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抗Human ABCC8 抗体:
抗Mouse (Murine) ABCC8 抗体:
抗Rat (Rattus) ABCC8 抗体:
Mammalian Monoclonal ABCC8 Primary Antibody for ISt, IHC - ABIN1304971
Harel, Cohen, Hussain, Flanagan, Schlade-Bartusiak, Patel, Courtade, Li, Van Karnebeek, Kurata, Ellard, Chanoine, Gibson: Alternating hypoglycemia and hyperglycemia in a toddler with a homozygous p.R1419H ABCC8 mutation: an unusual clinical picture. in Journal of pediatric endocrinology & metabolism : JPEM 2015
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Human Polyclonal ABCC8 Primary Antibody for ELISA, WB - ABIN314241
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
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Minor allele ABCC8 SNP genotypes have increased risk of cerebral edema, while major SNP alleles are protective in severe TBI.
Mutation in ABCC8 gene is associated with congenital hyperinsulinism.
ABCC8 mutation causing loss of function of beta-cell KATP channels lead to congenital hyperinsulinism, higher basal [Ca(2 (显示 CA2 抗体)+)] i and insulin (显示 INS 抗体) secretion, increased insulin (显示 INS 抗体) secretion in response to amino acids but not to glucose, increased basal rate of oxygen consumption and mitochondrial mass, increased rates of glycolysis, increased serine/glycine and glutamine (显示 GFPT1 抗体) biosynthesis, and low gamma-aminobutyric acid (GABA) levels.
Hyperinsulinism-causing mutations cause multiple molecular defects in SUR1 nucleotide-binding domains.
Genes ABCC7 (显示 CFTR 抗体), A3, A8, A12 (显示 UGT1A9 抗体), and C8 prevailed among the most upregulated or downregulated ones. In conclusion, the results supported our theory about general adenosine triphosphate-binding cassette gene expression profiles and their importance for cancer on clinical as well as research levels.
Cross-linking experiments showed that KATP channel inhibitors promoted interactions between the N terminus of Kir6.2 and SUR1, whereas channel openers did not, suggesting the inhibitors enhance intersubunit interactions to overcome channel biogenesis and trafficking defects.
Mutations of the ABCC8 gene is associated with congenital hyperinsulinism.
ABCC8 mutation is associated with neonatal diabetes mellitus and iDEND syndrome.
The most frequently seen mutations in Turkish patients with congenital hyperinsulinism (CHI) were ATP binding cassette subfamily C (显示 CYP 抗体) member 8 (ABCC8) gene, followed by 3-hydroxyacyl CoA dehydrogenase (HADH (显示 HADH 抗体)) and kcnj11 (显示 KCNJ11 抗体) channel (KCNJ11 (显示 KCNJ11 抗体)) genes.
Mutations in the ABCC8 gene were the most common cause of congenital hyperinsulinism in our cohort.
Despite its importance in central nervous system (CNS) injuries, sulfonylurea receptor 1 (SUR1) upregulation appears to play no part in rodent anterior ischemic optic neuropathy (rAION) injury.
study provides evidence for a role of Abcc8(ATP-binding cassette sub-family C) in early-phase glucose-mediated insulin (显示 INS 抗体) 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 (显示 INS 抗体) secretion due a failure of insulin (显示 INS 抗体) content to increase with age.
The results confirm that Kir6.2 (显示 KCNJ11 抗体) contributes to APD shortening in both atria and ventricle during metabolic stress, and that SUR1 is required for atrial APD shortening while SUR2A (显示 ABCC9 抗体) is required for ventricular APD shortening.
EPAC (显示 RAPGEF3 抗体) interaction with SUR1 controls seizure susceptibility and possibly acts via regulation of glutamate (显示 GRIN1 抗体) release.
the role of CpG methylation in regulating SUR1 and SUR2 (显示 ABCC9 抗体) expression
SUR1 controls K(ATP) channel activity but not TRPM4 (显示 TRPM4 抗体) channels.
Conserved intramolecular disulfide bond is critical to trafficking and fate of ATP-binding cassette (ABC (显示 ABCB6 抗体)) transporters ABCB6 (显示 ABCB6 抗体) 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.
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1), inward rectifying potassium channel (显示 KCNAB2 抗体) (Kir6.2 (显示 KCNJ11 抗体), associated with Sur1), glucagon-like peptide 1 receptor (GLP1R (显示 GLP1R 抗体)), and adrenergic receptor alpha 2A (显示 ADRA2A 抗体) (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