glut 4 level Search Results


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Thermo Fisher gene exp slc2a4 mm00436615 m1
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Santa Cruz Biotechnology antibodies for svct-2 and glut4
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Santa Cruz Biotechnology glut4 protein levels
Summary of <t> glucose transporter </t> family members
Glut4 Protein Levels, 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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Becton Dickinson separation tubes
Summary of <t> glucose transporter </t> family members
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Cusabio glut 4 level
Summary of <t> glucose transporter </t> family members
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Merck KGaA glut-4 protein
Summary of <t> glucose transporter </t> family members
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MyBiosource Biotechnology glut1 and glut4 levels from these fractions were measured using elisa assays
Plasma membrane GLUT1 and <t>GLUT4</t> levels. In line with previous evidences, H9c2 cells exposed to high glucose (33 mM D -glucose) exhibited lower GLUT4 levels and increased GLUT1 levels in plasma membrane, resulting in a higher GLUT1/GLUT4 levels compared to cells exposed to normal glucose (5.5 mM D -glucose). a-MSH (90 pM) and PG-901 (10 -10 M) significantly restored GLUT1/GLUT4 ratio, by increasing GLUT4 and consequently decreasing GLUT1 plasma membrane levels. PG-20N MC5R antagonist (130 nM) did not lead to any modification of the high GLUT1/GLUT4 ratio induced by high glucose. Values are expressed as mean ± S.E.M. of n = 9 values, obtained from the triplicates of three independent experiments. NG, normal glucose; Ang II, angiotensin II; HG, high glucose; ∗ P < 0,01 vs. NG; ° P < 0,01 vs. HG.
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Thermo Fisher cell surface protein isolation kits
Plasma membrane GLUT1 and <t>GLUT4</t> levels. In line with previous evidences, H9c2 cells exposed to high glucose (33 mM D -glucose) exhibited lower GLUT4 levels and increased GLUT1 levels in plasma membrane, resulting in a higher GLUT1/GLUT4 levels compared to cells exposed to normal glucose (5.5 mM D -glucose). a-MSH (90 pM) and PG-901 (10 -10 M) significantly restored GLUT1/GLUT4 ratio, by increasing GLUT4 and consequently decreasing GLUT1 plasma membrane levels. PG-20N MC5R antagonist (130 nM) did not lead to any modification of the high GLUT1/GLUT4 ratio induced by high glucose. Values are expressed as mean ± S.E.M. of n = 9 values, obtained from the triplicates of three independent experiments. NG, normal glucose; Ang II, angiotensin II; HG, high glucose; ∗ P < 0,01 vs. NG; ° P < 0,01 vs. HG.
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Image Search Results


Summary of  glucose transporter  family members

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Summary of glucose transporter family members

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques:

Schematic of insulin-induced translocation of glucose transporter 4 from cytosol to the cell membrane. The binding of insulin to its receptors initiates a signal transduction cascade, which results in the activation of Akt. Akt acts on the glucose transporter 4 (GLUT4) containing vesicles in the cytosol to facilitate their fusion with the cell membrane. When more GLUT4 molecules are present in the membrane, the rate of glucose uptake is elevated. GLUT4: Glucose transporter 4.

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Schematic of insulin-induced translocation of glucose transporter 4 from cytosol to the cell membrane. The binding of insulin to its receptors initiates a signal transduction cascade, which results in the activation of Akt. Akt acts on the glucose transporter 4 (GLUT4) containing vesicles in the cytosol to facilitate their fusion with the cell membrane. When more GLUT4 molecules are present in the membrane, the rate of glucose uptake is elevated. GLUT4: Glucose transporter 4.

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Translocation Assay, Membrane, Binding Assay, Transduction, Activation Assay

Recent studies of  glucose transporter 4  expression and translocation in the skeletal muscle

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Recent studies of glucose transporter 4 expression and translocation in the skeletal muscle

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Expressing, Translocation Assay, Membrane, Control, Western Blot, Muscles, Clinical Proteomics, Real-time Polymerase Chain Reaction, Negative Control, Positive Control, Immunoprecipitation, Isolation, Transgenic Assay, Immunofluorescence, Microscopy, Electron Microscopy, Saline, Injection, In Vitro, Activation Assay, Labeling, Protease Inhibitor

