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redd 1 (Santa Cruz Biotechnology)

Name: redd 1
Brand: Santa Cruz Biotechnology
Rating: 93 (18 reviews)

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Santa Cruz Biotechnology redd 1
Redd 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/redd 1/product/Santa Cruz Biotechnology
Average 93 stars, based on 18 article reviews

redd 1 - by Bioz Stars, 2026-03

93/100 stars

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DDIT4 in pan-cancers. A. Histogram of DDIT4 expression levels in BEAS-2B and A549 cell lines. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. Variables are presented as mean ± SD. B. Forest plot of cancer types whose prognosis was significantly correlated with DDIT4. C. Differential analysis of DDIT4 expression in pan-cancers obtained from the TIMER 2.0 database. *: P < 0.05, **: P < 0.01, ***: P < 0.001. Variables are presented as mean ± SD.

Journal: American Journal of Translational Research

Article Title: A novel signature based on twelve programmed cell death patterns to predict the prognosis of lung adenocarcinoma

doi: 10.62347/UAMN8558

Figure Lengend Snippet: DDIT4 in pan-cancers. A. Histogram of DDIT4 expression levels in BEAS-2B and A549 cell lines. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. Variables are presented as mean ± SD. B. Forest plot of cancer types whose prognosis was significantly correlated with DDIT4. C. Differential analysis of DDIT4 expression in pan-cancers obtained from the TIMER 2.0 database. *: P < 0.05, **: P < 0.01, ***: P < 0.001. Variables are presented as mean ± SD.

Article Snippet: Antibodies were purchased from manufacturers: DDIT4 (Santa Cruz, USA, sc-271158), β-Actin (CST, USA, #3700).

Techniques: Expressing

DDIT4 knock-down retarded the proliferation of LUAD cells in vitro. (A) qPCR and WB showed the efficiency of siRNAs. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. (B, C) Colony formation assays and growth curves (days 1-4) represent the proliferation of A549/PC9 cells infected with si-NC or DDIT4-si1/2. Representative images of the crystal violet staining of cells in 6-well plates were shown. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. (D, E) DDIT4 knockdown resulted in increased apoptosis in LUAD cells. Representative FACS images were shown. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference (D), and representative in situ fluorescence images (20× magnification) were also shown (E). Scale bars = 100 μm. *: P < 0.05, **: P < 0.01, ***: P < 0.001. Variables are presented as mean ± SD.

Journal: American Journal of Translational Research

Article Title: A novel signature based on twelve programmed cell death patterns to predict the prognosis of lung adenocarcinoma

doi: 10.62347/UAMN8558

Figure Lengend Snippet: DDIT4 knock-down retarded the proliferation of LUAD cells in vitro. (A) qPCR and WB showed the efficiency of siRNAs. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. (B, C) Colony formation assays and growth curves (days 1-4) represent the proliferation of A549/PC9 cells infected with si-NC or DDIT4-si1/2. Representative images of the crystal violet staining of cells in 6-well plates were shown. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference. (D, E) DDIT4 knockdown resulted in increased apoptosis in LUAD cells. Representative FACS images were shown. Data represent the means ± SD of 3 independent experiments and t test was used to analyze the difference (D), and representative in situ fluorescence images (20× magnification) were also shown (E). Scale bars = 100 μm. *: P < 0.05, **: P < 0.01, ***: P < 0.001. Variables are presented as mean ± SD.

Article Snippet: Antibodies were purchased from manufacturers: DDIT4 (Santa Cruz, USA, sc-271158), β-Actin (CST, USA, #3700).

Techniques: Knockdown, In Vitro, Infection, Staining, In Situ, Fluorescence

( a ) CK21 (50 mM) reduced the expression of DDIT4 in AsPC-1, Panc-1, U049MAI, and U123M15-T after 24 hoursr of culture. ( b ) Baseline expression of DDIT4 in different tumor cells (without CK21 treatment).

