Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE

Price:
927 EUR
1112 USD
769 GBP
known as: Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE
Catalog number: genta-SBA1100-09
Product Quantity: 0.25 mg.
Category:
Supplier: Accu

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Gene target: igg3 min x hu sr prot phycoerythrin rpe

Related genes to: Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE

Symbol : min NIH gene
Synonyms : mi
dbXrefs : FLYBASE:FBgn0002747
chromosome : 2
map location : 56E-56E|2-90 cM
description : mini
type of gene : unknown
Modification date : 2016-05-09
Symbol : Prot NIH gene
dbXrefs : MGI:MGI:107578
chromosome : 18
description : proline transporter
type of gene : protein-coding
Symbol from nomenclature authority : Prot
Full name from nomenclature authority : proline transporter
Nomenclature status : O
Modification date : 2016-07-02
Symbol : rpe NIH gene
LocusTag : NGR_c15200
description : Rpe; ribulose-phosphate 3-epimerase
type of gene : protein-coding
Modification date : 2014-10-31

Related Pathways to: Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE

Gene about :IgG3
Pathway :Hs Allograft Rejection
IgG3
Gene about :Rpe
Pathway :Rn Relationship between glutathione and NADPH
Rpe

Related product to: Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE

Related Articles about: Mouse IgG3 (min X Hu Sr Prot) Phycoerythrin RPE

MinE conformational dynamics regulate membrane binding, MinD interaction, and Min oscillation.

In Escherichia coli MinE induces MinC/MinD to oscillate between the ends of the cell, contributing to the precise placement of the Z ring at midcell. To do this, MinE undergoes a remarkable conformational change from a latent 6β-stranded form that diffuses in the cytoplasm to an active 4β-stranded form bound to the membrane and MinD. How this conformational switch occurs is not known. Here, using hydrogen-deuterium exchange coupled to mass spectrometry (HDX-MS) we rule out a model in which the two forms are in rapid equilibrium. Furthermore, HDX-MS revealed that a MinE mutant (D45A/V49A), previously shown to produce an aberrant oscillation and unable to assemble a MinE ring, is more rigid than WT MinE. This mutant has a defect in interaction with MinD, suggesting it has difficulty in switching to the active form. Analysis of intragenic suppressors of this mutant suggests it has difficulty in releasing the N-terminal membrane targeting sequences (MTS). These results indicate that the dynamic association of the MTS with the β-sheet is fine-tuned to balance MinE's need to sense MinD on the membrane with its need to diffuse in the cytoplasm, both of which are necessary for the oscillation. The results lead to models for MinE activation and MinE ring formation. - Source :PubMed

Chronic Trichuris muris infection causes neoplastic change in the intestine and exacerbates tumour formation in APC min/+ mice.

Incidences of infection-related cancers are on the rise in developing countries where the prevalence of intestinal nematode worm infections are also high. Trichuris muris (T. muris) is a murine gut-dwelling nematode that is the direct model for human T. trichiura, one of the major soil-transmitted helminth infections of humans. In order to assess whether chronic infection with T. muris does indeed influence the development of cancer hallmarks, both wild type mice and colon cancer model (APC min/+) mice were infected with this parasite. Parasite infection in wild type mice led to the development of neoplastic change similar to that seen in mice that had been treated with the carcinogen azoxymethane. Additionally, both chronic and acute infection in the APCmin/+ mice led to an enhanced tumour development that was distinct to the site of infection suggesting systemic control. By blocking the parasite specific T regulatory response in these mice, the increase in the number of tumours following infection was abrogated. Thus T. muris infection alone causes an increase in gut pathologies that are known to be markers of cancer but also increases the incidence of tumour formation in a colon cancer model. The influence of parasitic worm infection on the development of cancer may therefore be significant. - Source :PubMed

Reliability, validity, and norms of the 2-min walk test in children with and without neuromuscular disorders aged 6-12.

The 2-min walk test may be more appropriate functional exercise test for young children. This study aimed to examine the 2-min walk test's reliability; validity; and minimal clinically important difference; and to establish norms for children aged 6-12. - Source :PubMed

Effect of Endothelin-1 on proliferation, migration and fibrogenic gene expression in human RPE cells.

The pathology of the fibrotic proliferative vitreoretinopathy (PVR) membrane represents an excessive wound healing response characterised by cells' proliferation, migration and secretion of extracellular matrix molecules (ECMs). Retinal pigment epithelial (RPE) cells are a major cellular component of the fibrotic membrane. Endothelin-1 (ET-1) has been reported to be involved in the development of PVR in vivo research. However, little is known about the role of ET-1 in RPE cells in vitro. In the present study, we investigated the role of ET-1 in the proliferation, migration and secretion of ECMs (such as type I collagen and fibronectin) in RPE cells in vitro. Our results illustrated that ET-1 promoted the proliferation, migration and secretion of ECMs through the protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) signaling pathways in RPE cells in vitro. These findings strongly suggested that ET-1 may play a vital role in the development of PVR. - Source :PubMed

Complement-Mediated Regulation of Apolipoprotein E in Cultured Human RPE Cells.

Complement activation is implicated in the pathogenesis of age-related macular degeneration (AMD). Apolipoprotein E (ApoE) and complement activation products such as membrane attack complex (MAC) are present in eyes of individuals with AMD. Herein, we investigated the effect of complement activation on induction of ApoE accumulation in human retinal pigment epithelial (RPE) cells. - Source :PubMed

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