The movement of glucose transporter 4 in adipocytes. Adipose tissue is made of adipocytes. In adipocytes, glucose transporter 4 (GLUT4) can be found in the cell membrane and in the cytosol. The translocation of GLUT4 from cytosolic vesicles to the cell membrane leads to elevated glucose uptake, whereas endocytosis brings GLUT4 back to the cytosol. ( 1): In unstimulated cells, GLUT4 containing membrane portions are internalized in an endocytosis manner to generate vesicles containing GLUT4. GLUT4 vesicles are internalized into early (or sorted) endosomes. They can enter the recovery endoplasmic body, and follow the retrograde pathway to the trans-Golgi network and endoplasmic reticulum-Golgi intermediate compartment or other donor membrane compartments. (2): GLUT4 vesicles derived from the donor membrane structures are secured by tether containing a UBX domain for GLUT4 (TUG) protein. (3): During insulin signal stimulation, GLUT4 vesicles are released and loaded onto the microtubule motor to be transferred to the plasma membrane. The continuous presence of insulin leads to the direct movement of these vesicles to the plasma membrane. (4): GLUT4 vesicles are tethered to motor protein kinesin and other proteins. A stable ternary SNARE complex forms when this occurs. (5): The stable ternary SNARE complex is docked on the target membrane. (6): The docked vesicles rely on SNARE to move to and fuse with the target membrane[ , , ]. GLUT4: Glucose transporter 4.

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: The movement of glucose transporter 4 in adipocytes. Adipose tissue is made of adipocytes. In adipocytes, glucose transporter 4 (GLUT4) can be found in the cell membrane and in the cytosol. The translocation of GLUT4 from cytosolic vesicles to the cell membrane leads to elevated glucose uptake, whereas endocytosis brings GLUT4 back to the cytosol. ( 1): In unstimulated cells, GLUT4 containing membrane portions are internalized in an endocytosis manner to generate vesicles containing GLUT4. GLUT4 vesicles are internalized into early (or sorted) endosomes. They can enter the recovery endoplasmic body, and follow the retrograde pathway to the trans-Golgi network and endoplasmic reticulum-Golgi intermediate compartment or other donor membrane compartments. (2): GLUT4 vesicles derived from the donor membrane structures are secured by tether containing a UBX domain for GLUT4 (TUG) protein. (3): During insulin signal stimulation, GLUT4 vesicles are released and loaded onto the microtubule motor to be transferred to the plasma membrane. The continuous presence of insulin leads to the direct movement of these vesicles to the plasma membrane. (4): GLUT4 vesicles are tethered to motor protein kinesin and other proteins. A stable ternary SNARE complex forms when this occurs. (5): The stable ternary SNARE complex is docked on the target membrane. (6): The docked vesicles rely on SNARE to move to and fuse with the target membrane[ , , ]. GLUT4: Glucose transporter 4.

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Membrane, Translocation Assay, Derivative Assay, Clinical Proteomics

Recent studies of effects of bioactive compounds and chemical drugs on  glucose transporter 4  expression and translocation in adipocytes

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Recent studies of effects of bioactive compounds and chemical drugs on glucose transporter 4 expression and translocation in adipocytes

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Expressing, Translocation Assay, Fluorescence, Immunostaining, Western Blot, Inhibition, Immunoprecipitation, Real-time Polymerase Chain Reaction, Electrophoretic Mobility Shift Assay, Immunofluorescence, In Vitro, In Vivo, Enzyme-linked Immunosorbent Assay, Multiplex Assay, Activity Assay, Knockdown, Produced, Microscopy, Retroviral, Plasmid Preparation, Flow Cytometry

Recent studies of mechanisms of  glucose transporter 4  expression and translocation in adipocytes

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Recent studies of mechanisms of glucose transporter 4 expression and translocation in adipocytes

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Expressing, Translocation Assay, Real-time Polymerase Chain Reaction, Electrophoretic Mobility Shift Assay, Immunohistochemistry, Western Blot, Knockdown, Membrane, Transfection, Northern Blot, Nuclear Run-on Assay, Control, Plasmid Preparation, Flow Cytometry, Fluorescence, Microscopy, Over Expression, Isolation, Concentration Assay, Clinical Proteomics, Phospho-proteomics, Immunofluorescence

Recent studies of  glucose transporter 4  expression and translocation in the heart

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Recent studies of glucose transporter 4 expression and translocation in the heart

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Expressing, Translocation Assay, Membrane, Positive Control, Inhibition, Activation Assay, Isolation, Real-time Polymerase Chain Reaction, Western Blot, Immunofluorescence, Phospho-proteomics, Gene Expression, Control, Immunohistochemistry, Muscles, Saline

Recent studies of  glucose transporter 4  expression and translocation in the brain

Journal: World Journal of Biological Chemistry

Article Title: Current understanding of glucose transporter 4 expression and functional mechanisms

doi: 10.4331/wjbc.v11.i3.76

Figure Lengend Snippet: Recent studies of glucose transporter 4 expression and translocation in the brain

Article Snippet: Real-time PCR, Western blot. , 3T3-L1 transfected with Mmu-miR-29a/b/c. Anti-GLUT4 from Santa Cruz Biotechnology (SC-7938). , Cells with or without transfection. , Transfection of miR-29 family members inhibits Slc2a4 mRNA and GLUT4 protein levels in 3T3-L1 cells by inhibiting SPARC expression. , [ ] .