Journal: eLife

Article Title: A novel triptolide analog downregulates NF-κB and induces mitochondrial apoptosis pathways in human pancreatic cancer

doi: 10.7554/eLife.85862

Figure Lengend Snippet: ( a ) CK21 (50 mM) reduced the expression of DDIT4 in AsPC-1, Panc-1, U049MAI, and U123M15-T after 24 hoursr of culture. ( b ) Baseline expression of DDIT4 in different tumor cells (without CK21 treatment).

Article Snippet: Antibody , Recombinant anti-REDD-1/DDIT4 (Rabbit monoclonal) , Abcam , ab191871 , (1:1000).

Techniques: Expressing

( a ) knockdown of DDIT4 in Panc-1 did not alter response to CK21 (50 nM). ( b ) AsPC-1 overexpression of DDIT4 did not alter response to CK21 (50 nM).

Journal: eLife

Article Title: A novel triptolide analog downregulates NF-κB and induces mitochondrial apoptosis pathways in human pancreatic cancer

doi: 10.7554/eLife.85862

Figure Lengend Snippet: ( a ) knockdown of DDIT4 in Panc-1 did not alter response to CK21 (50 nM). ( b ) AsPC-1 overexpression of DDIT4 did not alter response to CK21 (50 nM).

Article Snippet: Antibody , Recombinant anti-REDD-1/DDIT4 (Rabbit monoclonal) , Abcam , ab191871 , (1:1000).

Techniques: Over Expression

Journal: eLife

Article Title: A novel triptolide analog downregulates NF-κB and induces mitochondrial apoptosis pathways in human pancreatic cancer

doi: 10.7554/eLife.85862

Figure Lengend Snippet:

Article Snippet: Antibody , Recombinant anti-REDD-1/DDIT4 (Rabbit monoclonal) , Abcam , ab191871 , (1:1000).

Techniques: Luciferase, Transfection, Staining, Bradford Assay, Recombinant, SYBR Green Assay

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

Fig. 1 Chemotherapeutic drugs induce REDD1 and downregulate VEGFR-2/3 expression without altering their mRNA levels. a, b REDD1 mRNA and protein levels in the HUVECs and HLECs treated with doxorubicin (DOX; 3 nM) for 24 h. c Microarray analysis of total and polysomal mRNAs puriﬁed from the HUVECs infected with control adenovirus (Ad-C) or Ad-Redd1 (Ad-R). Heat map of receptor genes involved in angiogenesis expressed as the fold change in total and polysomal mRNA levels in the Ad-Redd1-transfected HUVECs compared with the Ad-C- transfected cells (n = 3). d VEGFR-1, VEGFR-2, EGFR, and IGF-1Rβ expression levels in the HUVECs treated with DOX (3 nM), paclitaxel (PTX; 25 nM), or cisplatin (CisPt; 2 μM) for 24 h. e VEGFR-2 protein and mRNA levels in the HUVECs treated with chemotherapeutic drugs. f, g VEGFR- 3, EGFR, and IGF-1Rβ expression levels (f) and VEGFR-3 expression at the protein and mRNA levels (g) in the HLECs treated with chemotherapeutic drugs for 24 h. Data are presented as the mean ± SD (n = 4). ***P < 0.001; NS, not signiﬁcant.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 1 Chemotherapeutic drugs induce REDD1 and downregulate VEGFR-2/3 expression without altering their mRNA levels. a, b REDD1 mRNA and protein levels in the HUVECs and HLECs treated with doxorubicin (DOX; 3 nM) for 24 h. c Microarray analysis of total and polysomal mRNAs puriﬁed from the HUVECs infected with control adenovirus (Ad-C) or Ad-Redd1 (Ad-R). Heat map of receptor genes involved in angiogenesis expressed as the fold change in total and polysomal mRNA levels in the Ad-Redd1-transfected HUVECs compared with the Ad-C- transfected cells (n = 3). d VEGFR-1, VEGFR-2, EGFR, and IGF-1Rβ expression levels in the HUVECs treated with DOX (3 nM), paclitaxel (PTX; 25 nM), or cisplatin (CisPt; 2 μM) for 24 h. e VEGFR-2 protein and mRNA levels in the HUVECs treated with chemotherapeutic drugs. f, g VEGFR- 3, EGFR, and IGF-1Rβ expression levels (f) and VEGFR-3 expression at the protein and mRNA levels (g) in the HLECs treated with chemotherapeutic drugs for 24 h. Data are presented as the mean ± SD (n = 4). ***P < 0.001; NS, not signiﬁcant.

