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Description
Akt (E17K Mutant Specific) Rabbit Polyclonal AntibodyProduct Specification Host Rabbit Antigen Akt (E17K Mutant Specific) Synonyms RAC alpha serine threonine protein kinase; Protein kinase B (PKB); Protein kinase B alpha (PKB alpha); Proto oncogene c Akt; RAC PK alpha; PKB; RAC; AKT1 Immunogen Synthetic Peptide Location Cytoplasm, Nucleus, Cell membrane Accession P31749 Antibody Type Polyclonal antibody Isotype IgG Application WB Reactivity Hu Purification Immunogen Affinity Concentration 0. 5 mg ml
Product Specification
| Host | Rabbit |
| Antigen | Akt (E17K Mutant Specific) |
| Synonyms | RAC-alpha serine/threonine-protein kinase; Protein kinase B (PKB); Protein kinase B alpha (PKB alpha); Proto-oncogene c-Akt; RAC-PK-alpha; PKB; RAC; AKT1 |
| Immunogen | Synthetic Peptide |
| Location | Cytoplasm, Nucleus, Cell membrane |
| Accession | P31749 |
| Antibody Type | Polyclonal antibody |
| Isotype | IgG |
| Application | WB |
| Reactivity | Hu |
| Purification | Immunogen Affinity |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000 | Hu |
Background
The AKT1(E17K mutant protein) is a constitutively active serine/threonine kinase generated by a single glutamate-to-lysine substitution at position 17 within its pleckstrin homology (PH) domain; this mutation creates new hydrogen bonds that markedly increase affinity for membrane phosphoinositides, driving persistent plasma-membrane localization and PI3K-independent phosphorylation of T308 and S473, thereby locking the kinase in an “always-on” conformation that fuels oncogenic signaling through mTORC1, GSK3β and FOXO, promotes cell survival, proliferation and migration, and confers both tumorigenic potential and resistance to many allosteric AKT inhibitors while remaining selectively targetable by emerging ATP-competitive or covalent mutant-specific inhibitors.
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