Techniques: Expressing, Translocation Assay, Knock-Out, Western Blot, Cell Culture, Clinical Proteomics, Membrane, Activity Assay, Immunocytochemistry, Real-time Polymerase Chain Reaction, Muscles, Control, Phospho-proteomics, Immunofluorescence, Immunohistochemistry, Positive Control, Negative Control, Microscopy, Transgenic Assay

Plasma membrane GLUT1 and GLUT4 levels. In line with previous evidences, H9c2 cells exposed to high glucose (33 mM D -glucose) exhibited lower GLUT4 levels and increased GLUT1 levels in plasma membrane, resulting in a higher GLUT1/GLUT4 levels compared to cells exposed to normal glucose (5.5 mM D -glucose). a-MSH (90 pM) and PG-901 (10 -10 M) significantly restored GLUT1/GLUT4 ratio, by increasing GLUT4 and consequently decreasing GLUT1 plasma membrane levels. PG-20N MC5R antagonist (130 nM) did not lead to any modification of the high GLUT1/GLUT4 ratio induced by high glucose. Values are expressed as mean ± S.E.M. of n = 9 values, obtained from the triplicates of three independent experiments. NG, normal glucose; Ang II, angiotensin II; HG, high glucose; ∗ P < 0,01 vs. NG; ° P < 0,01 vs. HG.

Journal: Frontiers in Physiology

Article Title: The Melanocortin MC5R as a New Target for Treatment of High Glucose-Induced Hypertrophy of the Cardiac H9c2 Cells

doi: 10.3389/fphys.2018.01475

Figure Lengend Snippet: Plasma membrane GLUT1 and GLUT4 levels. In line with previous evidences, H9c2 cells exposed to high glucose (33 mM D -glucose) exhibited lower GLUT4 levels and increased GLUT1 levels in plasma membrane, resulting in a higher GLUT1/GLUT4 levels compared to cells exposed to normal glucose (5.5 mM D -glucose). a-MSH (90 pM) and PG-901 (10 -10 M) significantly restored GLUT1/GLUT4 ratio, by increasing GLUT4 and consequently decreasing GLUT1 plasma membrane levels. PG-20N MC5R antagonist (130 nM) did not lead to any modification of the high GLUT1/GLUT4 ratio induced by high glucose. Values are expressed as mean ± S.E.M. of n = 9 values, obtained from the triplicates of three independent experiments. NG, normal glucose; Ang II, angiotensin II; HG, high glucose; ∗ P < 0,01 vs. NG; ° P < 0,01 vs. HG.

Article Snippet: GLUT1 and GLUT4 levels from these fractions were measured using ELISA assays, according to the manufacturer’s instructions (MBS720405 and MBS451402 My BioSource, United Kingdom).

Techniques: Modification

MC5R signaling in cardiac hypertrophy induced by high glucose. H9c2 hypertrophy induced by hyperglycemia is characterized by increased miR-133a levels, leading to PI3K inactivation and GLUT1/GLUT4 elevation. Here, we show for the first time an up-regulation of MC5R, involved in glucose-uptake, as a defensive and anti-hypertrophic response to the high-glucose induced damage. MC5R agonism reduced H9c2 hypertrophic markers by decreasing miR-133a levels, consequently restoring PI3K activity and GLUT1/GLUT4 ratio.

Journal: Frontiers in Physiology

Article Title: The Melanocortin MC5R as a New Target for Treatment of High Glucose-Induced Hypertrophy of the Cardiac H9c2 Cells

doi: 10.3389/fphys.2018.01475

Figure Lengend Snippet: MC5R signaling in cardiac hypertrophy induced by high glucose. H9c2 hypertrophy induced by hyperglycemia is characterized by increased miR-133a levels, leading to PI3K inactivation and GLUT1/GLUT4 elevation. Here, we show for the first time an up-regulation of MC5R, involved in glucose-uptake, as a defensive and anti-hypertrophic response to the high-glucose induced damage. MC5R agonism reduced H9c2 hypertrophic markers by decreasing miR-133a levels, consequently restoring PI3K activity and GLUT1/GLUT4 ratio.

Article Snippet: GLUT1 and GLUT4 levels from these fractions were measured using ELISA assays, according to the manufacturer’s instructions (MBS720405 and MBS451402 My BioSource, United Kingdom).

Techniques: Activity Assay