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anti-Human ABCC8 Antibodies:
anti-Mouse (Murine) ABCC8 Antibodies:
anti-Rat (Rattus) ABCC8 Antibodies:
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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
Show all 5 Pubmed References
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
Show all 2 Pubmed References
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 (show CA2 Antibodies)+)] i and insulin (show INS Antibodies) secretion, increased insulin (show INS Antibodies) 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 (show GFPT1 Antibodies) biosynthesis, and low gamma-aminobutyric acid (GABA) levels.
Hyperinsulinism-causing mutations cause multiple molecular defects in SUR1 nucleotide-binding domains.
Genes ABCC7 (show CFTR Antibodies), A3, A8, A12 (show UGT1A9 Antibodies), 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 (show CYP Antibodies) member 8 (ABCC8) gene, followed by 3-hydroxyacyl CoA dehydrogenase (HADH (show HADH Antibodies)) and kcnj11 (show KCNJ11 Antibodies) channel (KCNJ11 (show KCNJ11 Antibodies)) 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 (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.
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