APC Anti-CXCR4 antibody [12G5] (ab270635)
Key features and details
- APC Mouse monoclonal [12G5] to CXCR4
- Suitable for: Flow Cyt
- Reacts with: Human, Non human primates
- Conjugation: APC. Ex: 645nm, Em: 660nm
- Isotype: IgG2a
Overview
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Product name
APC Anti-CXCR4 antibody [12G5]
See all CXCR4 primary antibodies -
Description
APC Mouse monoclonal [12G5] to CXCR4 -
Host species
Mouse -
Conjugation
APC. Ex: 645nm, Em: 660nm -
Tested applications
Suitable for: Flow Cytmore details -
Species reactivity
Reacts with: Human, Non human primates -
Immunogen
Tissue, cells or virus. CP-MAC-infected Sup-T1 cells
Database link: P61073 -
Positive control
- Flow: Peripheral whole blood cells, lymphocytes.
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General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C. Store In the Dark. -
Storage buffer
pH: 7.4
Preservative: 0.1% Sodium azide
Constituent: PBS -
Concentration information loading...
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Purity
Size exclusion -
Clonality
Monoclonal -
Clone number
12G5 -
Isotype
IgG2a -
Light chain type
kappa -
Research areas
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab270635 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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Flow Cyt |
Use 10µl for 106 cells.
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Notes |
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Flow Cyt
Use 10µl for 106 cells. |
Target
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Function
Receptor for the C-X-C chemokine CXCL12/SDF-1 that transduces a signal by increasing intracellular calcium ions levels and enhancing MAPK1/MAPK3 activation. Acts as a receptor for extracellular ubiquitin; leading to enhance intracellular calcium ions and reduce cellular cAMP levels. Involved in haematopoiesis and in cardiac ventricular septum formation. Plays also an essential role in vascularization of the gastrointestinal tract, probably by regulating vascular branching and/or remodeling processes in endothelial cells. Could be involved in cerebellar development. In the CNS, could mediate hippocampal-neuron survival. Acts as a coreceptor (CD4 being the primary receptor) for HIV-1 X4 isolates and as a primary receptor for some HIV-2 isolates. Promotes Env-mediated fusion of the virus. -
Tissue specificity
Expressed in numerous tissues, such as peripheral blood leukocytes, spleen, thymus, spinal cord, heart, placenta, lung, liver, skeletal muscle, kidney, pancreas, cerebellum, cerebral cortex and medulla (in microglia as well as in astrocytes), brain microvascular, coronary artery and umbilical cord endothelial cells. Isoform 1 is predominant in all tissues tested. -
Involvement in disease
Defects in CXCR4 are a cause of WHIM syndrome (WHIM) [MIM:193670]; also known as warts, hypogammaglobulinemia, infections and myelokathexis. WHIM syndrome is an immunodeficiency disease characterized by neutropenia, hypogammaglobulinemia and extensive human papillomavirus (HPV) infection. Despite the peripheral neutropenia, bone marrow aspirates from affected individuals contain abundant mature myeloid cells, a condition termed myelokathexis. -
Sequence similarities
Belongs to the G-protein coupled receptor 1 family. -
Domain
The amino-terminus is critical for ligand binding. Residues in all four extracellular regions contribute to HIV-1 coreceptor activity. -
Post-translational
modificationsPhosphorylated on agonist stimulation. Rapidly phosphorylated on serine and threonine residues in the C-terminal. Phosphorylation at Ser-324 and Ser-325 leads to recruitment of ITCH, ubiquitination and protein degradation.
Ubiquitinated by ITCH at the cell membrane on agonist stimulation. The ubiquitin-dependent mechanism, endosomal sorting complex required for transport (ESCRT), then targets CXCR4 for lysosomal degradation. This process is dependent also on prior Ser-/Thr-phosphorylation in the C-terminal of CXCR4. Also binding of ARRB1 to STAM negatively regulates CXCR4 sorting to lysosomes though modulating ubiquitination of SFR5S.
Sulfation on Tyr-21 is required for efficient binding of CXCL12/SDF-1alpha and promotes its dimerization.
O- and N-glycosylated. Asn-11 is the principal site of N-glycosylation. There appears to be very little or no glycosylation on Asn-176. N-glycosylation masks coreceptor function in both X4 and R5 laboratory-adapted and primary HIV-1 strains through inhibiting interaction with their Env glycoproteins. The O-glycosylation chondroitin sulfate attachment does not affect interaction with CXCL12/SDF-1alpha nor its coreceptor activity. -
Cellular localization
Cell membrane. In unstimulated cells, diffuse pattern on plasma membrane. On agonist stimulation, colocalizes with ITCH at the plasma membrane where it becomes ubiquitinated. - Information by UniProt
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Database links
- Entrez Gene: 7852 Human
- Omim: 162643 Human
- SwissProt: P61073 Human
- Unigene: 593413 Human
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Alternative names
- C-X-C chemokine receptor type 4 antibody
- CD184 antibody
- CD184 antigen antibody
see all
Images
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Flow cytometric analysis of lymphocytes (red) and monocytes (black) cells labeling CD184 using ab270635. Concentration of 10 μl reagent/100μl peripheral whole blood.
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Flow cytometric analysis of human peripheral whole blood cells labeling CD184 using ab270635, with the concentration of 10 µl reagent /100 µl of peripheral whole blood.
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
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SDS download
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Datasheet download
References (0)
ab270635 has not yet been referenced specifically in any publications.