| Observation/assay | Condition | Key result | Interpretation | Source |
|---|---|---|---|---|
| Tpx1 oxidation state and oligomerization | Low H2O2, 0.2 mM | Tpx1 accumulates mainly as a disulfide-linked dimer associated with active peroxidase function | Detoxification-competent catalytic cycle under mild peroxide stress; also compatible with signaling at low dose | da Silva Dantas 2011 (Tpx1 review/thesis context); https://doi.org/10.?? unavailable in retrieved metadata (pqac-00000022) |
| Tpx1 hyperoxidation state | High H2O2, 5 mM | Tpx1 accumulates as a hyperoxidized, inactive monomer; monomer formation appears to follow dimer hyperoxidation | High-dose peroxide switches Tpx1 away from peroxidase activity, altering signaling output | da Silva Dantas 2011; URL unavailable in retrieved metadata (pqac-00000022) |
| FlagTpx1 mutant pulldown / co-purifying proteins | FlagTpx1C169S, 0.2 mM H2O2 | 34 proteins co-purified with FlagTpx1C169S; these were not seen with C48S or C48S/C169S controls | Resolving-cysteine mutant traps mixed-disulfide interactors, supporting direct redox-signaling contacts | Latimer 2017; URL unavailable in retrieved metadata (pqac-00000019) |
| Genetic interaction screens | SGA/QFA with tpx1C169S versus tpx1Δ backgrounds | 31 candidate interacting genes with tpx1C169S; 21 with tpx1Δ; partial suppressors included pka1 and csn5 | Distinguishes signaling-specific versus deletion phenotypes and identifies pathway modifiers of Tpx1 function | Underwood 2019; URL unavailable in retrieved metadata (pqac-00000018) |
| Direct redox partner trapping | 0.2 mM H2O2 | Pka1 and Csn5 formed direct protein-protein disulfide complexes with Tpx1 | Experimental support that Tpx1 directly relays peroxide-dependent redox signals to signaling/regulatory proteins | Underwood 2019; URL unavailable in retrieved metadata (pqac-00000018) |
| Srk1 overexpression / cell length phenotype | Δtpx1 versus control; 84 cells measured | Reduced elongation response in Δtpx1; division-length difference significant (T test p = 7.8 × 10^-8; n = 84) | Tpx1 contributes to oxidation-dependent signaling affecting mitotic control, not just detoxification | Latimer 2017; URL unavailable in retrieved metadata (pqac-00000019) |
| Pap1 pathway requirement | Mild H2O2, 0.2 mM | Loss of Tpx1 abolishes Pap1 oxidation and Pap1-dependent gene induction; Trx1 is the main electron donor for Tpx1, with partial compensation by Trx3 | Tpx1 is a peroxide sensor/transducer in addition to being a scavenger; links thioredoxin oxidation to transcriptional signaling | Calvo Arnedo 2012; URL unavailable in retrieved metadata (pqac-00000020) |
| Localization / mitochondrial pool | After H2O2 treatment | Tpx1 is mostly cytosolic, but a small mitochondrial/IMS-associated pool is detected after oxidative stress | Supports compartment-specific roles in peroxide handling and redox signaling beyond bulk cytosolic detoxification | Underwood 2019; Latimer 2017; URLs unavailable in retrieved metadata (pqac-00000018, pqac-00000019) |


*Table: This table compiles the main quantitative and structured findings retrieved for Schizosaccharomyces pombe Tpx1, emphasizing peroxide-dose effects, genetic interaction counts, trapped redox partners, and signaling phenotypes. It is useful for separating Tpx1’s detoxification role from its experimentally supported signaling functions.*