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Rat (Rattus) IAPP ELISA Kit for Competition ELISA - ABIN431403
El Assar, Angulo, Santos-Ruiz, Moreno, Novials, Villanueva-Peñacarrillo, Rodríguez-Mañas: Differential effect of amylin on endothelial-dependent vasodilation in mesenteric arteries from control and insulin resistant rats. in PLoS ONE 2015
All-atom explicit-water molecular dynamics (MD) simulations studying adsorption, orientation, and surface interaction of hIAPP aggregates with different sizes (monomer to tetramer) and conformations (monomer with alpha-helix and tetramer with beta-sheet-rich U-turn) upon adsorption. hIAPP monomer with alpha-helical conformation and hIAPP pentamer with beta-sheet conformation can adsorb on both POPC and POPC/POPE (show HMBS ELISA Kits) bilayers.
Data (including data from studies using tissues from transgenic mice) suggest that IL1B (show IL1B ELISA Kits) plays dual roles by (1) mediating islet amyloid-induced FAS (show FAS ELISA Kits) up-regulation and apoptosis in pancreatic beta-cells and (2) down-regulating IAPP precursor processing thereby potentiating islet amyloid formation. (IL1B (show IL1B ELISA Kits) = interleukin-1beta; FAS (show FAS ELISA Kits) = FAS (show FAS ELISA Kits) cell surface death receptor; IAPP = islet amyloid polypeptide)
Data suggest that single aromatic/hydrophobic amino acid residues within IAPP (islet amyloid polypeptide) amyloid core region are able to control its interaction with amyloid-beta(1-40) or amyloid-beta(1-42) but not IAPP self-assembly; four aromatic/hydrophobic residues are able to control both IAPP amyloid self-assembly and its cross-interaction with amyloid-beta(1-40) or amyloid-beta(1-42).
Data show that aluminum (Al3+) could inhibit islet amyloid polypeptide hIAPP(11-28) fibrillogenesis.
The absence of BACE2 (show BACE2 ELISA Kits) ameliorates glucose tolerance defects induced by IAPP overexpression in the beta-cell and promotes beta-cell survival.
This study supports the elucidation of the structural basis of IAPP amyloid formation and highlights the extent of amyloid fibril polymorphism.
Data suggest that a single GlcNAc residue at CTR (show CALCR ELISA Kits) N130 (asparagine 130) is responsible for enhanced affinity of calcitonin (show CALCA ELISA Kits) for CTR (show CALCR ELISA Kits) ECD (show SHFM1 ELISA Kits); the same appears to apply for enhanced affinity of amylin for RAMP2 (show RAMP2 ELISA Kits)-CTR (show CALCR ELISA Kits) ECD (show SHFM1 ELISA Kits). [GlcNAc = N-acetylglucosamine; CTR (show CALCR ELISA Kits) = calcitonin receptor (show CALCR ELISA Kits); ECD (show SHFM1 ELISA Kits) = extracellular domain; RAMP2 (show RAMP2 ELISA Kits) = receptor (calcitonin) activity modifying protein 2 (show RAMP2 ELISA Kits)].
The kinetics of human amylin amyloid formation can be monitored by SYPRO-orange fluorescence and match the time course determined with thioflavin-T assays.
effect of cholesterol on the amyloidogenicity of IAPP
Chondroitin sulfate A has an intensive promotion effect on the fibrillation of human IAPP at the palmitoyloleoylphosphatidylcholine (POPC) membrane, which is larger than the total effect of Chondroitin sulfate A alone and POPC alone.
These data suggest participation by both soluble and fibrillar aggregates in IAPP-induced islet inflammation. IAPP-induced activation of TLR2 (show TLR2 ELISA Kits) and secretion of IL-1 (show IL1A ELISA Kits) may be important therapeutic targets to prevent amyloid-associated beta cell dysfunction.
Hypothalamic amylin is transcriptionally regulated by leptin (show LEP ELISA Kits), that it can act directly on ObRb (show LEPR ELISA Kits) neurons in concert with leptin (show LEP ELISA Kits), and that it regulates feeding.
Matrix Metalloproteinase-9 (show MMP9 ELISA Kits) Protects Islets from Amyloid-induced Toxicity.
Data indicate that T-cell receptors that react to chromogranin A (ChgA (show CHGA ELISA Kits)) and islet amyloid polypeptide precursor (IAPP) autoantigens were impaired when the thymic stromal cells lacked thymus-specific serine protease (TSSP (show PRSS16 ELISA Kits)).
Study the physiologic actions of IAPP on pancreatic beta cells, which secrete this peptide together with insulin (show INS ELISA Kits) upon glucose stimulation. Explore the signaling pathways and mitogenic actions of IAPP on beta cells.
deletion of the DeltaN isoforms of p63 (show CKAP4 ELISA Kits) or p73 (show ARHGAP24 ELISA Kits) leads to metabolic reprogramming and regression of p53 (show TP53 ELISA Kits)-deficient tumours through upregulation of IAPP, the gene that encodes amylin, a 37-amino-acid peptide co-secreted with insulin (show INS ELISA Kits) by the beta cells of the pancreas
The stability, conformational dynamics and association force of different single-layer models of the full-length wild-type and glycine mutants of amylin, were investigated.
studies have identified a novel TXNIP (show TXNIP ELISA Kits)/miR (show MLXIP ELISA Kits)-124a/FoxA2 (show FOXA2 ELISA Kits)/IAPP signaling cascade linking the critical beta-cell signaling pathways of TXNIP (show TXNIP ELISA Kits) and IAPP
MMP-9 (show MMP9 ELISA Kits) constitutes an endogenous islet protease that limits islet amyloid deposition and its toxic effects via degradation of hIAPP.
Data suggest that amylin and leptin (show LEP ELISA Kits) play additive roles in regulating energy homeostasis via activation of overlapping signalling pathways; mechanisms may be different in hypothalamus, muscle, and liver and in cases of endoplasmic reticulum stress.
Selectively inhibits insulin-stimulated glucose utilization and glycogen deposition in muscle, while not affecting adipocyte glucose metabolism.
Islet amyloid polypeptide (diabetes-associated peptide; amylin)
, diabetes-associated peptide
, insulinoma amyloid peptide
, islet amyloid polypeptide
, amyloid protein