By increasing intracellular cysteine levels, NRF2 engages a tumor suppressive metabolic pathway mediated by cysteine dioxygenase 1.

Cysteine dioxygenase, a conserved and critical enzyme in sulfur amino acid metabolism, is activated by the hypoxia-inducible transcription factor.

CysM and CysK2 play complementary and overlapping roles in Mtb's adaptation to environmental stress that are crucial for survival.

Structure-function analysis of the ROR2 cysteine-rich domain reveals a new mechanism of WNT5A reception at the cell surface and provides new insights into the pathogenic mechanisms of Robinow syndrome-driving ROR2 mutations.

A facile method is implemented to modify membrane proteins with biophysical reporters using cysteine-independent approaches in live cells.

Erastin and sorafenib inhibit system x_c^- and induce ER stress, suggesting these may be useful tools for probing the functions of system x_c^- and its role in inducing ER stress and ferroptosis.

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.

A combined chemical genetics, proximity labeling, and ADP-ribose site mapping approach shows that PARP-7 mono-ADP-ribosylates immune-relevant proteins on cysteine amino acids.

A cysteine-rich domain within the Smoothened receptor may represent a novel therapeutic target for cancers caused by abnormal functioning of the Hedgehog signaling pathway.

The crystal structure of Norrie Disease Protein in complex with the extracellular cysteine-rich domain of Frizzled4 receptor and sucrose octasulfate reveals binding sites for Frizzled4, low density lipoprotein receptor related protein 5/6, and proteoglycan.