Mouse SGLT1 (Sodium/glucose cotransporter 1) is a high-affinity electrogenic Na+-coupled symporter that actively transports D-glucose or D-galactose across the plasma membrane with a 2:1 Na+:sugar stoichiometry. It is pivotal for intestinal mass absorption of D-glucose and D-galactose across the apical brush-border membrane of enterocytes. SGLT1 knockout mice develop glucose-galactose malabsorption (GGM) syndrome and die within 2 days after weaning on standard diet. SGLT1 also triggers glucose-induced secretion of incretins GIP and GLP-1 in enteroendocrine cells, and reabsorbs approximately 3% of filtered glucose in the S3 segment of renal proximal tubules. The transporter also functions as a water channel enabling passive water transport.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005412 D-glucose:sodium symporter activity | IDA PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestina... | ACCEPT | Summary: Core molecular function directly demonstrated in mouse SGLT1 knockout studies. PMID:22124465 showed that passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1 (>80% of uptake), with 2:1 Na+:glucose stoichiometry. Reason: This is the primary molecular function of SGLT1 and was directly demonstrated using Sglt1-/- mice. The publication states "d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1" (PMID:22124465). UniProt confirms catalytic activity: "D-glucose(out) + 2 Na(+)(out) = D-glucose(in) + 2 Na(+)(in)". Supporting Evidence: file:mouse/Slc5a1/Slc5a1-uniprot.txt D-glucose(out) + 2 Na(+)(out) = D-glucose(in) + 2 Na(+)(in) PMID:22124465 Without d-glucose bolus the Vmax of AMG uptake via SGLT1 was 5.5 times higher than maximal d-glucose uptake via GLUT2, and after glucose gavage the Vmax of AMG uptake via SGLT1 was 8.7 times higher compared with d-glucose uptake via GLUT2 file:mouse/Slc5a1/Slc5a1-deep-research-falcon.md model: Edison Scientific Literature |
| GO:0005412 D-glucose:sodium symporter activity | IBA GO_REF:0000033 | ACCEPT | Summary: IBA annotation for the core symporter activity, supported by phylogenetic analysis and consistent with direct mouse experimental evidence. Reason: The IBA is at the correct level of specificity and is validated by direct mouse knockout evidence from PMID:22124465 demonstrating this exact function. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:0005412 D-glucose:sodium symporter activity | IEA GO_REF:0000117 | ACCEPT | Summary: Electronic annotation from ARBA machine learning models, redundant with but consistent with direct experimental evidence. Reason: Although IEA, this annotation is correct and consistent with IDA evidence from PMID:22124465. The automated assignment correctly identifies the core function. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0005412 D-glucose:sodium symporter activity | ISO GO_REF:0000096 | ACCEPT | Summary: ISO annotation transferred from rat ortholog, redundant with direct mouse IDA evidence. Reason: Correct function, though redundant given direct mouse IDA evidence exists. The ISO transfer is appropriate as SGLT1 function is highly conserved across mammals. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:0005412 D-glucose:sodium symporter activity | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation transferred from human ortholog (UniProtKB:P13866), consistent with direct mouse experimental evidence. Reason: Correct function, redundant with direct mouse IDA evidence but appropriately transferred given high conservation of SGLT1 function. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0005412 D-glucose:sodium symporter activity | ISS GO_REF:0000024 | ACCEPT | Summary: ISS annotation based on sequence similarity to human SGLT1 (UniProtKB:P13866), validated by direct mouse knockout studies. Reason: Correct and validated by direct mouse experimental evidence from PMID:22124465. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:0005412 D-glucose:sodium symporter activity | ISO GO_REF:0000008 | ACCEPT | Summary: ISO annotation from MGI based on curated orthology, consistent with direct mouse experimental evidence. Reason: Correct function, validated by mouse knockout data from PMID:22124465. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0015371 galactose:sodium symporter activity | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation transferred from human SGLT1, supported by the GGM phenotype in mouse knockouts which includes galactose malabsorption. Reason: SGLT1 knockout mice develop glucose-galactose malabsorption syndrome (PMID:22124465), demonstrating that SGLT1 is required for galactose absorption. The galactose:sodium symporter activity is a core function of SGLT1, with catalytic activity confirmed in UniProt: "D-galactose(out) + 2 Na(+)(out) = D-galactose(in) + 2 Na(+)(in)". Supporting Evidence: file:mouse/Slc5a1/Slc5a1-uniprot.txt D-galactose(out) + 2 Na(+)(out) = D-galactose(in) + 2 Na(+)(in) PMID:22124465 Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome |
| GO:0015371 galactose:sodium symporter activity | ISS GO_REF:0000024 | ACCEPT | Summary: ISS annotation for galactose transport, supported by knockout phenotype showing galactose malabsorption. Reason: Galactose transport is a core function validated by the GGM phenotype in Sglt1-/- mice. Supporting Evidence: PMID:22124465 Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome |
| GO:0005372 water transmembrane transporter activity | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation for water transport activity, supported by UniProt functional annotation based on structural and biochemical studies of SGLT1. Reason: UniProt describes SGLT1 as having "high water conductivity comparable to aquaporins" and states it "Acts as a water channel enabling passive water transport in response to the osmotic gradient created upon sugar and Na(+) uptake." This is a documented secondary function of sodium-glucose cotransporters. Supporting Evidence: file:mouse/Slc5a1/Slc5a1-uniprot.txt Acts as a water channel enabling passive water transport in response to the osmotic gradient created upon sugar and Na(+) uptake. Has high water conductivity comparable to aquaporins PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0005372 water transmembrane transporter activity | ISS GO_REF:0000024 | ACCEPT | Summary: ISS annotation for water transport based on sequence similarity to human SGLT1. Reason: Water transport is a well-documented secondary function of SGLT1, supported by biochemical studies showing high water conductivity. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0055056 D-glucose transmembrane transporter activity | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: ISO annotation for general glucose transporter activity. This is a parent term of the more specific D-glucose:sodium symporter activity. Reason: This term is accurate but less specific than GO:0005412 (D-glucose:sodium symporter activity) which better captures the Na+-coupled mechanism. Acceptable as a broader annotation but not the core descriptor of function. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:0055056 D-glucose transmembrane transporter activity | IMP PMID:10997927 Expression characteristics and relevance of sodium glucose c... | KEEP AS NON CORE | Summary: IMP annotation from renal tubulogenesis study showing SGLT1 activity via 14C-glucose uptake assays during kidney development. Reason: The study demonstrated glucose transport activity in developing kidney tubules. However, GO:0005412 (D-glucose:sodium symporter activity) is a more specific descriptor. This annotation is correct but less precise. Supporting Evidence: PMID:10997927 uptake, increased during gestation in the tubular segments where it is expressed |
| GO:0015151 alpha-glucoside transmembrane transporter activity | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: ISO annotation for alpha-glucoside transporter activity. This is broader than glucose-specific transport. Reason: While SGLT1 can transport alpha-methyl-D-glucopyranoside (AMG) as an experimental substrate, the physiological substrates are D-glucose and D-galactose. This term may overstate the range of natural substrates. The more specific symporter activity terms are preferred. Supporting Evidence: PMID:22124465 the Vmax of AMG uptake via SGLT1 was 5.5 times higher than maximal d-glucose uptake via GLUT2 |
| GO:0015293 symporter activity | IEA GO_REF:0000043 | ACCEPT | Summary: IEA annotation from UniProt keyword mapping. This is a very general parent term of the more specific sodium:glucose symporter activity. Reason: Correct but very general. SGLT1 is indeed a symporter (Na+:glucose cotransporter). More specific child terms exist but this IEA annotation is not incorrect. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0022857 transmembrane transporter activity | IEA GO_REF:0000002 | ACCEPT | Summary: IEA annotation from InterPro domain mapping. Very general parent term. Reason: Correct but uninformative. SGLT1 is a transmembrane transporter. More specific annotations exist so this provides minimal additional information. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0016324 apical plasma membrane | IDA PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestina... | ACCEPT | Summary: Core localization directly demonstrated in mouse intestinal and renal tissues by immunofluorescence and functional studies. Reason: This is the primary localization of SGLT1, directly demonstrated in mouse tissues. PMID:22124465 showed SGLT1 at the brush-border membrane (apical surface) of enterocytes and renal tubular cells. UniProt confirms: "Apical cell membrane". Supporting Evidence: file:mouse/Slc5a1/Slc5a1-uniprot.txt Apical cell membrane PMID:22124465 SGLT1 was located in luminal membranes of cells immunopositive for GIP and GLP-1 |
