Protein kinase B (PKB)

Where the papers sit

52 papers from the last 6 months study Protein kinase B (PKB) directly · updated from PubMed 12 Oct 2026

• PI3K/AKT Therapeutic Signaling

  PI3K/AKT activation is being used as a common therapeutic explanation across metabolic, neurological, vascular, fibrotic and cancer models. Natural products and exosomes recur, with reported benefits involving lipid homeostasis, ischemic injury, wound repair, neuronal survival and macrophage polarization. Nrf2, NF-κB, AMPK/PPAR-α and PTEN/p53 provide recurring pathway links. Lenvatinib plus PD-1 blockade extends the theme toward immune-modulating cancer combinations, but most evidence remains preclinical.

  16 papers · 30.8%

• Inflammatory Signaling Across Diseases

  Inflammation is being linked to AKT1, IL-6, TNF-α and related immune networks across liver, metabolic, reproductive, skeletal, neural and toxicological disease. Plant-derived compounds and traditional formulations dominate, usually combining network pharmacology with docking, molecular dynamics or animal validation. Gut microbiota, autophagy, oxidative stress and CXCL8/EGFR/PTPRC/MYC signaling recur as mechanistic bridges. The work is converging on multi-target anti-inflammatory intervention, though clinical evidence is largely absent.

  9 papers · 17.3%

• Cancer Growth and Drug Resistance

  Cancer studies are moving from single-pathway descriptions toward target selection and combination treatment. AKT1, EGFR, MET and MMP9 recur in proliferation, migration, senescence and kinase-inhibitor resistance, with CAMK2D-driven AKT phosphorylation implicated in gefitinib resistance. Capivasertib is tested with durvalumab and paclitaxel in triple-negative breast cancer, while other work remains computational or preclinical. Biomarker-defined combinations and validation beyond docking remain open.

  7 papers · 13.5%

• Others — AKT-Linked Liver and Cancer Biology

  Liver metabolism and hepatocellular carcinoma form the dominant thread, linking PPARγ, PGC-1α and AKT to lipid handling, inflammation, migration and tumor growth. Cilostazol, luteolin formulations and targeted PPARG/AKT1 activation are explored for metabolic or liver injury, whereas PRXL2B and prenylated flavonoids address PI3K/AKT-dependent HCC progression. AML induction and masitinib-driven lysosomal autophagy sit outside that main axis. The cluster therefore offers related liver biology but no single translational direction.

  8 papers · 15.4%

• Others — AKT-Linked Metabolic and Cancer Studies

  AKT-centered work is split between insulin resistance, type 2 diabetes, cancer drug resistance, and compound discovery. Evodiamine and puerarin are linked to IRS-1/PI3K/AKT/GLUT4 and AKT1-ferroptosis mechanisms, while exosomal p-AKT marks doxorubicin resistance. Capivasertib-associated hyperglycemia highlights a clinical toxicity issue. Network pharmacology and a reaction-aware design platform appear as tools rather than a shared biological direction.

  7 papers · 13.5%

• Others — mTOR-Related Cellular Stress

  mTOR- and AKT-linked studies here address distinct forms of cellular stress rather than a single disease program. The recurring endpoints are apoptosis, autophagy, metabolism and tissue injury, spanning mesothelioma, nerve repair, sepsis, Alzheimer-related peptide transport and breast-cancer metastasis. Monocyte epigenetic rewiring and TIGIT/CD155 signaling broaden the immune context. The set offers mechanistic leads, but no consistent treatment direction or clinical convergence.

  5 papers · 9.6%