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SLC5A2 encodes a member of the sodium glucose cotransporter family which are sodium-dependent glucose transport proteins. Zusätzlich bieten wir Ihnen SLC5A2 Antikörper (43) und SLC5A2 Kits (16) und viele weitere Produktgruppen zu diesem Protein an.
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cloning and distribution of SGLT2 mRNA expression in bovine tissues; SGLT2 mRNA was detected predominantly in the kidney; expression of SGLT2 mRNA in mammary gland increased more than 10-fold from late pregnancy to early lactation
C-peptide-based measurements of insulin (zeige INS Proteine) secretion are appropriate for assessing beta-cell function in SGLT2 inhibitor canagliflozin-treated participants.
The novel pathogenic SLC5A2 mutation p.S293C was responsible for the onset of FRG (zeige FOLR3 Proteine)
Molecular Interaction of Anti-Diabetic Drugs With Acetylcholinesterase (zeige AChE Proteine) and Sodium Glucose Co-Transporter 2.
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
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.
SGLT2/MAP17 (zeige PDZK1IP1 Proteine) functions as a low-affinity Na(+)-glucose cotransporter (zeige SLC5A1 Proteine) in the kidney.
reported nominal effects of individual SLC5A2 variants on fasting and post-challenge glucose levels may probably not be mediated by altered glucagon (zeige GCG Proteine) release
Findings suggest that there are subtypes of T2DM characterized by different urinary glucose excretion and cardiovascular risk factors. SLC5A2 and HNF1A (zeige HNF1A Proteine) mutations partially explain renal glycosuria in patients with T2DM.
SGLT2 inhibitors combined with insulin (zeige INS Proteine) might be an efficient and safe treatment modality for T1DM patients.
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.
SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3 (zeige NLRP3 Proteine)/ASC (zeige STS Proteine) inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 (zeige DPP4 Proteine) inhibitor Saxagliptin.
Taken together, it was concluded that the effect of SGLT2 inhibition on weight loss is in part mediated via the liver-brain-adipose neurocircuitry.
Tofogliflozin, a selective inhibitor of sodium-glucose cotransporter 2, suppress albuminuria and tubulointerstitial injury in obese and type 2 diabetic mice. Inhibition of glucose entry into tubular cells by tofogliflozin may exert renoprotective properties in diabetes.
SGLT2 inhibition induced gluconeogenesis mainly in the kidney, whereas for low carbohydrate diet, it was predominantly in the liver.
Suggest SGLT2 inhibitor pragliflozin may be effective when administered as part of a combination regimen in the treatment of type 2 diabetes.
these results suggest that SGLT2i treatment acutely suppresses energy expenditure in BAT (zeige BAAT Proteine) via regulation of an inter-organ neural network consisting of the common hepatic vagal branch and sympathetic nerves.
In conclusion, SGLT2 inhibitor luseogliflozin ameliorates glycemic control and thus exerts protective effects on pancreatic beta-cell mass and function.
SGLT2 can transport gentamicin and contribute to gentamicin-induced cytotoxicity.
SGLT2 is inhibited with dapagliflozin in pancreatic alpha cells, which triggers glucagon (zeige GCG Proteine) secretion
DNA sequencing of SGLT2 in SAMP10/TaSlc mice revealed a single nucleotide deletion of guanine at 1236, which resulted in a frameshift mutation that produced a truncated protein.
This gene encodes a member of the sodium glucose cotransporter family which are sodium-dependent glucose transport proteins. The encoded protein is the major cotransporter involved in glucose reabsorption in the kidney. Mutations in this gene are associated with renal glucosuria.
sodium/glucose cotransporter 2
, solute carrier family 5 (sodium/glucose cotransporter), member 2
, Na(+)/glucose cotransporter 2
, low affinity sodium-glucose cotransporter
, solute carrier family 5 (sodium/glucose transporter), member 2
, solute carrier family 5 member 2
, low affinity sodium-dependent glucose cotransporter
, low affinity Na-dependent glucose transporter (SGLT2)
, Na(+)/nucleoside cotransporter
, Na+/nucleoside cotransporter
, sodium/nucleoside cotransporter