| GO:0016324 apical plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: IBA annotation for apical membrane localization, consistent with direct mouse evidence. Reason: Phylogenetically conserved localization validated by direct mouse IDA evidence. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0016324 apical plasma membrane | IDA PMID:1702069 Antibodies to a renal Na+/glucose cotransport system localiz... | ACCEPT | Summary: IDA annotation from early embryo study showing apical localization in blastomeres using antibodies to SGLT1. Reason: Direct immunofluorescence and immunogold localization showed SGLT1 epitopes become restricted to apical plasma membrane domains by the 16-cell stage. Supporting Evidence: PMID:1702069 by the 16-cell stage epitope expression appeared to become restricted to FS Con A-labeled apical plasma membrane domains and was no longer evident on basolateral domains |
| GO:0016324 apical plasma membrane | IEA GO_REF:0000044 | ACCEPT | Summary: IEA annotation from UniProt subcellular location vocabulary mapping. Reason: Correct and consistent with direct IDA evidence from multiple mouse studies. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0016324 apical plasma membrane | ISO GO_REF:0000096 | ACCEPT | Summary: ISO annotation from rat ortholog, redundant with direct mouse IDA evidence. Reason: Correct localization, validated by multiple direct mouse studies. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0016324 apical plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation from human ortholog, consistent with mouse experimental data. Reason: Conserved apical localization validated by direct mouse evidence. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0005903 brush border | IDA PMID:15601832 Mice without the regulator gene Rsc1A1 exhibit increased Na+... | ACCEPT | Summary: IDA annotation showing SGLT1 localization to brush border in RS1 knockout study. Reason: Direct localization to brush border membrane shown in mouse intestine. This is a core localization for SGLT1's function in intestinal glucose absorption. Supporting Evidence: PMID:15601832 In the small intestines of RS1(-/-) mice, the SGLT1 protein was up-regulated sevenfold compared to that of wild-type mice PMID:22124465 Small intestinal mass absorption of d-glucose across the BBM is mainly mediated by SGLT1 |
| GO:0031526 brush border membrane | ISO GO_REF:0000096 | ACCEPT | Summary: ISO annotation for brush border membrane localization, consistent with direct mouse IDA evidence. Reason: Direct mouse evidence from PMID:22124465 and PMID:15601832 confirms brush border membrane localization in intestinal enterocytes. Supporting Evidence: PMID:22124465 passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1 |
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: IBA annotation for plasma membrane localization. This is a parent term of apical plasma membrane. Reason: Correct but less specific than apical plasma membrane. SGLT1 is indeed a plasma membrane transporter. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0005886 plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation for plasma membrane, correct but less specific than apical plasma membrane annotations. Reason: Correct general localization, validated by specific apical membrane evidence. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0016020 membrane | IEA GO_REF:0000002 | ACCEPT | Summary: IEA annotation from InterPro domain mapping. Very general term. Reason: Correct but uninformative. SGLT1 is a multi-pass membrane protein. More specific localizations are better captured by other annotations. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0005769 early endosome | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: ISO annotation for early endosome localization transferred from human. This likely represents transient trafficking rather than functional localization. Reason: SGLT1 may transit through endosomes during trafficking to/from the plasma membrane, but this is not its primary functional localization. The annotation may reflect transient trafficking intermediates rather than steady-state localization. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0005794 Golgi apparatus | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: ISO annotation for Golgi apparatus localization. This represents biosynthetic trafficking rather than functional localization. Reason: As a glycoprotein, SGLT1 transits through the Golgi during biosynthesis. However, the functional localization is at the apical plasma membrane. This annotation may overrepresent what is likely transient biosynthetic trafficking. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0031965 nuclear membrane | ISO GO_REF:0000119 | REMOVE | Summary: ISO annotation for nuclear membrane localization transferred from human. This seems unlikely for a transporter that functions at the apical plasma membrane. Reason: Nuclear membrane localization is not consistent with the known function and localization of SGLT1 as an apical plasma membrane transporter. There is no direct mouse evidence supporting nuclear membrane localization, and it is not mentioned in UniProt annotations. This is likely an artifact of the human annotation and not a genuine functional localization. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0048471 perinuclear region of cytoplasm | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: ISO annotation for perinuclear localization. May represent ER/Golgi localization during biosynthesis. Reason: Perinuclear localization may reflect biosynthetic intermediates in the ER/Golgi. Not a primary functional localization but may occur during trafficking. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0005911 cell-cell junction | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: ISO annotation for cell-cell junction localization transferred from rat. Reason: Cell-cell junction localization is not well-supported by the known biology of SGLT1. The transporter functions at the apical brush border membrane of polarized epithelial cells, not at lateral cell-cell junctions. This annotation may reflect proximity to junctional regions rather than true junctional localization. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0043226 organelle | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: Very general annotation stating SGLT1 is in an organelle. Reason: This term is too general to be informative. SGLT1's primary localization is at the apical plasma membrane, not within intracellular organelles. The annotation may be technically true (plasma membrane can be considered part of the endomembrane system) but provides no useful information about SGLT1 function. Supporting Evidence: PMID:22124465 SGLT1 was located in luminal membranes |
| GO:0001951 intestinal D-glucose absorption | IMP PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestina... | ACCEPT | Summary: Primary biological process directly demonstrated by knockout studies. Sglt1-/- mice develop GGM syndrome and die without glucose-free diet. Reason: This is THE core biological process of SGLT1 in intestine. The knockout study definitively demonstrated that SGLT1 is "pivotal for intestinal mass absorption of d-glucose" with >80% of glucose uptake mediated by SGLT1. Supporting Evidence: PMID:22124465 SGLT1 is 1) pivotal for intestinal mass absorption of d-glucose, 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2 |
| GO:0035623 renal D-glucose absorption | IMP PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestina... | ACCEPT | Summary: Core renal function demonstrated by micropuncture studies in knockout mice showing SGLT1 reabsorbs ~3% of filtered glucose in S3 segment. Reason: Direct evidence from micropuncture studies in Sglt1-/- mice demonstrated that SGLT1 is responsible for reabsorbing approximately 3% of filtered glucose in the S3 segment of proximal tubules. Supporting Evidence: PMID:22124465 Sglt1−/− mice lose ∼3% of the filtered glucose in the urine |
| GO:0035623 renal D-glucose absorption | IBA GO_REF:0000033 | ACCEPT | Summary: IBA annotation for renal glucose absorption, validated by direct mouse knockout micropuncture studies. Reason: Phylogenetically conserved function validated by direct mouse experimental evidence. Supporting Evidence: PMID:22124465 Sglt1−/− mice lose ∼3% of the filtered glucose in the urine |
| GO:0098708 D-glucose import across plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: IBA annotation for glucose import process, representing the transport activity in process terms. Reason: Correct process annotation that describes what SGLT1 does - imports glucose across the plasma membrane. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:0098708 D-glucose import across plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation for glucose import process from human ortholog. Reason: Correct process annotation consistent with direct mouse evidence. Supporting Evidence: PMID:22124465 passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1 |
| GO:1904659 D-glucose transmembrane transport | IMP PMID:10997927 Expression characteristics and relevance of sodium glucose c... | ACCEPT | Summary: IMP annotation from renal tubulogenesis study showing glucose transport during kidney development using antisense knockdown. Reason: Direct evidence from antisense experiments showing SGLT1 mediates glucose uptake in developing kidney tubules. Supporting Evidence: PMID:10997927 uptake, increased during gestation in the tubular segments where it is expressed. Glucose uptake was inhibited by the treatment with SGLT-1 antisense |
| GO:1904659 D-glucose transmembrane transport | ISO GO_REF:0000008 | ACCEPT | Summary: ISO annotation from MGI orthology curation, validated by direct mouse IMP evidence. Reason: Correct process annotation validated by direct mouse experimental evidence. Supporting Evidence: PMID:22124465 d-glucose uptake via the luminal membrane of small intestinal enterocytes is predominantly (>80%) mediated via SGLT1 |
| GO:1904659 D-glucose transmembrane transport | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation from human ortholog for glucose transport process. Reason: Correct process annotation consistent with mouse experimental evidence. Supporting Evidence: PMID:22124465 passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1 |
