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Anti AKT antibodies

AKT is one of the most actively studied kinase pathways in the basic research and drug development arenas:

Recent advances in AKT signaling have focused on understanding cellular processes and identifying cellular substrates that are physiologically relevant in vivo. These efforts have uncovered important roles for AKT regulation:

AKT Signaling Pathway Overview

AKT pathway poster

 

  Download the AKT pathway poster here

 

 

 

 

 

 

   

AKT Cell Signaling Antibodies & Assays

Activation of AKT results in phosphorylation of a wide range of proteins downstream of the AKT pathway. The phosphorylated substrates, present in various subcellular locations play an important role in directing different phenotypic outcomes. Faulty or aberrant activation of AKT underlies the pathophysiological properties of a variety of complex diseases, including type-2 diabetes, HIV and cancer. When constitutively active, AKT is utilized frequently by cancer cells to circumvent therapeutic intervention, promoting cellular survival and resistance to chemo and radiation therapy. Rockland's Anti-AKT antibodies help monitor levels of AKT and its phosphorylation at position S473, T308, as well as AKT isoforms AKT2 and AKT3.


Featured AKT Antibodies:

Anti-AKT pan    Immunohistochemistry of Mouse anti-AKT pT308 antibody. Tissue: human brain cerebellum tissue (40X). Fixation: formalin fixed paraffin embedded. Antigen retrieval: not required. Primary antibody: AKT pT308antibody at 20 µg/mL for 1 h at RT. Secondary antibody: Peroxidase rabbit secondary antibody at 1:10,000 for 45 min at RT. Localization: staining of Purkinje neurons and cell processes in the cerebellum, cytosolic as well as occasionally nuclear. Staining: AKT pT308 as precipitated red signal with hematoxylin purple nuclear counterstain.   Immunofluorescence Microscopy of Mouse Anti-AKTpS473 antibody using STED nanoscopy to evaluate AKT activation and migration. Tissue: A431 cells. Antigen retrieval: Panel A: serum starved,unstimulated cells. Panel B: serum starved, EGF stimulated for 15 mins. A massive increase in AKT-pS473 activation, as measured by intensity signal, peaked at 15 minutes and was associated with depolymerized tubulin. Staining: Panel A shows STED data (AKT-pS473, red channel) collected simultaneously with confocal signal (a-tubulin, green channel). Upon stimulation of cells with EGF, a rapid activation of AKT is observed (Panel B) along with a coincident change in the tubulin organization (yellow signal), as well as an extensive cell shape-change (cell membrane folding) and accumulation of AKTpS473 at the cell periphery.
         
   

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