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Bifurcation of the Tre1 G protein-coupled receptor signaling response via G protein-dependent and independent branches enables distinct spatiotemporal regulation of germ cell migration.
The scattershot allele results in an in-frame deletion of 8 amino acids at the junction of the third transmembrane domain and the second intracellular loop of Tre1 that dramatically impairs the function of this GPCR in germ cell migration.
plays an important role in regulation of germ cell migration, polarity , cell adhesion, and cadherin binding. (review)
Tre1 is a G protein-coupled receptor (Montrer GPBAR1 Kits ELISA) that directs transepithelial migration of Drosophila germ cells
Down-regulation of E-cadherin causes germ cell dispersal but is not sufficient for transepithelial migration in the absence of Tre1, suggesting a new mechanism for Tre1 GPCR function that links cell polarity, modulation of cell adhesion, and invasion.
CXCR7 mediates CD14 (Montrer NDUFA2 Kits ELISA)(+)CD16 (Montrer CD16 Kits ELISA)(+) monocyte transmigration across the blood brain barrier, and is a potential therapeutic target for neuro AIDS.
CXCR7 signaling could not be detected using impedance measurements. However, increasing levels of CXCR7 expression significantly reduced the CXCR4 (Montrer CXCR4 Kits ELISA)-mediated impedance readout, suggesting a regulatory role for CXCR7 on CXCR4 (Montrer CXCR4 Kits ELISA)-mediated signaling.
CXCR7 expression in gastric cancer tissues was significantly higher than that in adjacent non-cancer tissues and associated with tumor size, TNM (Montrer ODZ1 Kits ELISA) stage and lymph node metastasis. CXCR7 was identified as a novel promoter in gastric cancer initiation and progression.
the data identified the pivotal role of the receptor CXCR7 in pulmonary inflammation with a predominant effect on the pulmonary epithelium and polymorphonuclear neutrophils
SDF-1 (Montrer CXCL12 Kits ELISA)/CXCR7 plays a positive role in the proliferation and invasion of endometrial carcinoma cells.
our study demonstrates that the upregulation of CXCR7 signaling contributes to increased vasculogenic capacity of EOCs from CAD (Montrer CAD Kits ELISA) patients, indicating that CXCR7 signaling may be a novel therapeutic vasculogenic target for CAD (Montrer CAD Kits ELISA).
CXCR7 expression in the tumor cells and stromal cells from the metastatic foci was significantly more common in the group of male patients treated with cytotoxic drugs according to the FOLFOX6 regimen
hypoxia and CXCL12 (Montrer CXCL12 Kits ELISA)-CXCR7 axis appeared to be advantageous microenvironments to CD20 (Montrer MS4A1 Kits ELISA)(-) CD138 (Montrer SDC1 Kits ELISA)(-) cells in lymphoplasmacytic lymphoma
suppressing CXCR4 (Montrer CXCR4 Kits ELISA) is not enough to impede osteosarcoma invasion in bone marrow microenvironment since CXCR7 is activated to sustain invasion. Therefore, inhibiting both CXCR4 (Montrer CXCR4 Kits ELISA) and CXCR7 could be a promising strategy in controlling osteosarcoma invasion.
This short review intends to provide a concise summary of current knowledge with regards to cell-specific functions of CXCL12 (Montrer CXCL12 Kits ELISA) and its receptors CXCR4 (Montrer CXCR4 Kits ELISA) and CXCR7 with potential implications for the initiation and progression of atherosclerosis. [review]
High CXCR7 expression is associated with Prostate Cancer.
CXCR7 expression in adipose tissue macrophages is upregulated in obesity.
Elevated expression of CXCR7 enhances endothelial progenitor cell resistance to diabetes mellitus-induced oxidative damage.
expression of CXCR7 in normal and pathological nervous system suggests CXCR4 (Montrer CXCR4 Kits ELISA)-independent functions of SDF-1/CXCL12 (Montrer CXCL12 Kits ELISA) mediated through its interaction with CXCR7
confirm a pivotal role of the SDF-1 (Montrer CXCL12 Kits ELISA)/CXCR4 (Montrer CXCR4 Kits ELISA)/CXCR7 axis for chronic allograft vasculopathy development
our present study provided evidence that SDF-1 (Montrer CXCL12 Kits ELISA) mediated CSCs migration through CXCR4 (Montrer CXCR4 Kits ELISA) and CXCR7 via MEK (Montrer MDK Kits ELISA)/ERK (Montrer EPHB2 Kits ELISA) and PI3K/Akt (Montrer AKT1 Kits ELISA) pathway
Endothelial CXCR7 limits breast cancer metastasis at multiple steps in the metastatic cascade, advancing understanding of CXCL12 (Montrer CXCL12 Kits ELISA) pathways in tumor environments and informing ongoing drug development targeting CXCR7 in cancer.
Sata demonstrate that CXCR7 has a role in the positioning of hem and pallium-subpallium boundary-derived Cajal-Retzius (CR)cells, CXCL12 (Montrer CXCL12 Kits ELISA) regulating CR cell subpial localization through the combined action of CXCR4 (Montrer CXCR4 Kits ELISA) and CXCR7.
CXCR7 acts to prevent epithelial damage and ameliorate fibrosis after a single lung injury, repeated injury leads to suppression of CXCR7 expression and recruitment of VEGFR1 (Montrer FLT1 Kits ELISA) expressing macrophages, Wnt (Montrer WNT2 Kits ELISA) and Notch (Montrer NOTCH1 Kits ELISA) signaling, and enhanced fibrosis.
This gene encodes a member of the G-protein coupled receptor family. Although this protein was earlier thought to be a receptor for vasoactive intestinal peptide (VIP), it is now considered to be an orphan receptor, in that its endogenous ligand has not been identified. The protein is also a coreceptor for human immunodeficiency viruses (HIV). Translocations involving this gene and HMGA2 on chromosome 12 have been observed in lipomas.
, G protein coupled receptor
, trapped in endoderm 1
, trapped in endoderm-1
, C-X-C chemokine receptor type 7
, G protein-coupled receptor
, G-protein coupled receptor 159
, G-protein coupled receptor RDC1 homolog
, chemokine (C-X-C motif) receptor 7
, chemokine orphan receptor 1
, RDC1-like G protein-coupled receptor
, G-protein coupled receptor RDC1