glucose transporter glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter glut2
    Glucose Transporter Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter 2 glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut2
    Glucose Transporter 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter glut2
    Glucose Transporter Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter glut2
    Glucose Transporter Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter 2 glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut2
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    glucose transporter 2 glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut2
    Primer sequences used for semi-quantitative RT-qPCR analysis.
    Glucose Transporter 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Effect of Konjac Mannan Oligosaccharides on Glucose Homeostasis via the Improvement of Insulin and Leptin Resistance In Vitro and In Vivo"

    Article Title: Effect of Konjac Mannan Oligosaccharides on Glucose Homeostasis via the Improvement of Insulin and Leptin Resistance In Vitro and In Vivo

    Journal: Nutrients

    doi: 10.3390/nu11081705

    Primer sequences used for semi-quantitative RT-qPCR analysis.
    Figure Legend Snippet: Primer sequences used for semi-quantitative RT-qPCR analysis.

    Techniques Used:

    Effect of KMOS on liver damage and hepatic glucose metabolism disorder. ( A ) Representative photomicrographs of hematoxylin-eosin (H&E) staining in the liver (magnification 200×); ( B ) the liver dysfunction indices of activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); ( C ) serum triglyceride (TG) content; ( D ) hepatic TG content; ( E ) hepatic glycogen content; ( F ) the vitality of hepatic glycolytic and gluconeogenesis key enzymes of phosphoenolpyruvate carboxylase kinase (PEPCK) and pyruvate kinase (PK) in the liver; ( G ) mRNA levels of glycogen synthase (Gs) and glucose transporter 2 (Glut2) in the liver. Values are expressed as the fold change compared to the control, which was arbitrarily set to 1. Data are presented as the mean ± SD ( n = 5). ** p < 0.01 versus the control group, ## p < 0.01 versus the HFD group. HFD, high-fat diet (60% kcal from fat); L-KMOS, 400 mg/kg b.w./d KMOS; M-KMOS, 800 mg/kg b.w./d KMOS; H-KMOS, 1200 mg/kg b.w./d KMOS; Met, 400 mg/kg b.w./d metformin.
    Figure Legend Snippet: Effect of KMOS on liver damage and hepatic glucose metabolism disorder. ( A ) Representative photomicrographs of hematoxylin-eosin (H&E) staining in the liver (magnification 200×); ( B ) the liver dysfunction indices of activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); ( C ) serum triglyceride (TG) content; ( D ) hepatic TG content; ( E ) hepatic glycogen content; ( F ) the vitality of hepatic glycolytic and gluconeogenesis key enzymes of phosphoenolpyruvate carboxylase kinase (PEPCK) and pyruvate kinase (PK) in the liver; ( G ) mRNA levels of glycogen synthase (Gs) and glucose transporter 2 (Glut2) in the liver. Values are expressed as the fold change compared to the control, which was arbitrarily set to 1. Data are presented as the mean ± SD ( n = 5). ** p < 0.01 versus the control group, ## p < 0.01 versus the HFD group. HFD, high-fat diet (60% kcal from fat); L-KMOS, 400 mg/kg b.w./d KMOS; M-KMOS, 800 mg/kg b.w./d KMOS; H-KMOS, 1200 mg/kg b.w./d KMOS; Met, 400 mg/kg b.w./d metformin.

