| 项目编号 |
PRJCA028125 |
| 项目标题 |
AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis |
| 涉及领域 |
Medical |
| 数据类型 |
metalobome
|
| 物种名称 |
Homo sapiens
|
| 描述信息 |
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. |
| 样品范围 |
Monoisolate |
| 发布日期 |
2024-07-16 |
| 出版信息 |
| PubMed ID |
文章标题 |
杂志名称 |
Doi |
发表年份 |
|
|
AKT1 phosphorylation of cytoplasmic ME2 induces a metabolic switch to glycolysis for tumorigenesis
|
Nature communication
|
10.1038/s41467-024-44772-8
|
2024
|
|
|
| 项目资金来源 |
| 机构 |
项目类型 |
授权项目ID |
授权项目名称 |
| National Key Research and Development Program of China
|
|
2022YFA0806302
|
|
|
|
| 提交者 |
wei
li (942013819@qq.com)
|
| 提交单位 |
Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College |
| 提交日期 |
2024-07-16 |
