SLC5A2 Antibody

1. SGLT2-I therapy is a potential new strategy for the treatment of HCC. PMID:29205334
2. Sodium-glucose cotransporter-2 (SGLT2) is selectively expressed in the human kidney, where it executes reabsorption of filtered glucose with a high capacity; it may be overactive in patients with diabetes, especially in the early, hyperfiltering stage of the disease. As a therapeutic target, SGLT2 has been successfully engaged by orally active, selective agents. [review] PMID:28506519
3. In this study, more than 90% of patients were on Forxiga or Invokana. Merck and Pfizer are also collaborating to bring an SGLT2 rival drug, ertugliflozin, to market as well as on two combinations containing the drug to treat type 2 diabetes. PMID:28398306
4. Canagliflozin, an orally active inhibitor of sodium glucose co-transporter 2, is approved for the treatment of type-2 diabetes mellitus. Food did not affect canagliflozin pharmacokinetics. PMID:27136908
5. C-peptide-based measurements of insulin secretion are appropriate for assessing beta-cell function in SGLT2 inhibitor canagliflozin-treated participants. PMID:27127999
6. The novel pathogenic SLC5A2 mutation p.S293C was responsible for the onset of FRG PMID:28365451
7. Molecular Interaction of Anti-Diabetic Drugs With Acetylcholinesterase and Sodium Glucose Co-Transporter 2. PMID:28387957
8. the key pharmacodynamic effects of SGLT2 inhibitors and the clinical evidence that support the rationale for the use of SGLT2 inhibitors in patients with HF who have T2D. Because these favorable effects presumably occur independent of blood glucose lowering, we also explore the potential use of SGLT2 inhibition in patients without T2D with HF or at risk of HF, such as in patients with coronary artery disease PMID:29061576
9. Results provide evidence that common genetic variants in the SLC5A2 gene do not affect diabetes-related metabolic traits in subjects at increased risk of type 2 diabetes. PMID:28134748
10. SGLT2/MAP17 functions as a low-affinity Na(+)-glucose cotransporter in the kidney. PMID:28592437
11. reported nominal effects of individual SLC5A2 variants on fasting and post-challenge glucose levels may probably not be mediated by altered glucagon release PMID:28472182
12. Findings suggest that there are subtypes of T2DM characterized by different urinary glucose excretion and cardiovascular risk factors. SLC5A2 and HNF1A mutations partially explain renal glycosuria in patients with T2DM. PMID:28324025
13. SGLT2 inhibitors combined with insulin might be an efficient and safe treatment modality for T1DM patients. PMID:28399981
14. Data suggest that, by shunting substantial amounts of carbohydrate into urine, SGLT2-mediated glycosuria results in a progressive shift in energy metabolism toward fatty substrates; studies were conducted in subjects with/without diabetes type 2 treated with SGLT2 antagonist and hypoglycemic agent empagliflozin. PMID:26861783
15. Studies indicate that Sodium-glucose cotransporter 2 (SGLT2)T2 inhibitors are promising antidiabetic agents that are gaining attention in both clinical medicine and basic research. PMID:27754601
16. Data suggest that ketoacidosis (ketonuria/ketonemia) associated with the use of sodium-glucose cotransporter 2 protein (SGLT-2) inhibitors needs further research. PMID:27085074
17. In both men and women, grip strength increased in both hands after sodium-glucose cotransporter 2 protein (SGLT2) inhibitor treatment . PMID:27038414
18. Data suggest that SGLT2 plays central role in energy metabolism and renal elimination of circulating glucose; targeted inhibition of SGLT2 alters energy metabolism in diabetes and obesity. PMID:26403227
19. Mutations in the SLC5A2 gene did not find any evidence that chronic loss of glucose in the urine would protect from deterioration of the glucose tolerance over time. PMID:26735923
20. Data suggest that SGLT2 is transporter found in proximal renal tubules, responsible for reabsorption of most of glucose filtered by kidney; inhibition of SGLT2 lowers blood glucose level by promoting urinary excretion of excess glucose. [REVIEW] PMID:26362302
21. Data show that thiosugars bind to sodium-glucose co-transporters vSGLT and hSGLT2 stronger and dissociate more slowly than sugars. PMID:26260238
22. SGLT2 is functionally expressed in pancreatic and prostate adenocarcinomas PMID:26170283
23. Results identified six SLC5A2 variants including four novel variants in Chinese familial renal glucosuria. Variant SLC5A2 proteins had altered expression levels and patterns in addition to significantly lower glucose transport in cultured cells. PMID:25339128
24. SGLT2 inhibitor canagliflozin can be coadministered with oral contraceptives, warfarin, or digoxin without dose adjustments. PMID:25345427
25. SGLT2 is inhibited with dapagliflozin in pancreatic alpha cells, which triggers glucagon secretion PMID:25894829
26. Sodium glucose cotransporter 2 inhibitor empagliflozin is not associated with prolonged QT interval. PMID:23617452
27. A single dose of canagliflozin, a sodium glucose co-transporter 2 inhibitor, 300 mg reduced both fasting and postprandial PG. PMID:25110280
28. A possible role of common genetic variation in SLC5A2 in the control of glucose homeostasis. PMID:23651029
29. Studies indcate that glucose is present in the glomerular filtrate and is reabsorbed by a group of transport proteins in the renal tubular epithelium, with sodium glucose transporter (SGLT)-2 quantitatively the most important. PMID:23714218
30. Data suggest that SGLT2 plays role in tubular apoptosis in diabetic nephropathy; SGLT2-mediated, high glucose-induced generation of reactive oxygen species appears to augment apoptosis of renal tubular cells. PMID:23508966
31. It was concluded that human SGLT1 and SGLT2 are regulated by different mechanisms and suggest that insulin is an SGLT2 agonist in vivo. PMID:22673616
32. A total of 21 different SLC5A2 mutations were detected in a cohort of 23 unrelated Korean children with Familial renal glucosuria PMID:22314875
33. In this review, we summarize the available data concerning the mechanism of action, efficacy, and safety of this novel antidiabetic class of therapeutic agents. PMID:22528597
34. analysis of SGLT2 inhibitors containing the 1,2,3-triazole motif and evaluation of their urinary glucose excretion PMID:22079028
35. TS-071 inhibited SGLT2 activity in a concentration-dependent manner. PMID:21410690
36. Our data suggest a role of SGLT2 genetic variation in the regulation of glucose homeostasis and promote pharmacogenomic studies to clarify the efficacy of antidiabetic treatment by SGLT2 inhibitors PMID:21830867
37. Five novel SGLT2 mutations were identified in familial renal glucosuria patients. Mutant SGLT2 proteins had significantly lower glucose transport capacity upon reconstruction in cultured cells. PMID:21165652
38. SGLT2 plays an important role in renal tubular glucose reabsorption. PMID:14569097
39. homozygous missense mutation in exon 8 of SLC5A2, resulting in a lysine to arginine substitution at position 321 underlies autosomal-recessive renal glucosuria and aminoaciduria PMID:15610225
40. Thioglycoside I (phenyl-1'-thio-beta-D-glucopyranoside) inhibited hSGLT2. PMID:17505558
41. Within 17 pedigrees, we have identified a total of 20 different SLC5A2 mutations in familial renal glucosuria. PMID:18622023

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HGNC: 11037

UNIGENE: Hs.709195

KEGG: hsa:6524

STRING: 9606.ENSP00000327943

OMIM: 182381