Article Snippet: Some cells were infected with Redd1 (Ad-Redd1) or empty adenovirus (Ad-Control; Genenmed, Inc., Seoul, South Korea) at a multiplicity of infection (MOI) of 50 for 4 h or transfected with 80 nM small interfering RNA (siRNA), either the control (#SC-37007) or Redd1 (#SC45806; Santa Cruz Biotechnology, Dallas, TX), using Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions, followed by continuous culturing in fresh medium for 24 h. Tumor cells (HeLa, B16F1, and B16F10 cells) were cultured in Dulbecco’s modified Eagle’s medium supplemented with FBS (10%), penicillin (100 U/ mL), and streptomycin (100 μg/mL).

Techniques: Expressing, Microarray, Infection, Control, Transfection

Fig. 2 Low-dose DOX impairs Vegfr-2 translation and angiogenesis via REDD1 induction. VEGFR-1/2 expression and VEGF-A-induced angiogenesis were examined in HUVECs treated with DOX following transfection with control (siC) or Redd1 siRNA (siR). a, b Western blots of REDD1 and VEGFR-1/2 (a) as well as phosphorylated mTOR, 4E-BP1, and S6K (b). c Polysome proﬁling using sucrose density gradient ultracentrifugation. d qRT-PCR of Vegfr-1/2 mRNAs associated with high-molecular-weight polysomes (n = 4). e Western blots of phosphorylated VEGFR-2, ERK, and Akt in the HUVECs stimulated with VEGF-A. f Representative images of the migration (upper) and tube formation (lower) of the HUVECs stimulated with VEGF-A were obtained using Boyden chamber and Matrigel-based morphogenesis assays, respectively. g, h Quantitation of migration (g) and tube formation (h) was performed using ImageJ software (n = 4). Data are presented as the mean ± SD. **P < 0.01, ***P < 0.001; NS, not signiﬁcant.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 2 Low-dose DOX impairs Vegfr-2 translation and angiogenesis via REDD1 induction. VEGFR-1/2 expression and VEGF-A-induced angiogenesis were examined in HUVECs treated with DOX following transfection with control (siC) or Redd1 siRNA (siR). a, b Western blots of REDD1 and VEGFR-1/2 (a) as well as phosphorylated mTOR, 4E-BP1, and S6K (b). c Polysome proﬁling using sucrose density gradient ultracentrifugation. d qRT-PCR of Vegfr-1/2 mRNAs associated with high-molecular-weight polysomes (n = 4). e Western blots of phosphorylated VEGFR-2, ERK, and Akt in the HUVECs stimulated with VEGF-A. f Representative images of the migration (upper) and tube formation (lower) of the HUVECs stimulated with VEGF-A were obtained using Boyden chamber and Matrigel-based morphogenesis assays, respectively. g, h Quantitation of migration (g) and tube formation (h) was performed using ImageJ software (n = 4). Data are presented as the mean ± SD. **P < 0.01, ***P < 0.001; NS, not signiﬁcant.

Techniques: Expressing, Transfection, Control, Western Blot, Quantitative RT-PCR, High Molecular Weight, Migration, Quantitation Assay, Software

