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sglt2  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology sglt2
Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Sglt2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sodium-glucose cotransporter-2 (sglt-2) inhibitors  (Innov X Systems)
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Innov X Systems sodium-glucose cotransporter-2 (sglt-2) inhibitors
Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Sodium Glucose Cotransporter 2 (Sglt 2) Inhibitors, supplied by Innov X Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sodium-glucose cotransporter (sglt) 2 inhibitors  (Boehringer Ingelheim)
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Boehringer Ingelheim sodium-glucose cotransporter (sglt) 2 inhibitors
Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Sodium Glucose Cotransporter (Sglt) 2 Inhibitors, supplied by Boehringer Ingelheim, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti sglt2  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology anti sglt2
Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Anti Sglt2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse monoclonal anti sglt2  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology mouse monoclonal anti sglt2
Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Mouse Monoclonal Anti Sglt2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sglt-2 inhibitors  (Credence Genomics)
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Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Sglt 2 Inhibitors, supplied by Credence Genomics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sglt-2 inhibitors  (AstraZeneca ltd)
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Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and <t>SGLT2</t> in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.
Sglt 2 Inhibitors, supplied by AstraZeneca ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and SGLT2 in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.

Journal: Journal of Inherited Metabolic Disease

Article Title: Liver‐Directed Gene Therapy Mitigates Early Nephropathy in Murine Glycogen Storage Disease Type Ia

doi: 10.1002/jimd.70048

Figure Lengend Snippet: Assessment of kidney glucose homeostasis, reabsorption and early injury in L‐G6PC1‐low and L‐G6PC1‐high mice. L‐G6PC1‐low and L‐G6PC1‐high mice were generated from G6pc −/− mice and analyzed at 12 weeks of age. Age‐matched G6pc +/+ and G6pc +/− mice with a similar phenotype served as controls. (A) Oil Red O (neutral triglycerides and lipids) staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice. Three sets of representative staining are shown for each group of mice. Scale bar, 20 μm. (B) Ratio of kidney weight (KW) to body weight (BW) in control ( n = 26), L‐G6PC1‐low ( n = 15), and L‐G6PC1‐high ( n = 15) mice. (C) Body mass index (BMI) in control ( n = 50), L‐G6PC1‐low ( n = 29), and L‐G6PC1‐high ( n = 20) mice. (D) H&E staining of the kidneys in control ( n = 6), L‐G6PC1‐low ( n = 6), and L‐G6PC1‐high ( n = 6) mice at magnifications of x200 (top panels, Scale bar, 50 μm) and x400 (lower panels, Scale bar, 20 μm), Arrows point to the area of tubular dilation. Representative sets of staining are shown. (E) Western‐blot analyzes and quantitation of renal levels of GLUT2 and SGLT2 in control ( n = 20), L‐G6PC1‐low ( n = 23), and L‐G6PC1‐high ( n = 23) mice. Densitometric quantification was performed and normalized against β‐Actin. Values represent the mean ± SEM. * p < 0.05, ** p < 0.005.

Article Snippet: The antibodies used were: Abcam (Cambridge, MA), CTGF (ab6992); Cell Signaling Technology (Danvers, MA), rabbit β‐actin (#4970), β‐catenin (#8480), non‐phosphorylated β‐catenin (#8814), α‐SMA (#14968), E‐cadherin (#3195), N‐cadherin (#13116), Snail1 (#3879), and collagen‐Iα1 (#72026); Immuno‐Biological Laboratories (Minneapolis, MN, USA), Angiotensinogen (28101); LS Bio (Seattle, WA, USA), collagen‐IV (LS‐B8763); MyBioSource (San Diego, CA); Dkk3 (MBS840225) and SGLT2 (MBS821113); Santa Cruz Biotechnology (Dallas, TX), mouse β‐actin (sc‐47 778) and renin (sc‐133 145); Thermo Fisher Scientific (Waltham, MA), GLUT2 (MA5‐35162).

Techniques: Generated, Staining, Control, Western Blot, Quantitation Assay