Search results for AKT1 pT308 antibody

AKT1 pT308 antibody, Covalab, Ref 00014719

AKT Serine/threonine Kinase 1 Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx327723

AKT1 (pT308) Antibody is a Rabbit Polyclonal against AKT1 (pT308).

AKT Serine/threonine Kinase 1 Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx333194

AKT1 (pT308) Antibody is a Rabbit Polyclonal against AKT1 (pT308).

RAC-Alpha Serine/Threonine-Protein Kinase Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx012718

Rabbit polyclonal antibody against AKT1 protein. Immunogen region is Internal. Specificity is as follows for the reactive species: H:T308, M:T308, R:T308.

RAC-Alpha Serine/threonine-Protein Kinase Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx012525

Rabbit polyclonal antibody against Akt protein. Immunogen region is Internal. Specificity is as follows for the reactive species: H:T308, M:T308, R:T308.

RAC-Alpha Serine/threonine-Protein Kinase Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx032098

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/Teonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq].

RAC-Alpha Serine/threonine-Protein Kinase Phospho-Thr308 (AKT1 pT308) Antibody, Abbexa, abx000352

AKT1 (pT308) Antibody is a Rabbit Polyclonal antibody against AKT1 (pT308). 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.