Fig. 3 REDD1 overexpression suppresses Vegfr-2 translation and angiogenesis. a–f VEGFR-1/2 expression and VEGF-A-induced angiogenesis were examined in the HUVECs infected with control adenovirus (Ad-C) or Ad-Redd1 (Ad-R) at an MOI of 50. a, b Western blots of VEGFR-1/2, EGFR, and IGF-1Rβ (a) as well as phosphorylated mTOR, 4E-BP1, and S6K (b). c Polysome proﬁling using sucrose density gradient ultracentrifugation. d qRT-PCR of Vegfr-1/2 mRNAs associated with high-molecular-weight polysomes (n = 4). e Western blots of phosphorylated VEGFR-2, ERK, and Akt in the HUVECs stimulated with VEGF-A. f Quantitative migration and tube formation of HUVECs in response to VEGF-A were assessed using Boyden chamber and Matrigel-based morphogenesis assays, respectively. (n = 4). g Schematic representation of the 5′-UTRs of Egfr, Vegfr-1, Vegfr-2, and Vegfr-3; clover-like structures in the 5′-UTRs of Egfr (-54 to -25) and Vegfr-1 (−87 to −1) indicate authentic IRES and putative IRES sequences, respectively; +1 indicates the AUG start codon, and dotted lines indicate deleted regions of 5′-UTRs. NF, not found. h HEK-293 cells were cotransfected with the pGL4.13/5′-UTR-Fireﬂy luciferase construct and Renilla luciferase pGL4.74 vector, followed by treatment with or without DOX or infection with Ad-C or Ad-Redd1. Reporter activities were measured in cell lysates using a Dual Luciferase Assay Kit (n = 5). Data are presented as the mean ± SD. *P < 0.05, ***P < 0.001; NS, not signiﬁcant.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 3 REDD1 overexpression suppresses Vegfr-2 translation and angiogenesis. a–f VEGFR-1/2 expression and VEGF-A-induced angiogenesis were examined in the HUVECs infected with control adenovirus (Ad-C) or Ad-Redd1 (Ad-R) at an MOI of 50. a, b Western blots of VEGFR-1/2, EGFR, and IGF-1Rβ (a) as well as phosphorylated mTOR, 4E-BP1, and S6K (b). c Polysome proﬁling using sucrose density gradient ultracentrifugation. d qRT-PCR of Vegfr-1/2 mRNAs associated with high-molecular-weight polysomes (n = 4). e Western blots of phosphorylated VEGFR-2, ERK, and Akt in the HUVECs stimulated with VEGF-A. f Quantitative migration and tube formation of HUVECs in response to VEGF-A were assessed using Boyden chamber and Matrigel-based morphogenesis assays, respectively. (n = 4). g Schematic representation of the 5′-UTRs of Egfr, Vegfr-1, Vegfr-2, and Vegfr-3; clover-like structures in the 5′-UTRs of Egfr (-54 to -25) and Vegfr-1 (−87 to −1) indicate authentic IRES and putative IRES sequences, respectively; +1 indicates the AUG start codon, and dotted lines indicate deleted regions of 5′-UTRs. NF, not found. h HEK-293 cells were cotransfected with the pGL4.13/5′-UTR-Fireﬂy luciferase construct and Renilla luciferase pGL4.74 vector, followed by treatment with or without DOX or infection with Ad-C or Ad-Redd1. Reporter activities were measured in cell lysates using a Dual Luciferase Assay Kit (n = 5). Data are presented as the mean ± SD. *P < 0.05, ***P < 0.001; NS, not signiﬁcant.

Techniques: Over Expression, Expressing, Infection, Control, Western Blot, Quantitative RT-PCR, High Molecular Weight, Migration, Luciferase, Construct, Plasmid Preparation

