ArtNr |
BOS-M02656-30ul |
Hersteller |
Boster
|
Menge |
30ul |
Format |
Liquid |
Applikationen |
WB, FC |
Clon |
FEI-1 |
Specific against |
Human, Mouse, Rat |
Host |
Rabbit |
Isotype |
IgG |
Alias |
Atypical chemokine receptor 3;C-X-C chemokine receptor type 7;CXC-R7;CXCR-7;Chemokine orphan receptor 1;G-protein coupled receptor 159;G-protein coupled receptor RDC1 homolog;RDC-1;ACKR3;CMKOR1, CXCR7, GPR159, RDC1; |
Lieferbar |
|
Manufacturers Product Category |
Primary Antibodies, Rabbit Monoclonal Antibodies |
Manufacturers Research Category |
G Protein Signaling, Signal Transduction, Signaling Pathway |
Short Description |
Boster Bio Anti-CXCR7 ACKR3 Rabbit Monoclonal Antibody catalog # M02656. Tested in WB, Flow Cytometry applications. This antibody reacts with Human, Mouse, Rat. |
Description |
Boster Bio Anti-CXCR7 ACKR3 Rabbit Monoclonal Antibody catalog # M02656. Tested in WB, Flow Cytometry applications. This antibody reacts with Human, Mouse, Rat. |
Gene Name |
ACKR3 |
Application Details |
WB 1:500-1:2000 FC 1:50 |
Clonality |
Monoclonal |
Concentration |
Actual concentration vary by lot. Use suggested dilution ratio to decide dilution procedure. |
Contents |
Rabbit IgG in phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol, 0.4-0.5mg/ml BSA. |
Immunogen |
A synthesized peptide derived from human CXCR7 |
Purification |
Affinity-chromatography |
Storage |
Store at -20°C for one year. For short term storage and frequent use, store at 4°C for up to one month. Avoid repeated freeze-thaw cycles. |
Gene Full Name |
Atypical chemokine receptor 3 |
Molecular Weight |
41493 MW |
Protein Function |
Atypical chemokine receptor that controls chemokine levels and localization via high-affinity chemokine binding that is uncoupled from classic ligand-driven signal transduction cascades, resulting instead in chemokine sequestration, degradation, or transcytosis. Also known as interceptor (internalizing receptor) or chemokine-scavenging receptor or chemokine decoy receptor. Acts as a receptor for chemokines CXCL11 and CXCL12/SDF1. Chemokine binding does not activate G-protein- mediated signal transduction but instead induces beta-arrestin recruitment, leading to ligand internalization and activation of MAPK signaling pathway. Required for regulation of CXCR4 protein levels in migrating interneurons, thereby adapting their chemokine responsiveness. In glioma cells, transduces signals via MEK/ERK pathway, mediating resistance to apoptosis. Promotes cell growth and survival. Not involved in cell migration, adhesion or proliferation of normal hematopoietic progenitors but activated by CXCL11 in malignant hemapoietic cells, leading to phosphorylation of ERK1/2 (MAPK3/MAPK1) and enhanced cell adhesion and migration. Plays a regulatory role in CXCR4-mediated activation of cell surface integrins by CXCL12. Required for heart valve development. Acts as coreceptor with CXCR4 for a restricted number of HIV isolates.. |
Subcellular Localization |
Cell membrane; Multi-pass membrane protein. Cytoplasm, perinuclear region. Early endosome. Recycling endosome. Predominantly localizes to endocytic vesicles, and upon stimulation by the ligand is internalized via clathrin- coated pits in a beta-arrestin-dependent manner. Once internalized, the ligand dissociates from the receptor, and is targeted to degradation while the receptor is recycled back to the cell membrane. |
Tissue Specificity |
Expressed in monocytes, basophils, B-cells, umbilical vein endothelial cells (HUVEC) and B-lymphoblastoid cells. Lower expression detected in CD4+ T-lymphocytes and natural killer cells. In the brain, detected in endothelial cells and capillaries, and in mature neurons of the frontal cortex and hippocampus. Expressed in tubular formation in the kidney. Highly expressed in astroglial tumor endothelial, microglial and glioma cells. Expressed at low levels in normal CD34+ progenitor cells, but at very high levels in several myeloid malignant cell lines. Expressed in breast carcinomas but not in normal breast tissue (at protein level).. |
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