GLUT3 Antibody (YA7322)
(Synonyms: GLUT3, SLC2A3, GLUT-3)GLUT3 Antibody (YA7322) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to GLUT3.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in 10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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|---|---|
| Dilution Ratio | 1:1000-5000 |
Product Details
GLUT3 Antibody (YA7322) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to GLUT3.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 54 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 54 kDa
A synthesized peptide derived from human GLUT3
Endogenous
affinity purified by Protein A
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 10mM phosphate buffered saline(pH 7.4) with 150mM sodium chloride, 0.05% BSA, 0.02% Proclin300 and 50% glycerol.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
GLUT3 (SLC2A3) is a facilitative glucose transporter that supports high-affinity glucose uptake, especially in neurons and glucose-limited cellular environments[1][2]. Mechanistically, GLUT3 connects membrane glucose transport to glycolytic metabolism, nucleotide synthesis, and immune-cell inflammatory programming through GLUT3-dependent glucose uptake[3][4]. In disease models, high GLUT3 expression supports colorectal cancer growth under low-glucose stress through the AMPK/CREB1/GLUT3 axis and correlates with poor colorectal cancer outcomes[3]. Compared with GLUT1, GLUT3 shows distinct transport affinity despite conserved substrate coordination, and colorectal cancer studies report stronger GLUT3 dependence than GLUT1 dependence under glucose-limiting conditions[3][5]. For experimental applications, GLUT3 inhibitors identified by in silico ligand screening and yeast validation provide tools to probe GLUT3-dependent glucose transport and GLUT3-dependent cancer metabolism[6].
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Subcellular Localization
Cell membrane,Perikaryon,Cell projection
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Expression
Tissue_Specificity: Highly expressed in brain (PubMed:8457197). Expressed in many tissues -
Isoforms & Post-Translational Modification
P11169: 496 amino acids, molecular weight 53924 Da.
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Subunit
Interacts with SMIM43; the interaction may promote SLC2A3-mediated glucose transport to meet the energy needs of mesendoderm differentiation
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SwissProt ID
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Synonyms
GLUT3, SLC2A3, GLUT-3
Documentation
[1]. Simpson IA, et al. The facilitative glucose transporter GLUT3: 20 years of distinction. Am J Physiol Endocrinol Metab. 2008 Aug;295(2):E242-53. [Content Brief]
[2]. Peng W, et al. Glucose transporter 3 in neuronal glucose metabolism: Health and diseases. Metabolism. 2021 Oct;123:154869. [Content Brief]
[3]. Dai W, et al. GLUT3 induced by AMPK/CREB1 axis is key for withstanding energy stress and augments the efficacy of current colorectal cancer therapies. Signal Transduct Target Ther. 2020 Sep 2;5(1):177. [Content Brief]
[4]. Hochrein SM, et al. The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming. Cell Metab. 2022 Apr 5;34(4):516-532.e11. [Content Brief]
[5]. Custódio TF, et al. Structural comparison of GLUT1 to GLUT3 reveal transport regulation mechanism in sugar porter family. Life Sci Alliance. 2021 Feb 3;4(4):e202000858. [Content Brief]
[6]. Iancu CV, et al. GLUT3 inhibitor discovery through in silico ligand screening and in vivo validation in eukaryotic expression systems. Sci Rep. 2022 Jan 26;12(1):1429. [Content Brief]
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