    Techniques Used: Staining

    Effect of KMOS on glucose metabolism via the insulin signaling pathway and AMP-activated protein kinase (AMPK) pathway. The incubation of HepG2 cells with 18 mM glucosamine for 18 h was used for the construction of the high-glucosamine (HG)-induced insulin-resistant cell model. After starvation for 2 h with serum-free medium, cells were treated with different concentrations of KMOS (L-KMOS, 0.1 mg/mL; M-KMOS, 0.5 mg/mL; H-KMOS, 1 mg/mL) or Met (1 mg/mL metformin) for 24 h. ( A ) Protein expression in the insulin signaling pathway, including insulin receptor substrate (IRS-1), p-IRS-1 Tyr612 , p-IRS-1 Ser307 , protein kinase B (AKT), p-AKT, AKT substrate of 160 kDa (AS160), p-AS160, membrane GLUT2, and membrane NA + /K + -Pase α1; ( B ) densitometry quantification of the expressed protein bands of the insulin signaling pathway; ( C ) glucose uptake; ( D ) protein expressions of AMPK and p-AMPK; ( E ) densitometry quantification of the expressed protein bands of p-AMPK and AMPK; ( F ) protein expressions of p-AMPK, AMPK, p-AS160, AS160, membrane GLUT2, and membrane NA + /K + -Pase α1 in the presence of AMPK inhibitor Compound C (20 μmol/L); ( G ) densitometry quantification of the expressed protein bands in the presence of AMPK inhibitor Compound C; ( H ) glucose uptake in the presence of AMPK inhibitor Compound C. Met was used as a positive control. Results are expressed as the mean ± SD of at least three replicates. Values with different superscripts are significantly different at p < 0.05.
    Figure Legend Snippet: Effect of KMOS on glucose metabolism via the insulin signaling pathway and AMP-activated protein kinase (AMPK) pathway. The incubation of HepG2 cells with 18 mM glucosamine for 18 h was used for the construction of the high-glucosamine (HG)-induced insulin-resistant cell model. After starvation for 2 h with serum-free medium, cells were treated with different concentrations of KMOS (L-KMOS, 0.1 mg/mL; M-KMOS, 0.5 mg/mL; H-KMOS, 1 mg/mL) or Met (1 mg/mL metformin) for 24 h. ( A ) Protein expression in the insulin signaling pathway, including insulin receptor substrate (IRS-1), p-IRS-1 Tyr612 , p-IRS-1 Ser307 , protein kinase B (AKT), p-AKT, AKT substrate of 160 kDa (AS160), p-AS160, membrane GLUT2, and membrane NA + /K + -Pase α1; ( B ) densitometry quantification of the expressed protein bands of the insulin signaling pathway; ( C ) glucose uptake; ( D ) protein expressions of AMPK and p-AMPK; ( E ) densitometry quantification of the expressed protein bands of p-AMPK and AMPK; ( F ) protein expressions of p-AMPK, AMPK, p-AS160, AS160, membrane GLUT2, and membrane NA + /K + -Pase α1 in the presence of AMPK inhibitor Compound C (20 μmol/L); ( G ) densitometry quantification of the expressed protein bands in the presence of AMPK inhibitor Compound C; ( H ) glucose uptake in the presence of AMPK inhibitor Compound C. Met was used as a positive control. Results are expressed as the mean ± SD of at least three replicates. Values with different superscripts are significantly different at p < 0.05.

    Techniques Used: Incubation, Expressing, Positive Control

    glucose transporter 2 glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut2
    GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; <t>Glut2,</t> glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.
    Glucose Transporter 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Selenium Supplementation Alters Hepatic Energy and Fatty Acid Metabolism in Mice"

    Article Title: Selenium Supplementation Alters Hepatic Energy and Fatty Acid Metabolism in Mice

    Journal: The Journal of Nutrition

    doi: 10.1093/jn/nxy036

    GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; Glut2, glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.
    Figure Legend Snippet: GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; Glut2, glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.

    Techniques Used: Expressing

    Metabolome-wide association study of transcripts in 3 gene sets of mouse liver (from Figure 2) altered by supplemental selenium. Associations between 80 significant genes and the metabolome (12,421 features) from mouse liver (n = 5) are visualized at |ρ| ≥ 0.9, showing 2 central gene hubs and scattered connections (bottom left) and pathway associations of metabolites (bottom right). ACAA1B, peroxisomal 3-oxoacyl-CoA thiolase B; CL, cardiolipin; CPT2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; GLUT2, glucose transporter 2; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; LC, long-chain; PC, phosphatidylcholine; PE, phosphatidylethanolamine; Sc5dl, sterol-C5-desaturase; THC-CoA, 3α,7α,12α-trihydroxy-5β-cholest-24-enoyl-CoA; TrHOCCoA, 3α,7α,12α -trihydroxy-5β-24-oxocholestanoyl-CoA.
    Figure Legend Snippet: Metabolome-wide association study of transcripts in 3 gene sets of mouse liver (from Figure 2) altered by supplemental selenium. Associations between 80 significant genes and the metabolome (12,421 features) from mouse liver (n = 5) are visualized at |ρ| ≥ 0.9, showing 2 central gene hubs and scattered connections (bottom left) and pathway associations of metabolites (bottom right). ACAA1B, peroxisomal 3-oxoacyl-CoA thiolase B; CL, cardiolipin; CPT2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; GLUT2, glucose transporter 2; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; LC, long-chain; PC, phosphatidylcholine; PE, phosphatidylethanolamine; Sc5dl, sterol-C5-desaturase; THC-CoA, 3α,7α,12α-trihydroxy-5β-cholest-24-enoyl-CoA; TrHOCCoA, 3α,7α,12α -trihydroxy-5β-24-oxocholestanoyl-CoA.