Fig. 4 Metronomic DOX treatment inhibits in vivo angiogenesis and lymphangiogenesis in the WT but not Redd1−/−mice. a Representative images of Matrigel plugs containing saline or VEGF-A removed from the WT and Redd1−/−mice metronomically treated with or without DOX. b Quantitated levels of hemoglobin (Hb) extracted from the plugs (n = 6). c Representative immunostaining of CD31+ vessels in a Matrigel plug section. Scale bar, 100 μm. d Quantitated levels of CD31+ vessels in the plugs (n = 4). e Representative images of Matrigel plugs containing saline or VEGF-C removed from the WT and Redd1−/−mice metronomically treated with or without DOX. f Quantitated levels of Hb extracted from the plugs (n = 6). g Representative immunostaining of CD31+ and LYVE-1+ vessels in a Matrigel plug section. Scale bar, 100 μm. h Quantitated levels of LYVE-1+ lymphatic vessels (n = 4). Data are presented as the mean ± SD. *P < 0.05, ***P < 0.001; NS, not signiﬁcant.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 4 Metronomic DOX treatment inhibits in vivo angiogenesis and lymphangiogenesis in the WT but not Redd1−/−mice. a Representative images of Matrigel plugs containing saline or VEGF-A removed from the WT and Redd1−/−mice metronomically treated with or without DOX. b Quantitated levels of hemoglobin (Hb) extracted from the plugs (n = 6). c Representative immunostaining of CD31+ vessels in a Matrigel plug section. Scale bar, 100 μm. d Quantitated levels of CD31+ vessels in the plugs (n = 4). e Representative images of Matrigel plugs containing saline or VEGF-C removed from the WT and Redd1−/−mice metronomically treated with or without DOX. f Quantitated levels of Hb extracted from the plugs (n = 6). g Representative immunostaining of CD31+ and LYVE-1+ vessels in a Matrigel plug section. Scale bar, 100 μm. h Quantitated levels of LYVE-1+ lymphatic vessels (n = 4). Data are presented as the mean ± SD. *P < 0.05, ***P < 0.001; NS, not signiﬁcant.

Techniques: In Vivo, Saline, Immunostaining

Fig. 5 LDMC with DOX inhibits tumor growth, angiogenesis, and lymphangiogenesis in B16F1 tumor-bearing WT but not Redd1−/−mice. a Comparison of tumor growth in the WT and Redd1−/−mice metronomically treated with saline or DOX (n = 10 per group). The arrow indicates the start of DPX treatment. b Representative images of tumor sections showing CD31+ blood vessels and DAPI-stained nuclei. Scale bar, 100 μm. c Quantiﬁcation of CD31+ blood vessel density per high-power ﬁeld (HPF) (n = 10). d Representative images of tumor sections showing CD31+ blood vessels and REDD1 expression. Scale bar, 50 μm. e Quantiﬁcation of their colocalization (n = 10). f Representative images of tumor sections showing CD31+ vessels and VEGFR-2 expression. Scale bar, 100 μm. g Quantiﬁcation of their colocalization (n = 10). h Representative images of tumor sections showing LYVE-1+ lymphatic vessels and VEGFR-3 expression. Scale bar, 100 μm. i Quantiﬁcation of colocalization of VEGFR-3 and LYVE-1 (n = 10). j Quantiﬁcation of LYVE-1+ lymphatic vessel density (n = 10). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001; NS, not signiﬁcant. r, Pearson’s correlation coefﬁcient.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 5 LDMC with DOX inhibits tumor growth, angiogenesis, and lymphangiogenesis in B16F1 tumor-bearing WT but not Redd1−/−mice. a Comparison of tumor growth in the WT and Redd1−/−mice metronomically treated with saline or DOX (n = 10 per group). The arrow indicates the start of DPX treatment. b Representative images of tumor sections showing CD31+ blood vessels and DAPI-stained nuclei. Scale bar, 100 μm. c Quantiﬁcation of CD31+ blood vessel density per high-power ﬁeld (HPF) (n = 10). d Representative images of tumor sections showing CD31+ blood vessels and REDD1 expression. Scale bar, 50 μm. e Quantiﬁcation of their colocalization (n = 10). f Representative images of tumor sections showing CD31+ vessels and VEGFR-2 expression. Scale bar, 100 μm. g Quantiﬁcation of their colocalization (n = 10). h Representative images of tumor sections showing LYVE-1+ lymphatic vessels and VEGFR-3 expression. Scale bar, 100 μm. i Quantiﬁcation of colocalization of VEGFR-3 and LYVE-1 (n = 10). j Quantiﬁcation of LYVE-1+ lymphatic vessel density (n = 10). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001; NS, not signiﬁcant. r, Pearson’s correlation coefﬁcient.

