Mouse IgG2a, Control, FITC + Mouse IgG1, RPE, dual label

Price:
542 EUR
650 USD
449 GBP
known as: Mouse IgG2a, Control, FITC + Mouse IgG1, RPE, dual label
Catalog number: genta-YSRTDC014
Product Quantity: vial
Category:
Supplier: Accu

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Gene target: igg2a igg1 rpe

Related genes to: Mouse IgG2a, Control, FITC + Mouse IgG1, RPE, dual label

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 IgG2a, Control, FITC + Mouse IgG1, RPE, dual label

Gene about :IgG1
Pathway :Hs Allograft Rejection
IgG1
Gene about :Label
Pathway :Mm Hfe effect on hepcidin production
Label
Gene about :Rpe
Pathway :Rn Relationship between glutathione and NADPH
Rpe
Gene about :Control
Pathway :Rn Wnt Signaling Pathway NetPath
Control

Related product to: Mouse IgG2a, Control, FITC + Mouse IgG1, RPE, dual label

Related Articles about: Mouse IgG2a, Control, FITC + Mouse IgG1, RPE, dual label

Racing an Opponent Alters Pacing, Performance and Muscle Force Decline, But Not RPE.

Performing against a virtual opponent has been shown to invite a change in pacing and improve time trial (TT) performance. This study explored how this performance improvement is established by assessing changes in pacing, neuromuscular function and perceived exertion. - 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

Long-Term Efficacy of GMP Grade Xeno-Free hESC-Derived RPE Cells Following Transplantation.

Retinal pigment epithelium (RPE) dysfunction underlies the retinal degenerative process in age-related macular degeneration (AMD), and thus RPE cell replacement provides an optimal treatment target. We characterized longitudinally the efficacy of RPE cells derived under xeno-free conditions from clinical and xeno-free grade human embryonic stem cells (OpRegen) following transplantation into the subretinal space of Royal College of Surgeons (RCS) rats. - Source :PubMed

Semaphorin4D-PlexinB1 Signaling Attenuates Photoreceptor Outer Segment Phagocytosis by Reducing Rac1 Activity of RPE Cells.

Semaphorins form a family of secreted and membrane-bound molecules that were identified originally as axonal guidance factors during neuronal development. Given their wide distribution in many including mature tissues, semaphorin 4D (sema4D) and its main functional receptor plexin B1 (plxnB1) are expected to fulfill additional functions that remain to be uncovered. A main characteristic of the plexin receptor family is its ability to reorganize the cytoskeleton. PlxnB1 specifically may directly interact with Rho family GTPases to regulate F-actin driven pathways in cells in culture. Diurnal clearance phagocytosis by the retinal pigment epithelium (RPE) of photoreceptor outer segment fragments (POS) is critical for photoreceptor function and longevity. In this process, rearrangement of RPE cytoskeletal F-actin via activation of the Rho family GTPase Rac1 is essential for POS internalization. Here, we show a novel role in POS phagocytosis by RPE cells in culture and in vivo for plexin B1 and its ligand sema4D. Exogenous sema4D abolishes POS internalization (but not binding) by differentiated RPE cells in culture by decreasing the GTP load of Rac1. In the rat eye, sema4D localizes to retinal photoreceptors, while PlxnB1 is expressed by neighboring RPE cells. At the peak of diurnal retinal phagocytosis after light onset, plxnB1 phosphorylation and sema4D levels are reduced in wild-type rat retina in situ but not in mutant RCS rat retina in which the RPE lacks phagocytic activity. Finally, increased POS phagosome content after light onset is observed in the RPE in situ of mice with either plxnB1 or sema4D gene deletion. Altogether, our results demonstrate a novel physiological function for sema4D/plxnB1 signaling in RPE phagocytosis serving as attenuating brake prior to light onset whose release enables the diurnal phagocytic burst. - Source :PubMed

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