MOUSE ANTI HUMAN BLTR Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI HUMAN BLTR Azide Free
Catalog number: genta-ABS0282
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: bltr

Related genes to: MOUSE ANTI HUMAN BLTR Azide Free

Symbol : bltR NIH gene
LocusTag : BSU26580
description : multidrug-efflux transporter 2 regulator
type of gene : protein-coding
Modification date : 2016-04-19

Related Pathways to: MOUSE ANTI HUMAN BLTR Azide Free

Related product to: MOUSE ANTI HUMAN BLTR Azide Free

Related Articles about: MOUSE ANTI HUMAN BLTR Azide Free

[Regulation of multidrug resistance genes by transcriptional factors from the BltR subfamily].

BltR is a MerR family transcriptional factor, experimentally characterized in Bacillus subtilis. It activates transcription of genes encoding multidrug transporter Blt and spermine/spermidine acetyltransferase BltD. Here we studied BltR dependent regulons in 25 bacterial genomes using the comparative genomic approach. The structure of the promoter regions of regulated genes is typical for MerR family activators: the binding sites are located in long spacers between promoter elements. Regulated genes are usually co-localized with regulator genes and are divergently transcribed with them. The studied transcriptional factors regulate the transcription of multidrug transporter and spermine/spermidine acetyltransferase genes. These transporters can be either secondary or ATP-dependent. The phylogenetic analysis demonstrated that their role as multidrug transporters is conserved. - Source :PubMed

[Establishment of immortalized cell line BLTR-4 and primary identification of its biological character].

To establish immortalized cell line from the urothelium of the urinary bladder and identify the characteristics of the cell line. - Source :PubMed

BLTR mediates leukotriene B(4)-induced chemotaxis and adhesion and plays a dominant role in eosinophil accumulation in a murine model of peritonitis.

Leukotriene B(4) (LTB(4)) is a potent chemoattractant active on multiple leukocytes, including neutrophils, macrophages, and eosinophils, and is implicated in the pathogenesis of a variety of inflammatory processes. A seven transmembrane-spanning, G protein-coupled receptor, called BLTR (LTB(4) receptor), has recently been identified as an LTB(4) receptor. To determine if BLTR is the sole receptor mediating LTB(4)-induced leukocyte activation and to determine the role of LTB(4) and BLTR in regulating leukocyte function in inflammation in vivo, we generated a BLTR-deficient mouse by targeted gene disruption. This mouse reveals that BLTR alone is responsible for LTB(4)-mediated leukocyte calcium flux, chemotaxis, and firm adhesion to endothelium in vivo. Furthermore, despite the apparent functional redundancy with other chemoattractant-receptor pairs in vitro, LTB(4) and BLTR play an important role in the recruitment and/or retention of leukocytes, particularly eosinophils, to the inflamed peritoneum in vivo. These studies demonstrate that BLTR is the key receptor that mediates LTB(4)-induced leukocyte activation and establishes a model to decipher the functional roles of BLTR and LTB(4) in vivo. - Source :PubMed

Chemical probes that differentially modulate peroxisome proliferator-activated receptor alpha and BLTR, nuclear and cell surface receptors for leukotriene B(4).

Peroxisome proliferator-activated receptor alpha (PPARalpha)is a nuclear receptor for various fatty acids, eicosanoids, and hypolipidemic drugs. In the presence of ligand, this transcription factor increases expression of target genes that are primarily associated with lipid homeostasis. We have previously reported PPARalpha as a nuclear receptor of the inflammatory mediator leukotriene B(4) (LTB(4)) and demonstrated an anti-inflammatory function for PPARalpha in vivo (Devchand, P. R., Keller, H., Peters, J. M., Vazquez, M., Gonzalez, F. J., and Wahli, W. (1996) Nature 384, 39-43). LTB(4) also has a cell surface receptor (BLTR) that mediates proinflammatory events, such as chemotaxis and chemokinesis (Yokomizo, T., Izumi, T., Chang, K., Takuwa, Y., and Shimizu, T. (1997) Nature 387, 620-624). In this study, we report on chemical probes that differentially modulate activity of these two LTB(4) receptors. The compounds selected were originally characterized as synthetic BLTR effectors, both agonists and antagonists. Here, we evaluate the compounds as effectors of the three PPAR isotypes (alpha, beta, and gamma) by transient transfection assays and also determine whether the compounds are ligands for these nuclear receptors by coactivator-dependent receptor ligand interaction assay, a semifunctional in vitro assay. Because the compounds are PPARalpha selective, we further analyze their potency in a biological assay for the PPARalpha-mediated activity of lipid accumulation. These chemical probes will prove invaluable in dissecting processes that involve nuclear and cell surface LTB(4) receptors and also aid in drug discovery programs. - Source :PubMed

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