Techniques: Comparison, Saline, Staining, Expressing

Fig. 6 LDMC with DOX improves tumor vessel normalization in the WT but not Redd1−/−mice. a Representative images of α-SMA+ smooth muscle cell coverage on CD31+ tumor vessels in B16F1 tumors. Scale bar, 50 μm. b Quantiﬁcation of α-SMA+ smooth muscle cell coverage (n = 10). c Representative images of NG2+ pericyte coverage on CD31+ tumor vessels. Scale bar, 50 μm. d Quantiﬁcation of NG2+ pericyte coverage (n = 10). e Representative images of tumor sections showing FITC-dextran leakage, CD31+ blood vessels, and DAPI-stained nuclei. Scale bar, 50 μm. f Quantiﬁcation of FITC-dextran leakage (n = 10). g Representative images of tumor sections showing the hypoxyprobe+ area and CD31+ blood vessels. Scale bar, 50 μm. h Quantiﬁcation of hypoxyprobe+ area (n = 10). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 6 LDMC with DOX improves tumor vessel normalization in the WT but not Redd1−/−mice. a Representative images of α-SMA+ smooth muscle cell coverage on CD31+ tumor vessels in B16F1 tumors. Scale bar, 50 μm. b Quantiﬁcation of α-SMA+ smooth muscle cell coverage (n = 10). c Representative images of NG2+ pericyte coverage on CD31+ tumor vessels. Scale bar, 50 μm. d Quantiﬁcation of NG2+ pericyte coverage (n = 10). e Representative images of tumor sections showing FITC-dextran leakage, CD31+ blood vessels, and DAPI-stained nuclei. Scale bar, 50 μm. f Quantiﬁcation of FITC-dextran leakage (n = 10). g Representative images of tumor sections showing the hypoxyprobe+ area and CD31+ blood vessels. Scale bar, 50 μm. h Quantiﬁcation of hypoxyprobe+ area (n = 10). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques: Staining

Fig. 7 LDMC with DOX inhibits tumor progression and metastasis in B16F10 tumor-bearing WT but not Redd1−/−mice. a Comparison of tumor growth in the B16F10 tumor-bearing WT and Redd1−/−mice metronomically treated with saline or DOX (n = 12 per group). b Kaplan–Meier survival curves of the WT and Redd1−/−mice treated with saline or metronomic DOX (n = 20 per group). c Representative images of lung-metastatic tyrosinase+ colonies and CD31+ blood vessels. Scale bar, 50 μm. d Quantiﬁcation of tyrosinase+ colonies per high- power ﬁeld (HPF) (n = 10). e Representative images of spleen-metastatic tyrosinase+ colonies and CD31+ blood vessels. Scale bar, 50 μm. f Quantiﬁcation of tyrosinase+ colonies (n = 10). g Representative images of lymph node-metastatic tyrosinase+ colonies and LYVE-1+

Journal: Experimental & molecular medicine

Article Title: REDD1 is a determinant of low-dose metronomic doxorubicin-elicited endothelial cell dysfunction through downregulation of VEGFR-2/3 expression.

doi: 10.1038/s12276-021-00690-z

Figure Lengend Snippet: Fig. 7 LDMC with DOX inhibits tumor progression and metastasis in B16F10 tumor-bearing WT but not Redd1−/−mice. a Comparison of tumor growth in the B16F10 tumor-bearing WT and Redd1−/−mice metronomically treated with saline or DOX (n = 12 per group). b Kaplan–Meier survival curves of the WT and Redd1−/−mice treated with saline or metronomic DOX (n = 20 per group). c Representative images of lung-metastatic tyrosinase+ colonies and CD31+ blood vessels. Scale bar, 50 μm. d Quantiﬁcation of tyrosinase+ colonies per high- power ﬁeld (HPF) (n = 10). e Representative images of spleen-metastatic tyrosinase+ colonies and CD31+ blood vessels. Scale bar, 50 μm. f Quantiﬁcation of tyrosinase+ colonies (n = 10). g Representative images of lymph node-metastatic tyrosinase+ colonies and LYVE-1+

Techniques: Comparison, Saline

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