    Techniques Used:

    Correlations of selected metabolites with central genes (Glut2, Cpt2, and Acaa1b) in the major transcriptome-metabolome hubs (from Figure 3). (A) PE (36:5): m/z 738.5082, retention time 579 s (ρ = 0.72, P = 0.02); (B) PE (40:5): m/z 794.5710, retention time 582 s, confirmed by MS/MS (ρ = 0.88, P < 0.01); (C) propionylcarnitine: m/z 218.1274, retention time 45 s, confirmed by MS/MS (ρ = 0.71, P = 0.02); (D) octadecenylcarnitine: m/z 426.3561, time 563 s, confirmed by MS/MS (ρ = 0.67, P = 0.03); (E) dodecanoyl-CoA: m/z: 950.2873, retention time 38 s (ρ = 0.94, P < 0.01); (F) 3-oxocholic acid, m/z 407.2790, retention time 436 s (ρ = -0.84, P < 0.01). Values for the transcripts represent RMA average expression levels, and values for the metabolites represent log2 transformed, quantile-normalized mass spectral intensities; fold-changes for nontransformed values are provided in Supplemental Table 4. Acaa1b, peroxisomal 3-oxoacyl-CoA thiolase B; Cpt2, carnitine palmitoyltransferase 2; Glut2, glucose transporter 2; PE, phosphatidylethanolamine; RMA, robust multiarray average.
    Figure Legend Snippet: Correlations of selected metabolites with central genes (Glut2, Cpt2, and Acaa1b) in the major transcriptome-metabolome hubs (from Figure 3). (A) PE (36:5): m/z 738.5082, retention time 579 s (ρ = 0.72, P = 0.02); (B) PE (40:5): m/z 794.5710, retention time 582 s, confirmed by MS/MS (ρ = 0.88, P < 0.01); (C) propionylcarnitine: m/z 218.1274, retention time 45 s, confirmed by MS/MS (ρ = 0.71, P = 0.02); (D) octadecenylcarnitine: m/z 426.3561, time 563 s, confirmed by MS/MS (ρ = 0.67, P = 0.03); (E) dodecanoyl-CoA: m/z: 950.2873, retention time 38 s (ρ = 0.94, P < 0.01); (F) 3-oxocholic acid, m/z 407.2790, retention time 436 s (ρ = -0.84, P < 0.01). Values for the transcripts represent RMA average expression levels, and values for the metabolites represent log2 transformed, quantile-normalized mass spectral intensities; fold-changes for nontransformed values are provided in Supplemental Table 4. Acaa1b, peroxisomal 3-oxoacyl-CoA thiolase B; Cpt2, carnitine palmitoyltransferase 2; Glut2, glucose transporter 2; PE, phosphatidylethanolamine; RMA, robust multiarray average.

