Somatic mutations in AKT, particularly the , alter the PH domain structure, leading to constitutive membrane localization and hyperactivation of downstream effectors like mTOR and ERK1/2. This promotes uncontrolled proliferation and resistance to apoptosis. AKT1 Transcriptomic Landscape in Breast Cancer Cells - MDPI
: Predominantly expressed in the brain, where it regulates organ size and neurodevelopment. 3. Pathological Dysregulation 3.1 Cancer
: The primary regulator of insulin-dependent glucose uptake in muscle and adipose tissue. File: AKT_collection_compressed_2022-11-20.zip ...
AKT (Protein Kinase B) is a critical serine-threonine kinase existing in three isoforms (AKT1, AKT2, AKT3) that integrates signals from the PI3K pathway to regulate metabolism, survival, and proliferation. This paper analyzes the distinct and overlapping roles of these isoforms using transcriptomic landscapes and multi-omic profiling. We demonstrate that while AKT1 primarily drives somatic growth, AKT2 is essential for glucose metabolism, and AKT3 influences neuronal development. Furthermore, we explore how aberrant activation via somatic mutations, such as AKT1 (E17K), contributes to tumorigenesis in breast and colorectal cancers. 1. Introduction
Research indicates that AKT isoforms are not functionally redundant: Somatic mutations in AKT, particularly the , alter
We found that changes in the cellular levels of AKT1 lead to changes in the levels of a set of differentially expressed genes and, Akt isoforms in the immune system - Frontiers
The PI3K/AKT/mTOR signaling axis is one of the most frequently dysregulated pathways in human disease. AKT acts as a central hub, receiving signals from receptor tyrosine kinases (RTKs) and G-protein-coupled receptors (GPCRs). Upon recruitment to the plasma membrane via its PH domain, AKT is activated by phosphorylation at T308 and S473. 2. Isoform-Specific Functions This paper analyzes the distinct and overlapping roles
Multi-Isoform AKT Signaling: A Systems-Level Analysis of Cellular Homeostasis and Oncogenesis
