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]
Host
Rabbit
Immunogen
The antibody was produced against synthesized phosphopeptide derived from human AKT1 around the phosphorylation site of threonine 450 (T-I-TP-P-P).
Isotype
IgG
Quantity
100 µg
Reactivity
Rat, Mouse, Human
Recombinant
FALSE
Regulatory
RUO
Shipping Condition
Ice Packs
Buffer
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Concentration
100µg/100ul
Description
Specificity: AKT1 (phospho-Thr450) Antibody detects endogenous levels of AKT1 only when phosphorylated at threonine 450.
Format
Liquid
Purity
Affinity purified
Storage
This product is stable for several weeks at 4°C as an undiluted liquid. Dilute only prior to immediate use. For extended storage, aliquot contents and freeze at -20°C or below. Avoid cycles of freezing and thawing. Expiration date is one (1) year from date of receipt.