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Sestrin2 loss could be a universal mechanism of human colon carcinogenesis that allows for barrier dysfunction, mTORC1 hyperactivation, unrestricted tumor growth and chemoresistance.

Small molecule proteostasis regulators that activate the unfolded protein response transcription factor ATF6 reduce the secretion of amyloid disease-associated proteins.

Combinatorial signaling leads to transcription factor co-localization at Rev-erb sensitive enhancers, enabling a diversified cellular response to complex stimuli.

Post-translational processing of the SKN-1A/Nrf1 transcription factor regulates proteasome expression.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

Loss of KEAP1 modulates sensitivity to targeted therapies in lung cancer.

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.

Transient hormonal alterations during early critical developmental periods can have a crucial and long-lasting effect on lifespan in mice.

Cell culture models widely used in cancer research do not reflect metabolism in tumors; by altering culture systems to better model tumor metabolism we find that environmental cystine promotes tumor glutamine metabolism.

Activation of the NRF2 antioxidant program leads to an imbalance in central carbon metabolism and sensitizes cancers to glutaminase inhibition.