Figure 1
From: Disulfidptosis-associated lncRNAs predict breast cancer subtypes
Molecular mechanism of disulfidptosis-related genes. Under glucose-deficient conditions, high expression of SLC7A11 mediates cystine uptake into cells, consuming a large amount of NADPH and reducing cystine to cysteine, resulting in NADPH depletion. This promotes the oxidation of the sulfhydryl group (–SH) on the actin cytoskeleton protein’ s cysteine to form intermolecular or intramolecular disulfide bonds (–S–S–), leading to cytoskeleton collapse and plasma membrane separation, eventually inducing cell death. SLC3A2 encodes a chaperone protein for SLC7A11. NADPH promotes cytoskeleton reorganization by regulating actin polymerization and depolymerization and plays an important role in maintaining cytoskeleton stability and plasticity. INF2, DSTN, TLN1, CAPZB, RPN1, and NCKAP1 are involved in actin synthesis and cytoskeleton formation. FLNA, FLNB, IQGAP1, PDLIM1, and CD2AP are actin-binding proteins that regulate protein function by binding to actin. MYL6, MYH9, and MYH10 are myosin proteins that interact with actin to form part of the cytoskeleton. ACTN4 and ACTB are intracellular actins that maintain cytoskeleton stability. (Created by BioRender, https://www.biorender.com/).
