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The protein encoded by ABCC8 is a member of the superfamily of ATP-binding cassette (ABC) transporters. Additionally we are shipping ABCC8 Kits (9) and ABCC8 Proteins (7) and many more products for this protein.
Showing 10 out of 79 products:
Human Monoclonal ABCC8 Primary Antibody for ELISA, WB - ABIN396093
Jablonski, McAteer, de Bakker, Franks, Pollin, Hanson, Saxena, Fowler, Shuldiner, Knowler, Altshuler, Florez: Common variants in 40 genes assessed for diabetes incidence and response to metformin and lifestyle intervention in the diabetes prevention program. in Diabetes 2010
Show all 5 references for ABIN396093
Human Polyclonal ABCC8 Primary Antibody for DB, EIA - ABIN493480
Thomas, Cote, Wohllk, Haddad, Mathew, Rabl, Aguilar-Bryan, Gagel, Bryan: Mutations in the sulfonylurea receptor gene in familial persistent hyperinsulinemic hypoglycemia of infancy. in Science (New York, N.Y.) 1995
Show all 3 references for ABIN493480
Hamster Monoclonal ABCC8 Primary Antibody for ICC, IF - ABIN1027723
Campbell, Sansom, Ashcroft: Potassium channel regulation. in EMBO reports 2003
Show all 2 references for ABIN1027723
Dog (Canine) Polyclonal ABCC8 Primary Antibody for EIA, WB - ABIN375248
de Wet, Rees, Shimomura, Aittoniemi, Patch, Flanagan, Ellard, Hattersley, Sansom, Ashcroft: Increased ATPase activity produced by mutations at arginine-1380 in nucleotide-binding domain 2 of ABCC8 causes neonatal diabetes. in Proceedings of the National Academy of Sciences of the United States of America 2007
Cow (Bovine) Polyclonal ABCC8 Primary Antibody for IHC, WB - ABIN2781496
Babenko: A novel ABCC8 (SUR1)-dependent mechanism of metabolism-excitation uncoupling. in The Journal of biological chemistry 2008
A study of mutations in the ABCC8 gene that cause congenital hyperinsulinism demonstrate a clear functional distinction between SUR1 nucleotide-binding domain two (NBD2) and transmembrane domain (TMD (show TTN Antibodies)) mutants
up-regulation of SUR1 in humans point to this channel as one of the important molecular players in the pathophysiology of Post-traumatic brain contusions
HNF1A (show HNF1A Antibodies) gene mutations represented the second most frequent genetic cause of congenital hyperinsulinism of infancy in the Czech Republic
single amino acid difference can account for the markedly different diazoxide sensitivities between channels containing either the SUR1 or SUR2A (show ABCC9 Antibodies) subunit isoforms.
Mutations in ABCC8 are associated with neonatal diabetes mellitus.
First description of a homozygous p.R1419H mutation in ABCC8 in a family leading to postprandial hyperglycemia followed by hypoglycemia.
in a cohort of hyperinsulinemic hypoglycemia patients from Isfahan, Iran, 78% were noted to have disease-causing mutations: 48% had HADH (show HADHA Antibodies) mutations and 26% had ABCC8 mutations.
genome-wide association studies in population of Pima Indians in Arizona: Data suggest that R1420H loss-of-function variant in ABCC8 is associated with higher birth weights and twofold increased risk for type 2 diabetes with 7-year earlier onset age.
These calculations identified causal genetic variation within the ABCC8/KCNJ11 (show KCNJ11 Antibodies) region for type 2 diabetes mellitus.
Monoallelic ABCC8 mutations are a common cause of diazoxide-unresponsive diffuse form of congenital hyperinsulinism
study provides evidence for a role of Abcc8(ATP-binding cassette sub-family C) in early-phase glucose-mediated insulin (show INS Antibodies) secretion and validates this gene as a contributor to beta-cell dysfunction in type 2 diabetes
We conclude that the gradual development of glucose intolerance in patients with the SUR1-E1506K mutation might, as in the mouse model, result from impaired insulin (show INS Antibodies) secretion due a failure of insulin (show INS Antibodies) content to increase with age.
The results confirm that Kir6.2 (show KCNJ11 Antibodies) contributes to APD shortening in both atria and ventricle during metabolic stress, and that SUR1 is required for atrial APD shortening while SUR2A (show ABCC9 Antibodies) is required for ventricular APD shortening.
EPAC (show RAPGEF3 Antibodies) interaction with SUR1 controls seizure susceptibility and possibly acts via regulation of glutamate (show GRIN1 Antibodies) release.
the role of CpG methylation in regulating SUR1 and SUR2 (show ABCC9 Antibodies) expression
SUR1 controls K(ATP) channel activity but not TRPM4 (show TRPM4 Antibodies) channels.
Conserved intramolecular disulfide bond is critical to trafficking and fate of ATP-binding cassette (ABC (show ABCB6 Antibodies)) transporters ABCB6 (show ABCB6 Antibodies) and sulfonylurea receptor 1 (SUR1)/ABCC8.
ATP regulates pancreatic beta-cell K(ATP) channel activity, not only by its direct actions on Kir6.2 pore subunit, but also via ATP modulation of Syn-1A binding to SUR1.
Diazoxide does not open the ventricular sarcolemmal adenosine triphosphate-sensitive potassium channel but provides volume homeostasis via an SUR1-dependent pathway in mouse ventricular myocytes.
The role of Abcc8, which encodes sulfonylurea receptor 1 (SUR1), was assessed in progressive hemorrhagic necrosis.
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1), inward rectifying potassium channel (show KCNAB2 Antibodies) (Kir6.2 (show KCNJ11 Antibodies), associated with Sur1), glucagon-like peptide 1 receptor (GLP1R (show GLP1R Antibodies)), and adrenergic receptor alpha 2A (show ADRA2A Antibodies) (ADRalpha2A)
The protein encoded by this gene is a member of the superfamily of ATP-binding cassette (ABC) transporters. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the MRP subfamily which is involved in multi-drug resistance. This protein functions as a modulator of ATP-sensitive potassium channels and insulin release. Mutations and deficiencies in this protein have been observed in patients with hyperinsulinemic hypoglycemia of infancy, an autosomal recessive disorder of unregulated and high insulin secretion. Mutations have also been associated with non-insulin-dependent diabetes mellitus type II, an autosomal dominant disease of defective insulin secretion. Alternative splicing of this gene has been observed\; however, the transcript variants have not been fully described.
ATP-binding cassette, sub-family C (CFTR/MRP), member 8
, ATP-binding cassette, sub-family C, member 8
, ATP-binding cassette sub-family C member 8
, ATP-binding cassette transporter sub-family C member 8
, sulfonylurea receptor (hyperinsulinemia)
, sulfonylurea receptor 1
, sulfonylurea receptor
, sulphonylurea receptor 1