AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis
| Title | AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis |
|---|---|
| Description | Here we report that activation of AKT1 induces a metabolic switch to glycolysis from the mitochondrial metabolism via phosphorylation of cytoplasmic malic enzyme 2, namedmalic enzyme 2, favoring an enhanced glycolytic phenotype. In the cytoplasm, AKT phosphorylates malic enzyme 2 at serine 9 in the mitochondrial localization signal peptide at the N-terminus, preventing its mitochondrial translocation. Unlike mitochondrial malic enzyme 2, which accounts for adjusting the tricarboxylic acid cycle, ME functions as a scaffold that brings together the key glycolytic enzyme phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase and pyruvate kinase M2, as well as Lactate dehydrogenase A, to promote glycolysis in the cytosol. |
| Organism | Homo sapiens |
| Data Type | Metabolome Data by Mass Spectrometry (MS) |
| Data Accessibility | Open-access |
| BioProject | PRJCA028125 |
| Release Date | 2024-07-17 |
| Submitter | wei li (942013819@qq.com) |
| Organization | Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College |
| Submission Date | 2024-07-16 |
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| File ID | File Title | Number/Samples | File Type | File Size | File Suffix | Download Times | Download |
|---|---|---|---|---|---|---|---|
| OMIX006891-01 | AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis | 1 | Metabolome Data by Mass Spectrometry (MS) | 25.3 KB | xlsx | 0 |