Web13 nov. 2012 · MYC -transformed cells depend on both glutamate-oxaloacetate transaminase and glutamate dehydrogenase to maintain Gln homeostasis and suppress apoptosis. Consequently, either ATF4 agonists or glutaminolysis inhibitors potently induce apoptosis in vitro and inhibit tumor growth in vivo. Web5 jan. 2024 · While not as widely studied in the context of amino acid restriction as ATF4, c-MYC has emerged as an important regulator of glucose and glutamine metabolism in cancer cells. c-MYC supports non-oxidative glucose metabolism through transcriptional upregulation of glucose transporter GLUT1, multiple glycolytic enzymes, and the lactate …
ATF4 suppresses mTORC1-dependent signalling and inhibition of …
Web1 jul. 2024 · Inhibition of mTORC1 signalling can rescue ATF4-deficient cells from MYC-induced ER stress. Acute deletion of ATF4 significantly delays MYC-driven tumour progression and increases survival in mouse models. 105 Moreover, compared with normal tissues, the activation/overexpression of GCN2 and the increase in phosphorylated … Web22 aug. 2024 · Further studies revealed that MYC had a transcriptional effect on MTHFD2 and was also regulated by ATF4. PCR, and western blotting experiments with ATF4 … new wave optical
Harnessing the Co-vulnerabilities of Amino Acid-Restricted …
WebATF4 couples MYC-dependent translational activity to bioenergetic demands during tumour progression. The c-Myc oncogene drives malignant progression and induces robust … Web21 aug. 2014 · Mechanistically, we identified ATF4 as a novel regulator which coordinates with N-Myc to directly activate ASCT2 expression. Of note, ASCT2 expression, which correlates with that of N-Myc and ATF4, is markedly elevated in high-stage neuroblastoma tumour samples compared with low-stage ones. WebNational Center for Biotechnology Information new wave optic wall