Product nameAnti-SUR1 antibody
See all SUR1 primary antibodies
DescriptionRabbit polyclonal to SUR1
Tested applicationsSuitable for: IHC-FoFr, ELISA, WBmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide corresponding to SUR1 aa 1560-1582.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Storage bufferPreservative: 0.05% Sodium azide
DiluObuffer: Hepes, NaCl, KCl, glycerol, BSA and chaotropic agents(proprietary information). Preservative: 0.05% Sodium Azide
Concentration information loading...
PurityProtein A purified
- Pathways and Processes
- Metabolic signaling pathways
- Energy transfer pathways
- Integration of energy
Our Abpromise guarantee covers the use of ab32844 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-FoFr||Use at an assay dependent concentration. PubMed: 20304763|
|ELISA||1/10000 - 1/100000.|
|WB||1/500. Predicted molecular weight: 175 kDa.|
FunctionPutative subunit of the beta-cell ATP-sensitive potassium channel (KATP). Regulator of ATP-sensitive K(+) channels and insulin release.
Involvement in diseaseDefects in ABCC8 are a cause of leucine-induced hypoglycemia (LIH) [MIM:240800]; also known as leucine-sensitive hypoglycemia of infancy. LIH is a rare cause of hypoglycemia and is described as a condition in which symptomatic hypoglycemia is provoked by high protein feedings. Hypoglycemia is also elicited by administration of oral or intravenous infusions of a single amino acid, leucine.
Defects in ABCC8 are the cause of familial hyperinsulinemic hypoglycemia type 1 (HHF1) [MIM:256450]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. It causes nesidioblastosis, a diffuse abnormality of the pancreas in which there is extensive, often disorganized formation of new islets. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.
Defects in ABCC8 are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.
Defects in ABCC8 are the cause of transient neonatal diabetes mellitus type 2 (TNDM2) [MIM:610374]. Neonatal diabetes is a form of diabetes mellitus defined by the onset of mild-to-severe hyperglycemia within the first months of life. Transient neonatal diabetes remits early, with a possible relapse during adolescence.
Sequence similaritiesBelongs to the ABC transporter superfamily. ABCC family. Conjugate transporter (TC 3.A.1.208) subfamily.
Contains 2 ABC transmembrane type-1 domains.
Contains 2 ABC transporter domains.
- Information by UniProt
- ABC36 antibody
- Abcc8 antibody
- ABCC8_HUMAN antibody
This product has been referenced in:
- Zhou F et al. Neuroprotective potential of glibenclamide is mediated by antioxidant and anti-apoptotic pathways in intracerebral hemorrhage. Brain Res Bull 142:18-24 (2018). Read more (PubMed: 29933037) »
- Xu S et al. Autocrine insulin increases plasma membrane KATP channel via PI3K-VAMP2 pathway in MIN6 cells. Biochem Biophys Res Commun 468:752-7 (2015). WB ; Mouse . Read more (PubMed: 26585489) »