    Techniques Used: Tandem Mass Spectroscopy, Expressing, Transformation Assay

    glucose transporter 2 glut2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut2
    GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; <t>Glut2,</t> glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.
    Glucose Transporter 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/glucose transporter 2 glut2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
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    Images

    1) Product Images from "Selenium Supplementation Alters Hepatic Energy and Fatty Acid Metabolism in Mice"

    Article Title: Selenium Supplementation Alters Hepatic Energy and Fatty Acid Metabolism in Mice

    Journal: The Journal of Nutrition

    doi: 10.1093/jn/nxy036

    GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; Glut2, glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.
    Figure Legend Snippet: GSEA of supplemental selenium effect on mouse hepatic transcriptome. Enrichment plots of 3 significant pathways (FDR q < 0.05) from GSEA of supplemental selenium effect on mouse liver transcriptome (n = 5) (A) and heat map showing RMA normalized expression levels of genes that contributed to the enrichment (B) (marked as 1, 2 and 3 in panel A). Acaa1b, Acetyl-CoA acyltransferase B (also called peroxisomal 3-oxoacyl-CoA thiolase B); Cpt2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; FDR, false discovery rate; Foxo1, forkhead box protein class O; Glut2, glucose transporter 2; GSEA, Gene Set Enrichment Analysis; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; RMA, robust multiarray average.

    Techniques Used: Expressing

    Metabolome-wide association study of transcripts in 3 gene sets of mouse liver (from Figure 2) altered by supplemental selenium. Associations between 80 significant genes and the metabolome (12,421 features) from mouse liver (n = 5) are visualized at |ρ| ≥ 0.9, showing 2 central gene hubs and scattered connections (bottom left) and pathway associations of metabolites (bottom right). ACAA1B, peroxisomal 3-oxoacyl-CoA thiolase B; CL, cardiolipin; CPT2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; GLUT2, glucose transporter 2; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; LC, long-chain; PC, phosphatidylcholine; PE, phosphatidylethanolamine; Sc5dl, sterol-C5-desaturase; THC-CoA, 3α,7α,12α-trihydroxy-5β-cholest-24-enoyl-CoA; TrHOCCoA, 3α,7α,12α -trihydroxy-5β-24-oxocholestanoyl-CoA.
    Figure Legend Snippet: Metabolome-wide association study of transcripts in 3 gene sets of mouse liver (from Figure 2) altered by supplemental selenium. Associations between 80 significant genes and the metabolome (12,421 features) from mouse liver (n = 5) are visualized at |ρ| ≥ 0.9, showing 2 central gene hubs and scattered connections (bottom left) and pathway associations of metabolites (bottom right). ACAA1B, peroxisomal 3-oxoacyl-CoA thiolase B; CL, cardiolipin; CPT2, carnitine palmitoyltransferase 2; Dhcr7, 7-dehydrocholesterol reductase; GLUT2, glucose transporter 2; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; LC, long-chain; PC, phosphatidylcholine; PE, phosphatidylethanolamine; Sc5dl, sterol-C5-desaturase; THC-CoA, 3α,7α,12α-trihydroxy-5β-cholest-24-enoyl-CoA; TrHOCCoA, 3α,7α,12α -trihydroxy-5β-24-oxocholestanoyl-CoA.

    Techniques Used:

    Correlations of selected metabolites with central genes (Glut2, Cpt2, and Acaa1b) in the major transcriptome-metabolome hubs (from Figure 3). (A) PE (36:5): m/z 738.5082, retention time 579 s (ρ = 0.72, P = 0.02); (B) PE (40:5): m/z 794.5710, retention time 582 s, confirmed by MS/MS (ρ = 0.88, P < 0.01); (C) propionylcarnitine: m/z 218.1274, retention time 45 s, confirmed by MS/MS (ρ = 0.71, P = 0.02); (D) octadecenylcarnitine: m/z 426.3561, time 563 s, confirmed by MS/MS (ρ = 0.67, P = 0.03); (E) dodecanoyl-CoA: m/z: 950.2873, retention time 38 s (ρ = 0.94, P < 0.01); (F) 3-oxocholic acid, m/z 407.2790, retention time 436 s (ρ = -0.84, P < 0.01). Values for the transcripts represent RMA average expression levels, and values for the metabolites represent log2 transformed, quantile-normalized mass spectral intensities; fold-changes for nontransformed values are provided in Supplemental Table 4. Acaa1b, peroxisomal 3-oxoacyl-CoA thiolase B; Cpt2, carnitine palmitoyltransferase 2; Glut2, glucose transporter 2; PE, phosphatidylethanolamine; RMA, robust multiarray average.
    Figure Legend Snippet: Correlations of selected metabolites with central genes (Glut2, Cpt2, and Acaa1b) in the major transcriptome-metabolome hubs (from Figure 3). (A) PE (36:5): m/z 738.5082, retention time 579 s (ρ = 0.72, P = 0.02); (B) PE (40:5): m/z 794.5710, retention time 582 s, confirmed by MS/MS (ρ = 0.88, P < 0.01); (C) propionylcarnitine: m/z 218.1274, retention time 45 s, confirmed by MS/MS (ρ = 0.71, P = 0.02); (D) octadecenylcarnitine: m/z 426.3561, time 563 s, confirmed by MS/MS (ρ = 0.67, P = 0.03); (E) dodecanoyl-CoA: m/z: 950.2873, retention time 38 s (ρ = 0.94, P < 0.01); (F) 3-oxocholic acid, m/z 407.2790, retention time 436 s (ρ = -0.84, P < 0.01). Values for the transcripts represent RMA average expression levels, and values for the metabolites represent log2 transformed, quantile-normalized mass spectral intensities; fold-changes for nontransformed values are provided in Supplemental Table 4. Acaa1b, peroxisomal 3-oxoacyl-CoA thiolase B; Cpt2, carnitine palmitoyltransferase 2; Glut2, glucose transporter 2; PE, phosphatidylethanolamine; RMA, robust multiarray average.

