ArticleGenes2018
Phosphorylation-Dependent Inhibition of Akt1.
Article in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed.
- Food-Derived Natural Compounds as Molecular Targets in Cancer Prevention.Pharmaceutics · 2026Review
- Combining bioinformatics prediction with experimental validation to explore the ameliorative effect ofMolecular medicine reports · 2026Article
- SLC30A1, SLC30A5, and SLC30A9 transporters play crucial role in ligand-independent activation of ESR1 signalling in breast cancer cells via modulation of AKT activity by zinc.Metallomics : integrated biometal science · 2026Article
- Glyoxalase 1 is a proadipogenic gene.The Journal of biological chemistry · 2025Article
- Citrullination of AKT2 Catalyzed by PAD1 Facilitates the Maintenance of Stemness Characteristics of Ovarian Cancer Stem-Like Cells in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Flavonoids ofMediators of inflammation · 2025Article
- Network Pharmacology Analysis andCombinatorial chemistry & high throughput screening · 2025Article
- Genetic Encoding of Phosphorylated Amino Acids into Proteins.Chemical reviews · 2024Review
- Inhibition of lncRNA NFIA-AS1 Alleviates Abnormal Proliferation and Inflammation of Vascular Smooth Muscle Cells in Atherosclerosis by Regulating miR-125a-3p/AKT1 Axis.International journal of genomics · 2023Article
- Delivery of Active AKT1 to Human Cells.Cells · 2022Article
- Effects of urolithin A on osteoclast differentiation induced by receptor activator of nuclear factor-κB ligand via bone morphogenic protein 2.Bioengineered · 2022Article
- MicroRNA-149 suppresses osteogenic differentiation of mesenchymal stem cells via inhibition of AKT1-dependent Twist1 phosphorylation.Cell death discovery · 2022Article
- Duhuo Jisheng Decoction inhibits the activity of osteoclasts in osteonecrosis of the femoral head via regulation of the RELA/AKT1 axis.American journal of translational research · 2022Article
- Discovery of Herbacetin as a Novel SGK1 Inhibitor to Alleviate Myocardial Hypertrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Isoliensinine induces cervical cancer cell cycle arrest and apoptosis by inhibiting the AKT/GSK3α pathway.Oncology letters · 2022Article
- Analysis of the Molecular Mechanism ofJournal of healthcare engineering · 2022Article
- Integrating Network Pharmacology and Experimental Verification to Explore the Pharmacological Mechanisms of Aloin Against Gastric Cancer.Drug design, development and therapy · 2022Article
- Gld2 activity and RNA specificity is dynamically regulated by phosphorylation and interaction with QKI-7.RNA biology · 2021Article
- Multiple-Molecule Drug Design Based on Systems Biology Approaches and Deep Neural Network to Mitigate Human Skin Aging.Molecules (Basel, Switzerland) · 2021Article
- Minor and major circRNAs in virus and host genomes.Journal of microbiology (Seoul, Korea) · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Protein kinase B (Akt1) is a proto-oncogene that is overactive in most cancers. Akt1 activation requires phosphorylation at Thr308; phosphorylation at Ser473 further enhances catalytic activity. Akt1 activity is also regulated via interactions between the kinase domain and the N-terminal auto-inhibitory pleckstrin homology (PH) domain. As it was previously difficult to produce Akt1 in site-specific phosphorylated forms, the contribution of each activating phosphorylation site to auto-inhibition was unknown. Using a combination of genetic code expansion and in vivo enzymatic phosphorylation, we produced Akt1 variants containing programmed phosphorylation to probe the interplay between Akt1 phosphorylation status and the auto-inhibitory function of the PH domain. Deletion of the PH domain increased the enzyme activity for all three phosphorylated Akt1 variants. For the doubly phosphorylated enzyme, deletion of the PH domain relieved auto-inhibition by 295-fold. We next found that phosphorylation at Ser473 provided resistance to chemical inhibition by Akti-1/2 inhibitor VIII. The Akti-1/2 inhibitor was most effective against pAkt1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.