Search results for SLC5A1

Showing 17 results out of 23

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Protein (6 results from a total of 11)

Identifier: R-HSA-189243
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A1: P13866
Identifier: R-HSA-5656372
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A1: P13866
Identifier: R-HSA-5656373
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: P13866
Identifier: R-HSA-5656354
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: P13866
Identifier: R-HSA-5656370
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: P13866
Identifier: R-HSA-5656368
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: P13866

Set (1 results from a total of 1)

Identifier: R-HSA-5656360
Species: Homo sapiens
Compartment: plasma membrane

Reaction (6 results from a total of 7)

Identifier: R-HSA-5656356
Species: Homo sapiens
Compartment: plasma membrane, extracellular region
Sodium/glucose cotransporter 1 (SLC5A1 aka SGLT1) actively and reversibly transports glucose (Glc) into cells by Na+ cotransport with a Na+ to glucose coupling ratio of 2:1. SLC5A1 is mainly expressed in the microvilli of intestine and kidney and responsible for the absorption of sugars. Overexpressed SLC5A1 has been found in various cancers, possibly playing a role in preventing autophagic cell death by maintaining intracellular glucose levels. Defects in SLC5A1 can cause congenital glucose/galactose malabsorption (GGM; MIM:606824), an autosomal recessive disorder manifesting itself in newborns characterised by severe, life-threatening diarrhea which is usually fatal unless glucose and galactose are removed from the diet. Mutations that cause GGM include D28N, D28G, Y191*, R379*, R135W, G100V and Q457R (Turk et al. 1994, Wright et al. 2002).
Identifier: R-HSA-8932955
Species: Homo sapiens
Compartment: plasma membrane
The transport of extracellular glucose (Glc) and galactose (Gal) into the cytosol, coupled to the uptake of two sodium ions for each hexose transported, is mediated by sodium/glucose cotransporter 1 (SLC5A1, also known as SGLT1), localized on the luminal surfaces of enterocytes (Wright et al. 2004). The specificity of SLC5A1 has been worked out by studying sugar transport in plasma membrane vesicles containing recombinant human SLC5A1 protein (Quick et al. 2003). Consistent with these in vitro results, children lacking functional SLC5A1 protein fail to absorb dietary glucose and galactose (Martin et al. 1996). The transport activity of SLC5A1 was decreased upon co-expression of regulatory solute carrier protein family 1 member 1 (RSC1A1, aka RS1). RSC1A1 exhibits glucose-dependent, short-term inhibition of SLC5A1 by inhibiting the release of vesicles from the trans-Golgi network (Veyhl et al. 2006).
Identifier: R-HSA-8876283
Species: Homo sapiens
Compartment: cytosol, extracellular region, plasma membrane
The sodium/glucose cotransporter 5 (SLC5A10, sodium glucose cotransporter 5, SGLT5) is a plasma membrane-bound transport protein that possesses high capacity to transport mannose (Man) and fructose (Fru) into cells (Grempler et al. 2012). SLC5A10 is exclusively expressed in the kidney and is also able to transport glucose, alpha-methyl-D-glucose (AMG) and galactose, although to a much lower extent than Man and Fru.
Identifier: R-HSA-8876312
Species: Homo sapiens
Compartment: cytosol, extracellular region, plasma membrane
The sodium-coupled monocarboxylate transporter 2 (SLC5A12, SMCT2) acts as a plasma membrane-bound electroneutral and low-affinity Na+-dependent sodium-coupled solute transporter. It is highly expressed in the kidney cortex and may be responsible for the first step of reabsorption of monocarboxylates from the proximal tubule lumen. Functional studies of SLC5A12 expressed in mammalian cells show it can mediate cotransport of Na+ with lactate, pyruvate and nicotinate (Gopal et al. 2007).
Identifier: R-HSA-189242
Species: Homo sapiens
Compartment: plasma membrane
The reversible facilitated diffusion of fructose, galactose, and glucose from the cytosol to the extracellular space is mediated by tetrameric SLC2A2 (also known as GLUT2) transporter in the plasma membrane. In the epithelial cells of the small intestine, the basolateral localization of SLC2A2 (Thorens et al. 1990) enables hexose sugars derived from the diet and taken up by the action of the SLC5A1 (SGLT1) and SLC2A5 (GLUT5) transporters to be released into the circulation. The specificity of the SLC2A2 transporter has been established directly through biochemical assays of purified recombinant proteins (Colville et al. 1993; Wu et al. 1998) and indirectly through studies of patients deficient in SLC2A2 transporter protein (Santer et al. 1997).
Identifier: R-HSA-429613
Species: Homo sapiens
Compartment: plasma membrane, cytosol, extracellular region
The human gene SLC5A2 encodes a sodium-dependent glucose transporter, SGLT2 (Wells et al. 1992). SLC5A2 is expressed in many tissues but primarily in the kidney, specifically the renal proximal tubules (S1 and S2 segments). It is a low affinity, high capacity transporter of glucose across the apical membrane, with co-transport of Na+ ions in a 1:1 ratio. Unlike SGLT1, it doesn't transport galactose. SLC5A2 is the main transporter of glucose in the kidney, responsible for approximately 98% of glucose reabsorption (remainder by SGLT1). Defects in SLC5A2 are the cause of renal glucosuria (GLYS1), an autosomal recessive renal tubular disorder (Calado et al. 2004). A separate sodium dependent glucose transporter NAGLT1, was identified in the multifacilitator superfamily (MFS) and could be a transporter of glucose in kidney proximal tubules. Its rat orthologue, Naglt1, has been shown to mediate tubular reabsorption of glucose (Horiba et al. 2003). By similarity, SLC5A1, 4 and 9 are predicted proteins that transport glucose in a Na+-dependent manner.

