SLC2A9 Antibody [D8G2] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human, Pig, Rabbit

Usage Information

Dilution
WB1:5000-1:50000 IHC1:500-1:2000 IF1:200-1:800

Application
WB, IHC, IF

Reactivity
Mouse, Rat, Human, Pig, Rabbit

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
59 kDa 56-59 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
SLC2A9 Antibody [D8G2] detects endogenous levels of total SLC2A9 protein.

Clone
D8G2

Synonym(s)
Solute carrier family 2, facilitated glucose transporter member 9, Glucose transporter type 9, GLUT-9 ,SLC2A9, GLUT9

Background
SLC2A9 (GLUT9) is a member of the SLC2A facilitative glucose transporter family that functions primarily as a high-capacity urate transporter and contributes to systemic urate homeostasis, with additional residual transport activity for hexoses such as glucose and fructose. The protein is a multi-pass transmembrane transporter with two major isoforms, SLC2A9a and SLC2A9b, generated by alternative transcription start sites and differing in their N‑terminal cytoplasmic segments, which confer distinct subcellular targeting and polarity: SLC2A9a localizes predominantly to basolateral membranes of renal proximal tubular cells and hepatocytes, while SLC2A9b is enriched at apical or intracellular membranes in kidney, placenta, and liver. Functional characterization in heterologous systems shows that both isoforms mediate electrogenic, voltage-sensitive urate transport with much higher capacity for urate than for glucose, and that urate flux via SLC2A9 can be facilitated by co-transport or exchange with glucose and, to a lesser extent, fructose, integrating purine metabolism with carbohydrate availability. In renal proximal tubule, SLC2A9a on the basolateral membrane transports urate from the blood into tubular cells, complementing apical urate transporters to support reabsorption of filtered urate and determine net renal urate excretion; SLC2A9b may participate in apical or intracellular urate handling depending on species and nephron segment. SLC2A9 is also expressed in liver and intestine, where SLC2A9a contributes to hepatic and enterocyte urate transport and forms part of an entero-renal network for urate clearance, while expression in chondrocytes and other tissues suggests roles in local urate and fructose handling that may influence cell survival in cartilage and other matrices. Human genetic analyses identify SLC2A9 as a major locus controlling serum uric acid concentrations, with common variants explaining a measurable fraction of interindividual variance in serum urate and associating with altered fractional urate excretion, hypouricemia, or gout risk depending on the direction and functional impact of the allele. Loss-of-function mutations in SLC2A9 cause renal hypouricemia type 2, characterized by low serum urate, increased renal urate clearance, and risk of exercise-induced acute kidney injury, consistent with an essential role for SLC2A9-mediated urate reabsorption in preventing excessive urate loss. In contrast, alleles that enhance SLC2A9 urate transport or expression associate with higher serum urate levels and increased gout susceptibility, and SLC2A9 genotypes also modulate responses to diet and sex-specific differences in urate handling, positioning this transporter as a key determinant of purine metabolism relevant to hyperuricemia, gout, and possibly metabolic traits linked to fructose and glucose metabolism.

Background

SLC2A9 (GLUT9) is a member of the SLC2A facilitative glucose transporter family that functions primarily as a high-capacity urate transporter and contributes to systemic urate homeostasis, with additional residual transport activity for hexoses such as glucose and fructose. The protein is a multi-pass transmembrane transporter with two major isoforms, SLC2A9a and SLC2A9b, generated by alternative transcription start sites and differing in their N‑terminal cytoplasmic segments, which confer distinct subcellular targeting and polarity: SLC2A9a localizes predominantly to basolateral membranes of renal proximal tubular cells and hepatocytes, while SLC2A9b is enriched at apical or intracellular membranes in kidney, placenta, and liver. Functional characterization in heterologous systems shows that both isoforms mediate electrogenic, voltage-sensitive urate transport with much higher capacity for urate than for glucose, and that urate flux via SLC2A9 can be facilitated by co-transport or exchange with glucose and, to a lesser extent, fructose, integrating purine metabolism with carbohydrate availability. In renal proximal tubule, SLC2A9a on the basolateral membrane transports urate from the blood into tubular cells, complementing apical urate transporters to support reabsorption of filtered urate and determine net renal urate excretion; SLC2A9b may participate in apical or intracellular urate handling depending on species and nephron segment. SLC2A9 is also expressed in liver and intestine, where SLC2A9a contributes to hepatic and enterocyte urate transport and forms part of an entero-renal network for urate clearance, while expression in chondrocytes and other tissues suggests roles in local urate and fructose handling that may influence cell survival in cartilage and other matrices. Human genetic analyses identify SLC2A9 as a major locus controlling serum uric acid concentrations, with common variants explaining a measurable fraction of interindividual variance in serum urate and associating with altered fractional urate excretion, hypouricemia, or gout risk depending on the direction and functional impact of the allele. Loss-of-function mutations in SLC2A9 cause renal hypouricemia type 2, characterized by low serum urate, increased renal urate clearance, and risk of exercise-induced acute kidney injury, consistent with an essential role for SLC2A9-mediated urate reabsorption in preventing excessive urate loss. In contrast, alleles that enhance SLC2A9 urate transport or expression associate with higher serum urate levels and increased gout susceptibility, and SLC2A9 genotypes also modulate responses to diet and sex-specific differences in urate handling, positioning this transporter as a key determinant of purine metabolism relevant to hyperuricemia, gout, and possibly metabolic traits linked to fructose and glucose metabolism.

References
https://pubmed.ncbi.nlm.nih.gov/22647630/ https://pubmed.ncbi.nlm.nih.gov/18327257/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%