    Techniques Used: Tandem Mass Spectroscopy, Expressing, Transformation Assay

    ihc ab 2341188 glut2 glucose transporter type 2 antibody novus  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ihc ab 2341188 glut2 glucose transporter type 2 antibody novus
    Antibody Table
    Ihc Ab 2341188 Glut2 Glucose Transporter Type 2 Antibody Novus, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ihc ab 2341188 glut2 glucose transporter type 2 antibody novus/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
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    Images

    1) Product Images from "GRP94 Is an Essential Regulator of Pancreatic β -Cell Development, Mass, and Function in Male Mice"

    Article Title: GRP94 Is an Essential Regulator of Pancreatic β -Cell Development, Mass, and Function in Male Mice

    Journal: Endocrinology

    doi: 10.1210/en.2017-00685

    Antibody Table
    Figure Legend Snippet: Antibody Table

    Techniques Used: Purification

    glucose transporter 2 glut 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc glucose transporter 2 glut 2
    Glucose Transporter 2 Glut 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter type 2 glut2  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Cell Signaling Technology Inc glucose transporter type 2 glut2
    Primer sequences for quantitative polymerase chain reaction
    Glucose Transporter Type 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    1) Product Images from "Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats"

    Article Title: Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats

    Journal: World Journal of Gastroenterology : WJG

    doi: 10.3748/wjg.v19.i10.1572

    Primer sequences for quantitative polymerase chain reaction
    Figure Legend Snippet: Primer sequences for quantitative polymerase chain reaction

    Techniques Used:

    High-fat diets inhibited insulin pathway in liver of rats. Rats were fed with high-fat diets (HF) or normal control diets (Con) for 4 or 8 wk. A: The mRNA expression levels of mitofusin 2 (MFN2), insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were examined by quantitative real-time-polymerase chain reaction; B and C: The protein levels were detected by Western-blotting. bP < 0.01 vs normal diets for 4 wk; dP < 0.01 vs normal diets for 8 wk.
    Figure Legend Snippet: High-fat diets inhibited insulin pathway in liver of rats. Rats were fed with high-fat diets (HF) or normal control diets (Con) for 4 or 8 wk. A: The mRNA expression levels of mitofusin 2 (MFN2), insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were examined by quantitative real-time-polymerase chain reaction; B and C: The protein levels were detected by Western-blotting. bP < 0.01 vs normal diets for 4 wk; dP < 0.01 vs normal diets for 8 wk.

