Yiguo Zhang

This study identifies BACH1 as a tumor-promoting factor in hepatocellular carcinoma by activating the PI3K-AKT-mTOR pathway through PDP1 upregulation.

This study investigates how curcumin modulates Nrf1 and Nrf2 expression and their roles in redox metabolism and gene regulation in HepG2 cells and xenograft tumors.

This study shows that deleting Nrf1 increases oxidative stress-induced cellular senescence by disrupting homeostasis, as evidenced by increased senescence markers and impaired autophagy.

This study shows that deleting Nrf1α in HepG2 cells increases glutamine addiction and enhances cell death when glutamine is deprived.

This study shows that DDI2 deficiency reduces liver cancer growth by increasing ROS and DNA damage, which inhibits cell survival and tumor progression.

This study identifies how Nrf1 and Nrf2 regulate miRNAs to differentially modulate EMT in hepatocellular carcinoma cells, with Nrf1 inhibiting and Nrf2 promoting EMT through distinct miRNA pathways.

The paper investigates the regulatory relationship between Nrf1 and SREBP1, finding that Nrf1 is not a direct target of SREBP1, despite both being part of the rapamycin-responsive network in human hepatoma cells.

This study shows Nrf1 is essential for mitochondrial homeostasis by integrating redox regulatory networks, with loss of Nrf1 leading to increased ROS and oxidative damage.

This study shows that NFE2L1 dysfunction leads to AMPK-driven glucose metabolism reprogramming and mitochondrial damage in liver cancer.

The paper identifies synergistic and antagonistic roles of Nfe2l1 and Nfe2l2 in regulating -PalNRF1 and TFAM expression, with species-specific differences observed between mice and humans.

This paper investigates the opposing yet coordinated roles of Nrf1 and Nrf2 in response to tunicamycin-induced ER stress, showing how they regulate gene expression and maintain cellular homeostasis.

The paper investigates how different Nrf1 isoforms regulate distinct subsets of target genes, showing that Nrf1{gamma} acts as a dominant-negative competitor to Nrf1/{beta}.

This study shows that Nrf1 knockout leads to Nrf2 hyperactivation, promoting hepatoma, and reveals a feedback loop between Nrf1 and Nrf2 in tumor suppression.

The paper identifies a naturally-occurring Keap1 mutant, Keap1{Delta}C, that acts as a dominant-negative competitor, reducing Keap1's ability to inhibit Nrf2 and thereby increasing Nrf2-target gene expression.

The paper identifies a novel ancestral subfamily of CNC-bZIP transcription factors, Nach, tracing their evolutionary origin from marine bacteria to humans and showing distinct functional differences from Nrf1/2.