Pathway (3 results from a total of 3)

Identifier: R-HSA-5656364
Species: Homo sapiens
Sodium/glucose cotransporter 1 (SLC5A1 aka SGLT1) actively and reversibly transports glucose (Glc) into cells by Na+ cotransport with a Na+ to glucose coupling ratio of 2:1. SLC5A1 is mainly expressed in the microvilli of intestine and kidney and responsible for the absorption of sugars. Overexpressed SLC5A1 has been found in various cancers, possibly playing a role in preventing autophagic cell death by maintaining intracellular glucose levels. Defects in SLC5A1 can cause congenital glucose/galactose malabsorption (GGM; MIM:606824), an autosomal recessive disorder manifesting itself in newborns characterised by severe, life-threatening diarrhea which is usually fatal unless glucose and galactose are removed from the diet (Wright et al. 2002, Bergeron et al. 2008, Wright et al. 2007, Wright 2013).
Identifier: R-HSA-8981373
Species: Homo sapiens
Hexoses, notably fructose, glucose, and galactose generated in the lumen of the small intestine by breakdown of dietary carbohydrate, are taken up by enterocytes lining the microvilli of the small intestine and released from them into the blood. Uptake into enterocytes is mediated by two transporters localized on the luminal surfaces of the cells. SLC5A1, also known as SGLT1, mediates the co-transport of sodium ions and glucose and galactose, and SLC2A5, also known as GLUT5, mediates fructose uptake (Wright 1998). Tetrameric SLC2A2, also known as GLUT2, localized on the basolateral surfaces of enterocytes, mediates the release of these hexoses into the blood (Kellett & Brot-Laroche 2005; Wright et al. 2004).
Identifier: R-HSA-5619098
Species: Homo sapiens
The reversible facilitated diffusion of fructose, galactose, and glucose from the cytosol to the extracellular space is mediated by the SLC2A2 (GLUT2) transporter in the plasma membrane. In the epithelial cells of the small intestine, the basolateral localisation of SLC2A2 enables hexose sugars derived from the diet (and taken up by SLC5A1 and SLC2A5 transporters into cells) to be released into the circulation. SLC2A2 is a low affinity glucose transporter expressed mainly in the kidney, liver and pancreatic beta-cells. In beta-cells, it functions as a glucose-sensor for insulin secretion and in the liver, it allows for bi-directional glucose transport. Defects in SLC2A2 can cause Fanconi-Bickel syndrome (FBS; MIM:227810), a rare but well-defined disorder characterised by glycogen accumulation, proximal renal tubular dysfunction, and impaired utilisation of glucose and galactose (Leturque et al. 2009, Douard & Ferraris 2013).

Icon (1 results from a total of 1)

Species: Homo sapiens
Curator: Bijay Jassal
Designer: Cristoffer Sevilla
SLC5A1 icon
Sodium/glucose cotransporter 1
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