|Positive WB detected in||multi-cells, COLO 320 cells, MCF-7 cells|
|Positive IHC detected in||human breast cancer tissue, human cervical cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in||HeLa cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Immunofluorescence (IF)||IF : 1:10-1:100|
|Sample-dependent, check data in validation data gallery|
51077-1-AP targets AKT1 in WB, IHC, IF,ELISA applications and shows reactivity with human samples.
|Host / Isotype||Rabbit / IgG|
|Full Name||v-akt murine thymoma viral oncogene homolog 1|
|Calculated molecular weight||56 kDa|
|Observed molecular weight||56-62 kDa|
|GenBank accession number||BC084538|
|Gene ID (NCBI)||207|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Aliquoting is unnecessary for -20oC storage.|
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.
Cancer Cell Int
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Gelsolin-like actin-capping protein is associated with patient prognosis, cellular apoptosis and proliferation in prostate cancer.
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Clinical significance of combined detection of interleukin-6 and tumour markers in lung cancer.
Oestrogen receptor β5 and epidermal growth factor receptor synergistically promote lung cancer progression.
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Interaction between epidermal growth factor receptor and interleukin-6 receptor in NSCLC progression.