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DRD2 Antibody (C-term) (Ascites)
Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P14416 |
| Other Accession | NP_057658.2 |
| Reactivity | Mouse, Rat |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG2a |
| Clone/Animal Names | 629CT62.2.2 |
| Calculated MW | 50619 Da |
| Antigen Region | 307-336 aa |
| Gene ID | 1813 |
|---|---|
| Other Names | D(2) dopamine receptor, Dopamine D2 receptor, DRD2 |
| Target/Specificity | This DRD2 antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 307-336 amino acids from the C-terminal region of human DRD2. |
| Dilution | WB~~1:200~800 |
| Format | Mouse monoclonal antibody supplied in crude ascites with 0.09% (W/V) sodium azide. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | DRD2 Antibody (C-term) (Ascites) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | DRD2 |
|---|---|
| Function | Dopamine receptor whose activity is mediated by G proteins which inhibit adenylyl cyclase (PubMed:21645528). Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity). |
| Cellular Location | Cell membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein |
| Tissue Location | [Isoform 1]: Expressed in the anterior pituitary gland. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes the D2 subtype of the dopamine receptor. This G-protein coupled receptor inhibits adenylyl cyclase activity. A missense mutation in this gene causes myoclonus dystonia; other mutations have been associated with schizophrenia. Alternative splicing of this gene results in two transcript variants encoding different isoforms. A third variant has been described, but it has not been determined whether this form is normal or due to aberrant splicing.
References
Verma, V., et al. J. Biol. Chem. 285(45):35092-35103(2010)
Borroto-Escuela, D.O., et al. Biochem. Biophys. Res. Commun. 401(4):605-610(2010)
Stelzel, C., et al. J. Neurosci. 30(42):14205-14212(2010)
Huang, H.Y., et al. J. Formos. Med. Assoc. 109(10):736-739(2010)
Itokawa, M., et al. J. Pharmacol. Sci. 114(1):1-5(2010)
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