Phospho-AKT1 (Thr450) Polyclonal Antibody

Supplier: Elabscience
Product Category: Phospho/Acetyl/Methyl
Description: The serine-threonine protein kinase AKT1 is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery.
Research Areas: Cancer, Epigenetics and Nuclear Signaling, Metabolism, Signal transduction
Size: 200 uL
Concentration: 1mg/mL
Applications: WB,IHC-p,ELISA
Recommended Dilutions: WB 1:500-1:2000, IHC 1:100-1:300, ELISA 1:5000
Clonality: Polyclonal
Clone No:
SwissProt: P31749
Gene ID: 207
Reactivity: Human,Mouse,Rat
Host: Rabbit
Isotype: IgG
Immunogen: Synthesized peptide derived from human Akt1 around the phosphorylation site of Thr450
Formulation: PBS with 0.02% sodium azide, 0.5% BSA and 50% glycerol, pH7.4
Purification: Affinity purification
Conjugation: Unconjugated
Observed MW: 55kDa
Storage: Store at -20C. Avoid freeze / thaw cycles.
Cellular Localization: Cytoplasm. Nucleus. Cell membrane. Nucleus after activation by integrin-linked protein kinase 1 (ILK1). Nuclear translocation is enhanced by interaction with TCL1A. Phosphorylation on Tyr-176 by TNK2 results in its localization to the cell membrane where it is targeted for further phosphorylations on Thr-308 and Ser-473 leading to its activation and the activated form translocates to the nucleus.

Product Link: https://www.elabscience.com/p-phospho_akt1_(thr450)_polyclonal_antibody-25393.html
Manaul Link: https://www.elabscience.com/viewpdf-25393-elabscience-E-AB-20804.PDF