The PI3K-PKB/Akt pathway is a critical signaling cascade involved in various cellular processes, including growth, proliferation, survival, and metabolism. It was first identified in the early 1980s through studies on insulin receptor signaling. The pathway involves the activation of PI3K, which generates PIP3, a molecule that recruits and activates PKB/Akt. PKB/Akt is then phosphorylated at specific sites, such as T308 and S473, leading to its full activation. This activation triggers downstream effects, including the regulation of mTORC1 and mTORC2, which control protein synthesis and cell growth. Additionally, PKB/Akt influences apoptosis, transcription, and angiogenesis. The pathway is tightly regulated by negative regulators such as PP2A, PHLPP1/2, and PTEN, which dephosphorylate Akt or convert PIP3 back to PIP2. The PI3K-PKB/Akt pathway is highly conserved across species and plays a significant role in tumorigenesis. Recent studies have identified additional components, such as mTORC2 and DNA-PK, which contribute to the full activation of Akt. The pathway is essential for maintaining cellular homeostasis and is a target for therapeutic interventions in diseases such as cancer. The pathway is regulated through a complex network of interactions, involving multiple kinases and phosphatases, and is a key focus of current research in cell signaling.The PI3K-PKB/Akt pathway is a critical signaling cascade involved in various cellular processes, including growth, proliferation, survival, and metabolism. It was first identified in the early 1980s through studies on insulin receptor signaling. The pathway involves the activation of PI3K, which generates PIP3, a molecule that recruits and activates PKB/Akt. PKB/Akt is then phosphorylated at specific sites, such as T308 and S473, leading to its full activation. This activation triggers downstream effects, including the regulation of mTORC1 and mTORC2, which control protein synthesis and cell growth. Additionally, PKB/Akt influences apoptosis, transcription, and angiogenesis. The pathway is tightly regulated by negative regulators such as PP2A, PHLPP1/2, and PTEN, which dephosphorylate Akt or convert PIP3 back to PIP2. The PI3K-PKB/Akt pathway is highly conserved across species and plays a significant role in tumorigenesis. Recent studies have identified additional components, such as mTORC2 and DNA-PK, which contribute to the full activation of Akt. The pathway is essential for maintaining cellular homeostasis and is a target for therapeutic interventions in diseases such as cancer. The pathway is regulated through a complex network of interactions, involving multiple kinases and phosphatases, and is a key focus of current research in cell signaling.