Phospho-AKT1S1 (T246) antibody
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935106861
info@markelab.com
name
Phospho-AKT1S1 (T246) antibody
category
Primary Antibodies
provider
FineTest
reference
FNab09943
tested applications
ELISA, WB, IHC
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | A synthetic phosphorylated peptide around Thr246 of human AKT1S1 (Phospho-AKT1S1 (T246)) |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | WB: 1:500 - 1:2000; IHC: 1:20 - 1:200 |
| Clonality | polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | 50 kDa |
| Purity | ≥95% as determined by SDS-PAGE |
| Purification | Immunogen affinity purified |
| Size 1 | 100µg |
| Form | liquid |
| Tested Applications | ELISA, WB, IHC |
| Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
| UniProt ID | Q96B36 |
| Alias | AKT1S1,PRAS40 |
| Background | Antibody anti-AKT1S1 |
| Status | RUO |
| Note | Mol. Weight 50 kDa |
AKT1S1, also known as proline-rich AKT1 substrate 1 or PRAS40, is a protein that acts as a substrate for AKT1 (Protein Kinase B, isoform 1). It plays a crucial role in regulating the mTOR (mechanistic target of rapamycin) signaling pathway, which is involved in controlling cell growth, proliferation, and survival. AKT1S1 contains proline-rich motifs that serve as docking sites for protein-protein interactions. When phosphorylated by AKT1 at specific sites, such as Serine 183, AKT1S1 dissociates from mTORC1 (mTOR Complex 1), leading to activation of mTORC1 and subsequent stimulation of protein synthesis and cell growth.The regulation of AKT1S1 by AKT1 and its involvement in mTOR signaling make it a key player in cellular processes such as cell growth, proliferation, and metabolism. Dysregulation of this pathway can contribute to various diseases, including cancer and metabolic disorders. Therefore, understanding the function of AKT1S1 and its interactions with AKT1 and mTOR is important for elucidating disease mechanisms and developing potential therapeutic strategies.
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