Shaofan Hu

Curcumin activates distinct programming of redox metabolism towards differential regulation of gene expression mediated by Nrf1 and Nrf2

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.

Deletion of Nrf1 exacerbates oxidative stress-induced cellular senescence by disrupting the cell homeostasis

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

Deletion of Nrf1α promotes glutamine addiction of HepG2 cells and thus enhances its apoptosis caused by glutamine deprivation

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

Deficiency of DDI2 suppresses liver cancer progression byworsening cell survival conditions

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

The opposing mechanisms by which miRNAs critically contribute to differential roles of Nrf1 and Nrf2 in modulating the epithelial-mesenchymal transformation of hepatocellular carcinoma

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.

Nrf1 is not a direct target gene of SREBP1, albeit both are integrated into the rapamycin-responsive regulatory network in human hepatoma cells

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.

Nrf1 is an indispensable redox-determining factor for mitochondrial homeostasis by integrating multi-hierarchical regulatory networks

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.

Synergism and antagonism of two distinct, but confused, Nrf1 factors in integral regulation of the nuclear-to mitochondrial respiratory and antioxidant transcription networks

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.

A unity of opposites in between Nrf1- and Nrf2-mediated responses to the endoplasmic reticulum stressor tunicamycin

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.

Oncogenic activation of Nrf2 by specific knockout of Nrf1α that acts as a dominant tumor repressor

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

Nach is a novel ancestral subfamily of the CNC-bZIP transcription factors selected during evolution from the marine bacteria to human

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.