| Accession |
PRJCA028125 |
| Title |
AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis |
| Relevance |
Medical |
| Data types |
metalobome
|
| Organisms |
Homo sapiens
|
| 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, named ME2, favoring an enhanced glycolytic phenotype. mechanistically, in the cytoplasm, AKT phosphorylates ME2 at serine 9 in the mitochondrial localization signal peptide at the N-terminus, preventing its mitochondrial translocation. Unlike mitochondrial ME2, which accounts for adjusting the tricarboxylic acid cycle, ME2 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. |
| Sample scope |
Monoisolate |
| Release date |
2024-07-16 |
| Publication |
| PubMed ID |
Article title |
Journal name |
DOI |
Year |
|
|
AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis
|
Nature communication
|
10.1038/s41467-024-44772-8
|
2024
|
|
|
| Grants |
| Agency |
program |
Grant ID |
Grant title |
| National Key Research and Development Program of China
|
|
2022YFA0806302
|
|
|
|
| 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 |