| GO:0015757 galactose transmembrane transport | IEA GO_REF:0000108 | ACCEPT | Summary: IEA annotation inferred from galactose:sodium symporter activity (GO:0015371). Reason: Galactose transport is a core function of SGLT1, validated by the GGM phenotype in knockout mice which includes galactose malabsorption. Supporting Evidence: PMID:22124465 Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome |
| GO:0050892 intestinal absorption | IDA PMID:15601832 Mice without the regulator gene Rsc1A1 exhibit increased Na+... | ACCEPT | Summary: IDA annotation from RS1 knockout study showing SGLT1 role in intestinal absorption. Reason: Direct evidence showing SGLT1 is required for intestinal absorption. The RS1 knockout study showed upregulation of SGLT1 increases intestinal glucose absorption. Supporting Evidence: PMID:15601832 Small intestinal d-glucose uptake measured in jointly perfused small bowel and liver was increased twofold compared to that of the wild-type |
| GO:0000017 alpha-glucoside transport | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: ISO annotation for alpha-glucoside transport from human ortholog. Reason: While SGLT1 can transport alpha-methyl-D-glucopyranoside (AMG) in experimental assays, the physiological substrates are D-glucose and D-galactose, not alpha- glucosides in general. This term may overstate the natural substrate range. Supporting Evidence: PMID:22124465 the Vmax of AMG uptake via SGLT1 |
| GO:0009758 carbohydrate utilization | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: ISO annotation for carbohydrate utilization from rat ortholog. Reason: This is a high-level process that SGLT1 contributes to indirectly through glucose absorption. More specific annotations (intestinal D-glucose absorption, renal D-glucose absorption) better capture SGLT1's role. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0006814 sodium ion transport | IEA GO_REF:0000043 | ACCEPT | Summary: IEA annotation from UniProt keyword mapping indicating sodium transport involvement. Reason: SGLT1 couples glucose transport to sodium import with 2:1 Na+:glucose stoichiometry. Sodium transport is an integral part of SGLT1 function. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0098719 sodium ion import across plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: ISO annotation for sodium import process from human ortholog. Reason: Sodium import is mechanistically coupled to glucose transport in SGLT1. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0006811 monoatomic ion transport | IEA GO_REF:0000043 | ACCEPT | Summary: IEA annotation from UniProt keyword for ion transport. Reason: Correct but very general - SGLT1 transports sodium ions as part of its cotransport mechanism. The more specific sodium ion transport term is preferred. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0055085 transmembrane transport | IEA GO_REF:0000002 | ACCEPT | Summary: IEA annotation from InterPro domain mapping for general transmembrane transport. Reason: Correct but uninformative parent term. More specific transport annotations exist. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0035377 transepithelial water transport | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: ISO annotation for water transport process from human ortholog. Reason: SGLT1 has high water conductivity and contributes to transepithelial water transport, particularly in the small intestine. This is a secondary but documented function. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
| GO:0001656 metanephros development | IMP PMID:10997927 Expression characteristics and relevance of sodium glucose c... | KEEP AS NON CORE | Summary: IMP annotation from antisense study showing SGLT1 knockdown affects tubule population in metanephric explants. Reason: The antisense study showed that SGLT1 knockdown "selectively decreased the population of tubules in the metanephric explants". However, SGLT1 is not a developmental signaling molecule - the effect is likely secondary to its metabolic role in glucose transport for tubular cell survival/proliferation. This is a non-core/indirect function. Supporting Evidence: PMID:10997927 Treatment with SGLT-1 antisense selectively decreased the population of tubules in the metanephric explants. Expression of glomerular mRNA and WGA binding were unchanged |
| GO:0150104 transport across blood-brain barrier | ISO GO_REF:0000119 | UNDECIDED | Summary: ISO annotation for blood-brain barrier transport transferred from human. SGLT1's role in BBB glucose transport is debated. Reason: The role of SGLT1 in blood-brain barrier glucose transport is controversial. GLUT1 is the primary glucose transporter at the BBB. While SGLT1 expression has been reported in some brain endothelial studies, this is not its primary physiological function. No direct mouse evidence is available for this annotation. Requires further evaluation. Supporting Evidence: PMID:22124465 Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption |
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