Zeheng Lv

Correction: mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated ubiquitination of eIF4A1 in cancer cells

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

FBXW7 mutations reprogram glucose metabolism by activating the ETV6-GLUT1 axis

Siqi Fei, Xiayun Xu, Tingrui Wang, Xinyue Jiang et autres

The progression of endometrial cancer (EC) involves substantial metabolic reprogramming, frequently driven by mutations in tumor suppressors and oncogenes. In this study, we identify a previously unrecognized pathway through which FBXW7 mutations rewire glucose metabolism in EC cells. Specifically, we demonstrate that …

cn (code pays fourni par la source)

Editorial Expression of Concern: DCAF12 promotes apoptosis and inhibits NF-κB activation by acting as an endogenous antagonist of IAPs

Dongyue Jiao, Yingji Chen, Yalan Wang, Huiru Sun et autres

cn (code pays fourni par la source)

mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated ubiquitination of eIF4A1 in cancer cells

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …

cn (code pays fourni par la source)

Author response: mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated ubiquitination of eIF4A1 in cancer cells

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

cn (code pays fourni par la source)

mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated non-degradative ubiquitination of eIF4A1

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Abstract Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, …

cn (code pays fourni par la source)

Author response: mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated non-degradative ubiquitination of eIF4A1

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …

cn (code pays fourni par la source)

Reviewer #1 (Public Review): mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated non-degradative ubiquitination of eIF4A1

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …

cn (code pays fourni par la source)

Reviewer #2 (Public Review): mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated non-degradative ubiquitination of eIF4A1

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …

Phosphorylation of INF2 by AMPK promotes mitochondrial fission and oncogenic function in endometrial cancer

Yan Ding, Zeheng Lv, Wenxin Cao, Wenming Shi et autres

Mitochondria are highly dynamic organelles capable of altering their sizes and shapes to maintain metabolic balance through coordinated fission and fusion processes. In various cancer types, mitochondrial hyperfragmentation has been frequently observed, contributing to the progression of cancer toward metastasis. Inverted formin …

cn, hk (code pays fourni par la source)

mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated ubiquitination of eIF4A1 in cancer cells

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …

cn (code pays fourni par la source)

Reviewer #2 (Public Review): mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3IBTK-mediated non-degradative ubiquitination of eIF4A1

Huiru Sun, Dongyue Jiao, Xiaying Zhao, Yingji Chen et autres

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the …