Mouse IgG2a (1b allotype specific), Biotin

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1077 EUR
1292 USD
893 GBP
known as: Mouse IgG2a (1b allotype specific), Biotin
Catalog number: genta-YNShMIgG2a1bBio
Product Quantity: 1 ml.
Category:
Supplier: Accu

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Gene target: igg2a 1b allotype specific

Related genes to: Mouse IgG2a (1b allotype specific), Biotin

Symbol : 1b NIH gene
LocusTag : AL352_gp2
description : 1b
type of gene : protein-coding
Modification date : 2016-05-06
Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26

Related Pathways to: Mouse IgG2a (1b allotype specific), Biotin

Gene about :biotin
Pathway :Sc Protein Modifications
biotin

Related product to: Mouse IgG2a (1b allotype specific), Biotin

Related Articles about: Mouse IgG2a (1b allotype specific), Biotin

Protein-Tyrosine Phosphatase-1B Mediates Sleep Fragmentation-Induced Insulin Resistance and Visceral Adipose Tissue Inflammation in Mice.

Sleep fragmentation (SF) is highly prevalent and has emerged as an important contributing factor to obesity and metabolic syndrome. We hypothesized that SF-induced increases in protein tyrosine phosphatase-1B (PTP-1B) expression and activity underlie increased food intake, inflammation, and leptin and insulin resistance. - Source :PubMed

Outcomes of oral biotin treatment in patients with biotinidase deficiency - Twenty years follow-up.

Biotinidase deficiency (BTD) is an inborn error of biotin metabolism inherited as an autosomal recessive trait. Due to the, biotinidase deficiency, biotin is not recycled. Individuals with BTD usually exhibit neurological and cutaneous abnormalities unless treated with biotin. Supplementation with biotin may either ameliorate or if early introduced even prevent symptoms when introduced presymptomatically. - Source :PubMed

Pseudohypoparathyroidism type 1B - a rare cause of tetany: case report.

Pseudohypoparathyroidism (PHP) is a rare group of disorders characterised by end-organ resistance to the parathyroid hormone (PTH). A 16-year-old boy presented with a 2-year history of involuntary dystonic movements involving mainly the left hand, initially after writing and later during physical exercise. Serum calcium was 1.37 mmol/L (2.20-2.69), phosphate 2.1 mmol/L (0.8-1.45) and PTH 302 ng/L (12-88). CT scan of the head demonstrated multiple subcortical and diffuse basal ganglia calcifications. Genetic analysis confirmed a methylation defect in the GNAS cluster on chromosome 20q13.32 which established the diagnosis. Treatment with calcitriol and calcium carbonate led to complete remission of symptoms. Causes of hypocalcaemia should be considered in evaluating patients with movement disorders. The diagnosis of PHP-1B is challenging but the overall prognosis is excellent. - Source :PubMed

Analysis of K-Ras Interactions by Biotin Ligase Tagging.

Mutations of the human K-Ras 4B (K-Ras) G protein are associated with a significant proportion of all human cancers. Despite this fact, a comprehensive analysis of K-Ras interactions is lacking. Our investigations focus on characterization of the K-Ras interaction network. - Source :PubMed

Alendronate treatment induces IL-1B expression and apoptosis in glioblastoma cell line.

Alendronate (ALD), one among the nitrogen-containing bisphosphonates (NBPs), is currently used for the treatment of many pathological conditions. Unfortunately, although generally tolerated, NBPs treatment has been associated with central nervous system (CNS) adverse outcomes, such as amnesia, hallucinations and visual disturbances. So, we analyzed the effect of ALD treatment in glial cells, the main sources of cholesterol for neurons and principal cells involved in the immunological defense of the brain. We treated a glial cell line (U87-MG) with increasing doses of ALD (0.1, 1, 10, 25, 50 μM) for 48 h, aimed at evaluating the influence of this drug treatment on IL-1B expression, NLRP3 and CASP1 expression, mitochondrial activity and apoptotic cell death. We observed that ALD treatment, at the higher concentrations, induced a significant increase of IL-1B, NLRP3, CASP1 expression, provoked apoptosis and also mitochondrial damage in U87-MG. Considering the reported CNS adverse outcomes of NBPs treatment, our results confirm ALD side-effects on glial cell model. - Source :PubMed

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