Which Antioxidant System Shapes Intracellular H₂O₂ Gradients?

Oxidative Stress-Induced STIM2 Cysteine Modifications Suppress Store-Operated Calcium Entry

“…The conserved cysteines within the lumen of the ER, shown previously to be regulated in STIM1 (described earlier), were identified neither in our analysis nor in an in vivo redox proteomic study (Xiao et al, 2020). These findings do not negate the role of the STIM2 luminal cysteines in SOCE redox regulation but rather suggest that oxidative stress needs to be discussed as a localized subcellular event, not as a generalized state of a cell (Mishina et al, 2019). In terms of SOCE, spatially limited, i.e., local, redox regulation would be physiologically plausible.…”

Redox Signaling from Mitochondria: Signal Propagation and Its Targets

“…At the vicinity of the target protein, H 2 O 2 may either directly oxidize certain amino acid residues of the target protein or affect the target protein indirectly via peroxiredoxins. Interestingly, recent reports based on cytosolic H 2 O 2 -selective probes receiving matrix-originating artificially generated H 2 O 2 showed that these cytosolic fluorescent probes were affected only when some cytosolic thioredoxins were ablated [96]. If confirmed, this would suggest the participation of peroxiredoxins in the spreading of the redox signal beyond the OMM surface.…”

hTERT-Driven Immortalization of RDEB Fibroblast and Keratinocyte Cell Lines Followed by Cre-Mediated Transgene Elimination

“…The insert encoding hTERT cDNA was cloned into modified plasmid pLCMV-Puro that was previously described in [52]. In this plasmid, the CMV promoter was changed to a relatively less stronger pGK promoter; under its control, a cassette with a pair of LoxP sites surrounded hTERT cDNA with a "stop" codon placed upstream of the TurboFP635 NLS (i.e., LoxP hTERT "stop" codon LoxP TurboFP635 NLS).…”