HPA013796
Anti-P2RY12 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
P2RY12 Antibody - Anti-P2RY12 antibody produced in rabbit, P2Ry12 Antibody, Anti-ADP-glucose receptor, Anti-ADPG-R, Anti-P2T(AC), Anti-P2Y purinoceptor 12, Anti-P2Y(AC), Anti-P2Y(ADP), Anti-P2Y(cyc), Anti-P2Y12, Anti-P2Y12 platelet ADP receptor, Anti-SP1999
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About This Item
Recommended Products
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
enhanced validation
orthogonal RNAseq
Learn more about Antibody Enhanced Validation
technique(s)
immunohistochemistry: 1:20-1:50
immunogen sequence
LTNRQPRDKNVKKCSFLKSEFGLVWHEIV
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... P2RY12(64805)
General description
Purinergic receptor (P2Y12) is expressed in platelets. P2Y12 is mapped to human chromosome 3q25.1. It belongs to the P2Y receptors family and is predominantly expressed in astrocytes. P2Y12 is predicted to have three ATP binding regions. It has seven transmembrane regions.
Immunogen
P2Y purinoceptor 12 recombinant protein epitope signature tag (PrEST)
Application
Anti-P2RY12 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level.
Biochem/physiol Actions
The gene P2RY12 (purinergic receptor P2Y, G-protein coupled, 12) encodes a G-protein coupled receptor for ADP and ATP coupled to G-proteins that are involved in the negative regulation of adenylyl cyclase second messenger system. It functions in normal platelet aggregation and blood coagulation. Defects in this gene may cause bleeding disorder, platelet type 8 (BDPLT8). It serves as a potential target for the treatment of thromboembolisms and other clotting disorders.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST72772
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
10 - Combustible liquids
wgk_germany
WGK 1
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Does i-T744C P2Y12 Polymorphism Modulate Clopidogrel Response among Moroccan Acute Coronary Syndromes Patients?
Hassani I, et al.
Genetics research international, 2017 (2017)
Identification of the P2Y12 receptor: a novel member of the P2Y family of receptors activated by extracellular nucleotides
Nicholas RA
Molecular Pharmacology, 60(3), 416-420 (2001)
Molecular modeling of purinergic receptor P2Y12 and interaction with its antagonists
Zhan C, et al.
Journal of Molecular Graphics & Modelling, 26(1), 20-31 (2007)
Marco Cattaneo et al.
Proceedings of the National Academy of Sciences of the United States of America, 100(4), 1978-1983 (2003-02-13)
We have identified structural attributes required for signal transduction through a seven-transmembrane-domain receptor. Platelets from a patient (AC) with a congenital bleeding disorder had normal shape change but reduced and reversible aggregation in response to 4 microM ADP, similar to
Rocío Rojo et al.
Nature communications, 10(1), 3215-3215 (2019-07-22)
The proliferation, differentiation and survival of mononuclear phagocytes depend on signals from the receptor for macrophage colony-stimulating factor, CSF1R. The mammalian Csf1r locus contains a highly conserved super-enhancer, the fms-intronic regulatory element (FIRE). Here we show that genomic deletion of
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