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GNAQ Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P50148 |
| Other Accession | P38410, P82471, Q2PKF4, P21279, NP_002063.2 |
| Reactivity | Human |
| Predicted | Mouse, Pig, Rat, Xenopus |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 42142 Da |
| Antigen Region | 52-78 aa |
| Gene ID | 2776 |
|---|---|
| Other Names | Guanine nucleotide-binding protein G(q) subunit alpha, Guanine nucleotide-binding protein alpha-q, GNAQ, GAQ |
| Target/Specificity | This GNAQ antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 52-78 amino acids from the N-terminal region of human GNAQ. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| 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 | GNAQ Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | GNAQ |
|---|---|
| Synonyms | GAQ |
| Function | Guanine nucleotide-binding proteins (G proteins) function as transducers downstream of G protein-coupled receptors (GPCRs) in numerous signaling cascades (PubMed:37991948). The alpha chain contains the guanine nucleotide binding site and alternates between an active, GTP-bound state and an inactive, GDP-bound state (PubMed:37991948). Signaling by an activated GPCR promotes GDP release and GTP binding (PubMed:37991948). The alpha subunit has a low GTPase activity that converts bound GTP to GDP, thereby terminating the signal (PubMed:37991948). Both GDP release and GTP hydrolysis are modulated by numerous regulatory proteins (PubMed:37991948). Signaling is mediated via phospholipase C-beta-dependent inositol lipid hydrolysis for signal propagation: activates phospholipase C-beta: following GPCR activation, GNAQ activates PLC-beta (PLCB1, PLCB2, PLCB3 or PLCB4), leading to production of diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3) (PubMed:37991948). Required for platelet activation (By similarity). Regulates B-cell selection and survival and is required to prevent B-cell-dependent autoimmunity (By similarity). Regulates chemotaxis of BM-derived neutrophils and dendritic cells (in vitro) (By similarity). Transduces FFAR4 signaling in response to long-chain fatty acids (LCFAs) (PubMed:27852822). Together with GNA11, required for heart development (By similarity). |
| Cellular Location | Cell membrane; Lipid-anchor. Golgi apparatus. Nucleus {ECO:0000250|UniProtKB:P21279} Nucleus membrane {ECO:0000250|UniProtKB:P21279}. Note=Colocalizes with the adrenergic receptors, ADREN1A and ADREN1B, at the nuclear membrane of cardiac myocytes. {ECO:0000250|UniProtKB:P21279} |
| Tissue Location | Predominantly expressed in ovary, prostate, testis and colon. Down-regulated in the peripheral blood lymphocytes (PBLs) of rheumatoid arthritis patients (at protein level) |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
This locus encodes a guanine nucleotide-binding protein. The encoded protein, an alpha subunit in the Gq class, couples a seven-transmembrane domain receptor to activation of phospolipase C-beta. Mutations at this locus have been associated with problems in platelet activation and aggregation. A related pseudogene exists on chromosome 2.
References
Dratviman-Storobinsky, O., et al. Invest. Ophthalmol. Vis. Sci. 51(12):6180-6182(2010)
Crouthamel, M., et al. Mol. Pharmacol. 78(4):767-777(2010)
Chillar, A., et al. Biochemistry 49(30):6365-6374(2010)
Klenke, S., et al. Pharmacogenet. Genomics 20(8):476-484(2010)
Salmanian, S., et al. Biochem. Biophys. Res. Commun. 395(4):577-582(2010)
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