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Biotinyl-Neuropeptide Y (human, rat) - CAS 213779-13-6

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Category
Main Product
Product Name
Biotinyl-Neuropeptide Y (human, rat)
Catalog Number
213779-13-6
Synonyms
BIOTIN-TYR-PRO-SER-LYS-PRO-ASP-ASN-PRO-GLY-GLU-ASP-ALA-PRO-ALA-GLU-ASP-MET-ALA-ARG-TYR-TYR-SER-ALA-LEU-ARG-HIS-TYR-ILE-ASN-LEU-ILE-THR-ARG-GLN-ARG-TYR-NH2;BIOTINYL-TYR-PRO-SER-LYS-PRO-ASP-ASN-PRO-GLY-GLU-ASP-ALA-PRO-ALA-GLU-ASP-MET-ALA-ARG-TYR-TYR-SER-AL
CAS Number
213779-13-6
Molecular Weight
0
Molecular Formula
C199H299N57O59S2
COA
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MSDS
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Specification
Purity
95%
Reference Reading
1.Grape pomace and grape pomace extract improve insulin signaling in high-fat-fructose fed rat-induced metabolic syndrome.
Rodriguez Lanzi C1, Perdicaro DJ1, Antoniolli A2, Fontana AR2, Miatello RM1, Bottini R2, Vazquez Prieto MA1. Food Funct. 2016 Mar 16;7(3):1544-53. doi: 10.1039/c5fo01065a.
In this study the effect of diet supplementation with grape pomace (GP) and grape pomace extract (GPE) on insulin sensitive tissues (adipose, liver and muscle) was evaluated in an experimental model of metabolic syndrome (MetS). MetS was developed by giving a high-fat-fructose (HFF) diet to Wistar rats. Six weeks of HFF diet induced weight gain, which was partially attenuated by GP (1 g per kg per day) and GPE (300 mg per kg per day) supplementation. HFF diet increased systolic blood pressure, triglycerides, insulin resistance (HOMA:IR) and inflammation (c-reactive protein (CRP)). Supplementation with GP prevented SBP, triglycerides and CRP increased and partially attenuated insulin resistance. On the other hand, GPE partially reduced SBP and triglycerides and significantly prevented insulin resistance and inflammation. Also, HFF diet induced higher triglycerides content and enhanced NADPH oxidase activity in the liver. Also, HFF diet increased the epididymal adipose tissue weight, enlarged adipocyte size, and c-jun N-terminal kinase (JNK) activation, probably contributing to a pro-inflammatory cytokine pattern (higher resistin) and lower adiponectin protein expression.
2.Allosteric Modulation of Kv11.1 (hERG) Channels Protects Against Drug-Induced Ventricular Arrhythmias.
Yu Z1, Liu J1, van Veldhoven JP1, IJzerman AP1, Schalij MJ1, Pijnappels DA1, Heitman LH2, de Vries AA2. Circ Arrhythm Electrophysiol. 2016 Apr;9(4). pii: e003439. doi: 10.1161/CIRCEP.115.003439.
BACKGROUND: Ventricular arrhythmias as a result of unintentional blockade of the Kv11.1 (hERG [human ether-à-go-go-related gene]) channel are a major safety concern in drug development. In past years, several highly prescribed drugs have been withdrawn for their ability to cause such proarrhythmia. Here, we investigated whether the proarrhythmic risk of existing drugs could be reduced by Kv11.1 allosteric modulators.
3.Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury.
Calvo M1, Richards N2, Schmid AB3, Barroso A4, Zhu L4, Ivulic D5, Zhu N6, Anwandter P7, Bhat MA8, Court FA9, McMahon SB2, Bennett DL10. Elife. 2016 Apr 1;5. pii: e12661. doi: 10.7554/eLife.12661. [Epub ahead of print]
Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with αDTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury.
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