SLC13A5 Antibody (YA9364)
(Synonyms: NACT, SLC13A5, Na(+)/citrate cotransporter, NaCT, Sodium-coupled citrate transporter, Sodium-dependent citrate transporter, Solute carrier family 13 member 5)
Based on 1 Customer Validation
SLC13A5 Antibody (YA9364) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to SLC13A5.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, ICC/IF, IF-Tissue, IHC-P, IP, ELISA
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Reactivity :
human
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Formulation:
Supplied in PBS(pH7.4) containing 0.1% gelatin and < 0.1% sodium azide.
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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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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IF-Tissue
IF-Tissue: Immunofluorescence-Tissue
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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IP
IP: Immunoprecipitation
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|---|---|---|
| Dilution Ratio | 1:500-1000 | 1:50-500 | 1:50-500 | 1:100-500 | 1-2μg per 100-500μg Total protein | 1:50-3000 |
Product Details
SLC13A5 Antibody (YA9364) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to SLC13A5.
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Host Mouse
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Species Reactivityhuman
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Calculated Molecular Weight Predicted band size: 63 kDa
A synthesized peptide derived from human SLC13A5.
Endogenous
Affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS(pH7.4) containing 0.1% gelatin and < 0.1% sodium azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at 2-8°C for 1 year, do not freeze.
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Shipping
Shipping with blue ice.
Background
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Function
SLC13A5 is a High-affinity sodium/citrate cotransporter that mediates the entry of citrate into cells, which is a critical participant of biochemical pathways. May function in various metabolic processes in which citrate has a critical role such as energy production (Krebs cycle), fatty acid synthesis, cholesterol synthesis, glycolysis, and gluconeogenesis. Transports citrate into the cell in a Na(+)-dependent manner, recognizing the trivalent form of citrate (physiological pH) rather than the divalent form. Can recognize succinate as a substrate, but its affinity for succinate is several fold lower than for citrate. The stoichiometry is probably 4 Na(+) for each carboxylate, irrespective of whether the translocated substrate is divalent or trivalent, rendering the process electrogenic. Involved in the regulation of citrate levels in the brain (By similarity)[1][2][3][4][5][6][7].
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Subcellular Localization
Cell membrane
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Expression
Tissue_Specificity: Expressed most predominantly in the liver, with moderate expression detectable in the brain and testis. -
Isoforms & Post-Translational Modification
SLC13A5 has 4 isoforms, Q86YT5-1: amino acid length is 568, molecular weight is 63062 Da (predicted); Q86YT5-2: amino acid length is 522, molecular weight is 58110 Da (predicted); Q86YT5-3: amino acid length is 551, molecular weight is 61210 Da (predicted); Q86YT5-4: amino acid length is 525, molecular weight is 58092 Da (predicted).
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Subunit
Homodimer; the dimer shifts between outward and inward conformations to generate an elevator-type movement for substrate transport.
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SwissProt ID
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Synonyms
NACT, SLC13A5, Na(+)/citrate cotransporter, NaCT, Sodium-coupled citrate transporter, Sodium-dependent citrate transporter, Solute carrier family 13 member 5
Documentation
[1]. Inoue K, et al. Human Na+ -coupled citrate transporter: primary structure, genomic organization, and transport function. Biochem Biophys Res Commun. 2002 Dec 6;299(3):465-71. [Content Brief]
[2]. Inoue K, et al. Human sodium-coupled citrate transporter, the orthologue of Drosophila Indy, as a novel target for lithium action. Biochem J. 2003 Aug 15;374(Pt 1):21-6. [Content Brief]
[3]. Zwart R, et al. Electrophysiological characterization of human and mouse sodium-dependent citrate transporters (NaCT/SLC13A5) reveal species differences with respect to substrate sensitivity and cation dependence. J Pharmacol Exp Ther. 2015 Nov;355(2):247-54. [Content Brief]
[4]. Hardies K, et al. Recessive mutations in SLC13A5 result in a loss of citrate transport and cause neonatal epilepsy, developmental delay and teeth hypoplasia. Brain. 2015 Nov;138(Pt 11):3238-50. [Content Brief]
[5]. Selch S, et al. Analysis of naturally occurring mutations in the human uptake transporter NaCT important for bone and brain development and energy metabolism. Sci Rep. 2018 Jul 27;8(1):11330. [Content Brief]
[6]. Sauer DB, et al. Structure and inhibition mechanism of the human citrate transporter NaCT. Nature. 2021 Mar;591(7848):157-161. [Content Brief]
[7]. Li Y, et al. Substrate translocation and inhibition in human dicarboxylate transporter NaDC3. Nat Struct Mol Biol. 2025 Mar;32(3):502-512. [Content Brief]
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