

Figure Lengend Snippet: REDD1 is required for Aβ-induced synaptic dysfunction. ( A ) REDD1 inducer suppressed hippocampal long-term potentiation (LTP). Hippocampal slices incubated with REDD1 inducer (50 μM) for 4 h. Data represented as mean ± SD. ( B ) REDD1 inducer suppressed mTOR signaling in the hippocampus. Data represented as mean ± SD with raw data. ( C ) Aβ suppressed hippocampal LTP. Hippocampal slices incubated with Aβ (1 μM) for 4 h. Data represented as mean ± SD. ( D ) REDD1 knockdown blocked Aβ-induced LTP impairment. REDD1 shRNA (m) lentiviral particle or scramble lentiviral particle was bilaterally injected into hippocampal fissure layer. Hippocampal slices prepared and incubated with Aβ for 4 h, 7 d after lentiviral injection. Data represented as mean ± SD.

Article Snippet: REDD1 shRNA (m) lentiviral particles were purchased from Santa Cruz Biotechnology (sc-45807-V, Santa Cruz, CA, USA).

Techniques: Incubation, Knockdown, shRNA, Injection

REDD1 reduction rescued Aβ-induced memory impairment. ( A ) REDD1 shRNA (m) lentiviral particle or control lentiviral particle was bilaterally injected into hippocampal fissure layer. Aβ was injected into the lateral ventricle 7 d later than the shRNA injection was. ( B , C ) REDD1 knockdown blocked Aβ-induced passive-avoidance memory deficit. Data represented as mean ± SD. ** p < 0.01 vs. sham group; # p < 0.05 vs. scramble + Aβ group. ( D , E ) REDD1 knockdown blocked Aβ-induced object-recognition memory deficit. Data represented as mean ± SD. # p < 0.05. ** p < 0.01.

Journal: International Journal of Molecular Sciences

Article Title: REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment

doi: 10.3390/ijms21249482

Figure Lengend Snippet: REDD1 reduction rescued Aβ-induced memory impairment. ( A ) REDD1 shRNA (m) lentiviral particle or control lentiviral particle was bilaterally injected into hippocampal fissure layer. Aβ was injected into the lateral ventricle 7 d later than the shRNA injection was. ( B , C ) REDD1 knockdown blocked Aβ-induced passive-avoidance memory deficit. Data represented as mean ± SD. ** p < 0.01 vs. sham group; # p < 0.05 vs. scramble + Aβ group. ( D , E ) REDD1 knockdown blocked Aβ-induced object-recognition memory deficit. Data represented as mean ± SD. # p < 0.05. ** p < 0.01.

Article Snippet: REDD1 shRNA (m) lentiviral particles were purchased from Santa Cruz Biotechnology (sc-45807-V, Santa Cruz, CA, USA).

Techniques: shRNA, Control, Injection, Knockdown

REDD1 expression in different ovarian epithelial tissues

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: REDD1 expression in different ovarian epithelial tissues

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

Correlation between cytoplasmic REDD1 expression and clinicopathologic factors

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Correlation between cytoplasmic REDD1 expression and clinicopathologic factors

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

Immunoreactivity patterns of REDD1 in ovarian carcinomas. a REDD1-high expression in serous carcinoma. b Serous carcinoma cells show no REDD1 staining. c Diffuse and strong positive staining for REDD1 in endometrioid carcinoma. d Endometrioid carcinoma cells show very weak cytoplasmic REDD1 staining. e REDD1-positive staining in mucinous adenocarcinoma. f Mucinous adenocarcinoma do not exhibit REDD1 staining. g Positive nuclear staining for REDD1 in clear cell carcinoma. h Clear cell carcinoma cells do not show staining for REDD1 (original magnification × 200)

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Immunoreactivity patterns of REDD1 in ovarian carcinomas. a REDD1-high expression in serous carcinoma. b Serous carcinoma cells show no REDD1 staining. c Diffuse and strong positive staining for REDD1 in endometrioid carcinoma. d Endometrioid carcinoma cells show very weak cytoplasmic REDD1 staining. e REDD1-positive staining in mucinous adenocarcinoma. f Mucinous adenocarcinoma do not exhibit REDD1 staining. g Positive nuclear staining for REDD1 in clear cell carcinoma. h Clear cell carcinoma cells do not show staining for REDD1 (original magnification × 200)

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing, Staining

Correlation between nuclear REDD1 expression and clinicopathologic factor

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Correlation between nuclear REDD1 expression and clinicopathologic factor

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Cytoplasmic REDD1 expression and OS

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Cytoplasmic REDD1 expression and DFS

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

Kaplan–Meier survival curves ovarian carcinoma patients grouped by low and high REDD1 expression levels. a OS curves in all patients with ovarian cancer ( n = 229). b DFS curves in all patients ( n = 229). c OS curves in patients with ovarian serous carcinoma ( n = 125). d DFS curves in patients with ovarian serous carcinoma ( n = 125)

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Kaplan–Meier survival curves ovarian carcinoma patients grouped by low and high REDD1 expression levels. a OS curves in all patients with ovarian cancer ( n = 229). b DFS curves in all patients ( n = 229). c OS curves in patients with ovarian serous carcinoma ( n = 125). d DFS curves in patients with ovarian serous carcinoma ( n = 125)

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

The multivariate Cox proportional- hazards regression for OS

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: The multivariate Cox proportional- hazards regression for OS

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

The multivariate Cox proportional- hazards regression for DFS

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: The multivariate Cox proportional- hazards regression for DFS

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Expressing

REDD1 enhance cell migration and invasion in ovarian cancer. a Western blotting detected REDD1 expression level in human ovarian epithelial cancer cell lines. b Construction of ovarian cancer cell lines with REDD1 overexpression or knockdown. c Transwell assays illustrate that REDD1 enhances ovarian cancer cell migration and invasion ability

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: REDD1 enhance cell migration and invasion in ovarian cancer. a Western blotting detected REDD1 expression level in human ovarian epithelial cancer cell lines. b Construction of ovarian cancer cell lines with REDD1 overexpression or knockdown. c Transwell assays illustrate that REDD1 enhances ovarian cancer cell migration and invasion ability

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: Migration, Western Blot, Expressing, Over Expression, Knockdown

Research of REDD1 in different tumor types

Journal: Diagnostic Pathology

Article Title: Overexpression of the recently identified oncogene REDD1 correlates with tumor progression and is an independent unfavorable prognostic factor for ovarian carcinoma

doi: 10.1186/s13000-018-0754-4

Figure Lengend Snippet: Research of REDD1 in different tumor types

Article Snippet: REDD1 short hairpin RNAs (shRNAs) were purchased from Genechem (Shanghai, China).

Techniques: In Vitro, Expressing, Over Expression, Inhibition, Activation Assay, Phospho-proteomics, In Vivo

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