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Metabolic reprogramming in suppressing oxidative stress during TH17 cell differentiation.

Global changes in gene expression associated with differential DNA methylation underlie epigenetic inheritance of circadian periodicity in cells.

Utilizing a conserved mechanism, a ribosome can initiate translation from a site within the insulin receptor mRNA to maintain protein synthesis even when standard mechanisms of initiating translation have been inhibited by stress.

Transcription factors KLF2 and ETV1 repress the transcriptional program of mitochondrial biogenesis, resulting in impaired mitochondrial function in lysosomal storage diseases.

LRH-1/NR5A2 responds to ER stress by inducing a novel pathway that is required for stress resolution in mice and can be targeted by LRH-1 agonists.

An integrative genome-wide approach supports a direct and collaborative role of ETS and AP-1 transcription factors in maintaining endothelial cell-specific and anti-inflammatory gene expression programs.

Airborne PM2.5 exposure triggers oxidative stress and mitochondrial apoptosis in placental trophoblast cells via the KLF9/CYP1A1 transcriptional axis, ultimately leading to adverse pregnancy outcomes.

ATF4 is a metabolic effector of mTORC1 signaling, co-opted to induce gene targets involved in amino acid synthesis, uptake, and tRNA charging, contributing to mTORC1-driven protein and glutathione synthesis.

Organ-selective drug action of traditional Chinese medicine that generates systemic immune mediators is proposed and reviewed as a novel mechanistic angle to develop new immunomodulatory drugs.