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Mitofusin-2 over-expression up-regulated the expression of insulin pathway related genes in liver of rats. Rats were fed with high-fat diets for 8 wk, and then were infected with Ad-mitofusin-2 (MFN2) or empty Ad adenovirus or phosphate-buffered saline (PBS) control for 3 wk. The expression levels of insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were determined by quantitative real-time-polymerase chain reaction (RT-PCR) (A) and Western-blot (B). The phosphorylation levels of PI3K and AKT2 were assayed by Western-blotting (B). The expression level of suppressor of cytokine signaling 3 (SOCS3) was determined by quantitative RT-PCR (C) and Western-blot (D). aP < 0.05, bP < 0.01 vs Ad.
    Figure Legend Snippet: Mitofusin-2 over-expression up-regulated the expression of insulin pathway related genes in liver of rats. Rats were fed with high-fat diets for 8 wk, and then were infected with Ad-mitofusin-2 (MFN2) or empty Ad adenovirus or phosphate-buffered saline (PBS) control for 3 wk. The expression levels of insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were determined by quantitative real-time-polymerase chain reaction (RT-PCR) (A) and Western-blot (B). The phosphorylation levels of PI3K and AKT2 were assayed by Western-blotting (B). The expression level of suppressor of cytokine signaling 3 (SOCS3) was determined by quantitative RT-PCR (C) and Western-blot (D). aP < 0.05, bP < 0.01 vs Ad.

    Techniques Used: Over Expression, Expressing, Infection, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Western Blot, Quantitative RT-PCR

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    ihc ab 2341188 glut2 glucose transporter type 2 antibody novus  (Cell Signaling Technology Inc)
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    Ihc Ab 2341188 Glut2 Glucose Transporter Type 2 Antibody Novus, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    glucose transporter 2 glut 2  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc glucose transporter 2 glut 2
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    glucose transporter type 2 glut2  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc glucose transporter type 2 glut2
    Primer sequences for quantitative polymerase chain reaction
    Glucose Transporter Type 2 Glut2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Antibody Table

    Journal: Endocrinology

    Article Title: GRP94 Is an Essential Regulator of Pancreatic β -Cell Development, Mass, and Function in Male Mice

    doi: 10.1210/en.2017-00685

    Figure Lengend Snippet: Antibody Table

    Article Snippet: Species Raised in; Monoclonal or Polyclonal Dilution Used RRID GRP94 Grp94 monoclonal antibody (9G10) Enzo Life Sciences, ADI-SPA-850-F Rat; monoclonal 1:2000 (WB), 1:100 (IHC) AB_777179 PDX1 Anti-PDX1 antibody Abcam, ab47267 Rabbit; polyclonal 1:2000 (IHC) AB_777179 Insulin Insulin antibody Thermo Fisher Scientific, PA1-26938 Guinea pig; polyclonal antibody 1:100 (IHC) AB_794668 HSPA5 GRP 78 (H-129) antibody Santa Cruz Biotechnology, sc-13968 Rabbit; polyclonal 1:1000 (WB) AB_2119991 Glucagon Mouse antiglucagon antibody Abcam, ab82270 Mouse; monoclonal 1:2000 (IHC) AB_1658481 Somatostatin Rabbit antisomatostatin antibody Abcam, ab64053 Rabbit; polyclonal 1:300 (IHC) AB_1143012 β -Actin β -Actin antibody (C4) Santa Cruz Biotechnology, SC-47778 Mouse; monoclonal 1:2000 (IHC) AB_2714189 E-cadherin Purified mouse anti–E-cadherin antibody BD Bioscience, 610181 Mouse; monoclonal 1:100 (IHC) AB_397580 Histone H3 Rabbit anti–histone H3, phospho (Ser10) antibody Cell Signaling Technology, 3377s Rabbit; monoclonal 1:200 (IHC) AB_1549592 Cleaved caspase-3 (Asp175) Cleaved caspase-3 (Asp175) antibody Cell Signaling Technology, 9661s Rabbit; polyclonal 1:200 (IHC) AB_2341188 Glut2 Glucose transporter type 2 antibody Novus, NBP2-22218 Rabbit; polyclonal 1:1000 (WB) AB_2335858 Open in a separate window Abbreviations: IHC, immunohistochemistry; RRID, Research Resource Identifier.

