Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:500 - 1:1000 |
1:50 - 1:100 |
Not tested in other applications.
Calculated MW
Predict Reactivity
Mouse, Rat(>80% identity)
Form
Liquid
Buffer
PBS, 150mM NaCl, 50% Glycerol
Preservative
0.02% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
Batch dependent (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
The antiserum was produced against synthesized phosphopeptide derived from human Akt around the phosphorylation site of threonine 308 (M-K-Tp-F-C).
Purification
Purified by sequential chromatography on phospho- and non-phospho-peptide affinity columns.
From serum
Conjugation
Unconjugated
RRID
AB_11163439
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
AKT,AKT serine/threonine kinase 1,AKT1,CWS6,PKB,PKBALPHA,PRKBA,RAC,RACALPHA,AKT phospho
Cellular Localization
Cytoplasm,Nucleus,Cell membrane
Background
The serine-threonine protein kinase encoded by the AKT1 gene 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. Mutations in this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2011]
Database
Research Area