RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin

Price:
694 EUR
832 USD
576 GBP
known as: RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin
Catalog number: genta-ABS0480
Product Quantity: 50 µg
Category:
Supplier: AbD

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Gene target: interleukin 1 beta

Related genes to: RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin

Symbol : betA NIH gene
LocusTag : NGR_c06990
description : choline dehydrogenase
type of gene : protein-coding
Modification date : 2016-04-19
Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26

Related Pathways to: RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin

Gene about :biotin
Pathway :Sc Protein Modifications
biotin

Related product to: RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin

Related Articles about: RABBIT ANTI MOUSE INTERLEUKIN_1 BETA Biotin

PCOS and diabetes mellitus: from insulin resistance to altered beta pancreatic function, a link in evolution.

- Source :PubMed

Structural insights into the inclusion complexes between clomiphene citrate and β-cyclodextrin: The mechanism of preferential isomeric selection.

A major challenge in pharmaceuticals for clinical applications is to alter the solubility, stability, and toxicity of drug molecules in living systems. Cyclodextrins (CDs) have the ability to form host-guest inclusion complexes with pharmaceuticals for further development of new drug formulations. The inclusion complex of clomiphene citrate (CL), a poorly water-soluble drug, with native β-cyclodextrin (β-CD) was characterized by a one and two-dimensional nuclear magnetic resonance (NMR) spectroscopic approach and also by molecular docking techniques. Here we report NMR and a computational approach in preferential isomeric selection of CL, which exists in two stereochemical isomers, enclomiphene citrate (ENC; E isomer) and zuclomiphene citrate (ZNC; Z isomer) with β-CD. β-CD cavity protons, namely, H-3' and H-5', experienced shielding in the presence of CL. The aromatic ring protons of the CL molecule were observed to be deshielded in the presence of β-CD. The stoichiometric ratio of the β-CD:CL inclusion complex was observed by NMR and found to be 1:1. The overall binding constant of β-CD:CL inclusion complexes was based on NMR chemical shifts and was calculated to be 50.21 M(-1) . The change in Gibb's free energy (∆G) was calculated to be -9.80 KJ mol(-1) . The orientation and structure of the β-CD:CL inclusion complexes are proposed on the basis of NMR and molecular docking studies. 2D (1) H-(1) H ROESY confirmed the involvement of all three aromatic rings of CL in the inclusion complexation with β-CD in the solution, confirming the multiple equilibria between β-CD and CL. Molecular docking and 2D (1) H-(1) H ROESY provide insight into the inclusion complexation of two isomers of CL into the β-CD cavity. A molecular docking technique further provided the different binding affinities of the E and Z isomers of CL with β-CD and confirmed the preference of the Z isomer binding for β-CD:CL inclusion complexes. The study indicates that the formation of a hydrogen bond between -O- of CL and the hydrogen atom of the hydroxyl group of β-CD was the main factor for noncovalent β-CD:CL inclusion complex formation and stabilization in the aqueous phase. - Source :PubMed

Stabilizing amyloid-β peptide by the N-terminus capture is capable of preventing and eliminating amyloid-β oligomers.

Elimination of amyloid-β (Aβ) oligomers remains challenging. We describe here a novel strategy to prevent and eliminate the Aβ oligomers from either the early aggregation or the fibril dissolution pathway by targeting the flexible N-terminus, but not the widely investigated hydrophobic segment, with a rationally designed cyclopeptide. - Source :PubMed

Potentiating role of copper on spatial memory deficit induced by beta amyloid and evaluation of mitochondrial function markers in the hippocampus of rats.

Mounting evidence suggests that copper, a crucial element in normal brain function, plays an important role in the etiology of Alzheimer's disease, which is known as a neurodegenerative mitochondrial disorder. However, the precise mechanisms of its effects on cognitive and mitochondrial functions through the CNS have not been thoroughly recognized yet. In this study, we aimed to investigate the long-term (3-week) effects of copper sulfate (50, 100 and 200 mg kg(-1) day(-1)) exposure on learning and memory as well as on mitochondrial function in the hippocampus of rats in the presence and absence of beta amyloid (1 μg μl(-1) per side) intrahippocampally (IH). After three weeks of copper exposure through drinking water, acquisition and retention of spatial memory were measured by the Morris water maze (MWM) test. Various parameters of mitochondrial function were also evaluated. Our data show that copper damaged the spatial learning and memory and also exacerbated the memory deficit induced by Aβ injection in rats in a dose-dependent manner. Mitochondria isolated from the hippocampus of rats treated with copper showed significant increases in ROS formation, mitochondrial swelling, lipid peroxidation, glutathione oxidation, outer membrane damage, and collapse of MMP, decreased cytochrome c oxidase activity, and finally increased ADP/ATP ratios. Our results indicate that copper overloading in the hippocampus of rats causes mitochondrial dysfunction and subsequent oxidative stress leading to cognitive impairment. This study also reveals that copper can potentiate Aβ deleterious effects on spatial memory and brain mitochondrial function. - Source :PubMed

Susac syndrome misdiagnosed as multiple sclerosis with exacerbation by interferon beta therapy.

Susac syndrome is a rare autoimmune disorder characterised by the clinical triad of encephalopathy, retinopathy (branch retinal artery occlusions) and hearing loss. The diagnosis of Susac syndrome may be difficult initially, and it is not uncommon for patients with Susac syndrome to be misdiagnosed with multiple sclerosis. In this case report, we describe a patient who was diagnosed as having multiple sclerosis for three years, with further deterioration after starting treatment with interferon beta-1a. The patient had the triad of encephalopathy, branch retinal artery occlusions and sensorineural hearing loss. She had the classic magnetic resonance imaging appearance, with normal magnetic resonance imaging of the spinal cord and absence of oligoclonal bands in the cerebrospinal fluid. Our patient responded well to treatment with a combination therapy and discontinuation of interferon beta-1a. Our observations raise awareness about the importance of the early and correct diagnosis of Susac syndrome, which usually affects young patients, with an excellent prognosis if treated aggressively at an early stage of the disease. Susac syndrome is underdiagnosed and is not uncommonly misdiagnosed as multiple sclerosis. Susac syndrome is a great mimicker of multiple sclerosis, and establishing diagnostic criteria for this syndrome is very useful. In any patient presenting with a progressive disabling neurological disorder associated with callosal lesions and/or hearing loss, and/or visual loss especially in women, Susac syndrome should be suspected. - Source :PubMed

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