    Techniques: Purification

    Primer sequences for quantitative polymerase chain reaction

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats

    doi: 10.3748/wjg.v19.i10.1572

    Figure Lengend Snippet: Primer sequences for quantitative polymerase chain reaction

    Article Snippet: Membranes were incubated with appropriate diluted primary antibodies of MFN2, insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K-P85), p-PI3K-P85, AKT2, p-AKT2, glucose transporter type 2 (GLUT2) or β-actin (all from Santa Cruz or Cell Signaling Technology, United states) respectively overnight at 4 °C, and then with the respective secondary antibody for 2 h. Proteins were detected with the enhanced chemiluminescence detection system. β-actin served as an internal control protein.

    Techniques:

    High-fat diets inhibited insulin pathway in liver of rats. Rats were fed with high-fat diets (HF) or normal control diets (Con) for 4 or 8 wk. A: The mRNA expression levels of mitofusin 2 (MFN2), insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were examined by quantitative real-time-polymerase chain reaction; B and C: The protein levels were detected by Western-blotting. bP < 0.01 vs normal diets for 4 wk; dP < 0.01 vs normal diets for 8 wk.

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats

    doi: 10.3748/wjg.v19.i10.1572

    Figure Lengend Snippet: High-fat diets inhibited insulin pathway in liver of rats. Rats were fed with high-fat diets (HF) or normal control diets (Con) for 4 or 8 wk. A: The mRNA expression levels of mitofusin 2 (MFN2), insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were examined by quantitative real-time-polymerase chain reaction; B and C: The protein levels were detected by Western-blotting. bP < 0.01 vs normal diets for 4 wk; dP < 0.01 vs normal diets for 8 wk.

    Article Snippet: Membranes were incubated with appropriate diluted primary antibodies of MFN2, insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K-P85), p-PI3K-P85, AKT2, p-AKT2, glucose transporter type 2 (GLUT2) or β-actin (all from Santa Cruz or Cell Signaling Technology, United states) respectively overnight at 4 °C, and then with the respective secondary antibody for 2 h. Proteins were detected with the enhanced chemiluminescence detection system. β-actin served as an internal control protein.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Mitofusin-2 over-expression up-regulated the expression of insulin pathway related genes in liver of rats. Rats were fed with high-fat diets for 8 wk, and then were infected with Ad-mitofusin-2 (MFN2) or empty Ad adenovirus or phosphate-buffered saline (PBS) control for 3 wk. The expression levels of insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were determined by quantitative real-time-polymerase chain reaction (RT-PCR) (A) and Western-blot (B). The phosphorylation levels of PI3K and AKT2 were assayed by Western-blotting (B). The expression level of suppressor of cytokine signaling 3 (SOCS3) was determined by quantitative RT-PCR (C) and Western-blot (D). aP < 0.05, bP < 0.01 vs Ad.

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Mitofusin-2 ameliorates high-fat diet-induced insulin resistance in liver of rats

    doi: 10.3748/wjg.v19.i10.1572

    Figure Lengend Snippet: Mitofusin-2 over-expression up-regulated the expression of insulin pathway related genes in liver of rats. Rats were fed with high-fat diets for 8 wk, and then were infected with Ad-mitofusin-2 (MFN2) or empty Ad adenovirus or phosphate-buffered saline (PBS) control for 3 wk. The expression levels of insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K), AKT2 and glucose transporter type 2 (GLUT2) were determined by quantitative real-time-polymerase chain reaction (RT-PCR) (A) and Western-blot (B). The phosphorylation levels of PI3K and AKT2 were assayed by Western-blotting (B). The expression level of suppressor of cytokine signaling 3 (SOCS3) was determined by quantitative RT-PCR (C) and Western-blot (D). aP < 0.05, bP < 0.01 vs Ad.

    Article Snippet: Membranes were incubated with appropriate diluted primary antibodies of MFN2, insulin receptor (INSR), insulin receptor substrate 2 (IRS2), phosphoinositide-3-kinase (PI3K-P85), p-PI3K-P85, AKT2, p-AKT2, glucose transporter type 2 (GLUT2) or β-actin (all from Santa Cruz or Cell Signaling Technology, United states) respectively overnight at 4 °C, and then with the respective secondary antibody for 2 h. Proteins were detected with the enhanced chemiluminescence detection system. β-actin served as an internal control protein.

    Techniques: Over Expression, Expressing, Infection, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Western Blot, Quantitative RT-PCR