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AKT3 Antibody (aa119-136, clone 66C1247.1)
Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P |
|---|---|
| Primary Accession | Q9Y243 |
| Reactivity | Human, Mouse, Rat, Rabbit, Monkey, Pig, Chicken, Horse, Bovine, Dog |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | 66C1247.1 |
| Calculated MW | 56kDa |
| Dilution | IHC-P (10 µg/ml), WB (1-2 µg/ml), |
| Gene ID | 10000 |
|---|---|
| Other Names | RAC-gamma serine/threonine-protein kinase, 2.7.11.1, Protein kinase Akt-3, Protein kinase B gamma, PKB gamma, RAC-PK-gamma, STK-2, AKT3, PKBG |
| Target/Specificity | A synthetic peptide corresponding to amino acid residues 119-136 (CSPTSQIDNIGEEEMDAS) of human Akt3, GenBank no. gi|4574744|gb|AAD24196.1|AF135794_1. This sequence is identical in human, mouse, rat, cow, dog, and chicken. |
| Reconstitution & Storage | Long term: -20°C; Short term: +4°C; Avoid freeze-thaw cycles. |
| Precautions | AKT3 Antibody (aa119-136, clone 66C1247.1) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | AKT3 |
|---|---|
| Synonyms | PKBG |
| Function | AKT3 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT3 is the least studied AKT isoform. It plays an important role in brain development and is crucial for the viability of malignant glioma cells. AKT3 isoform may also be the key molecule in up-regulation and down-regulation of MMP13 via IL13. Required for the coordination of mitochondrial biogenesis with growth factor-induced increases in cellular energy demands. Down- regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase- dependent apoptosis. |
| Cellular Location | Nucleus. Cytoplasm. Membrane; Peripheral membrane protein Note=Membrane-associated after cell stimulation leading to its translocation |
| Tissue Location | In adult tissues, it is highly expressed in brain, lung and kidney, but weakly in heart, testis and liver. In fetal tissues, it is highly expressed in heart, liver and brain and not at all in kidney |
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
AKT3 is one of 3 closely related serine/threonine- protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT3 is the least studied AKT isoform. It plays an important role in brain development and is crucial for the viability of malignant glioma cells. AKT3 isoform may also be the key molecule in up-regulation and down-regulation of MMP13 via IL13. Required for the coordination of mitochondrial biogenesis with growth factor-induced increases in cellular energy demands. Down-regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase- dependent apoptosis.
References
Brodbeck D.,et al.J. Biol. Chem. 274:9133-9136(1999).
Nakatani K.,et al.Biochem. Biophys. Res. Commun. 257:906-910(1999).
Masure S.,et al.Eur. J. Biochem. 265:353-360(1999).
Li X.,et al.Submitted (AUG-1998) to the EMBL/GenBank/DDBJ databases.
Wiemann S.,et al.Genome Res. 11:422-435(2001).
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