Evidence-qualified experimental proposals · Updated September 07, 2026
Cross readout degree (linear vs quadratic) with coupling (absent vs single-CZ), using identical reservoir trajectories, with paired bootstrap confidence intervals for NMSE and 1-PLV.
Evidence: Hypothesis untested — the source study does not test cross-subreservoir entanglement; the benchmark gap is large (NMSE 0.4208 vs 0.0330; 1-PLV 0.1880 vs 0.0110), so a single CZ must close a substantial fraction of it to matter.
Sweep CZ placement and timing at fixed gate count, testing whether gains survive hardware noise and transpilation, and whether they reflect cross-frequency information or regularization.
Evidence: Unresolved mechanism — whether a CZ adds predictive information or merely relocates nonlinear mixing is unknown without held-out comparison against quadratic readout augmentation.
Live-cell lysate assays ± X6632 to detect direct USP1 engagement, working around the recombinant-protein SPR false-negative.
Evidence: USP1 hypothesis is indirect — pan-ID suppression without ID1 binding fits a deubiquitinase-inhibition signature, but no direct X6632–USP1 binding has been demonstrated and SPR negativity could reflect true non-binding.
Pre-saturate USP1 with TNG348, then add X6632; additive versus occlusive thermal shifts distinguish shared allosteric sites from independent binding.
Evidence: Controls built in — known USP1 binders (TNG348, ML323) serve as positive controls at 1–30 µM X6632, bracketing reported 0.9–3 µM IC50s; non-binding ID1 acts as an internal negative control.
If X6632 loses all activity in USP1-null cells, the post-transcriptional degradation mechanism is confirmed genetically with a clean epistasis readout.
Evidence: Mechanistic inference — USP1 inhibitors are known to promote ID1 degradation without binding ID1 directly, making USP1 the leading candidate upstream target.
Paired ub-PCNA kinetics (1, 3, 6, 12, 24 h at 3 µM) with ID1 mRNA qPCR to separate proteostasis effects from transcriptional ID suppression.
Evidence: Discriminating time-course — protein loss within 24 hours alongside unchanged mRNA would support degradation; the alternative upstream-transcription route remains possible.
Cross Myo10-Halo zebrafish with ctgfa:eGFP CA-yap/DN-yap lines and image extracellular vesicle transport in proximal versus distal blastema zones at 48 hours post-amputation.
Evidence: Coupled mechanism test — links the Yap/F-actin density axis to vesicle transport within a single experiment; causal direction between vesicle position and filopodial extension still requires Granger analysis.
Ex vivo actin disruption at 2-second imaging intervals: if tip PI(3,4)P2 drains before filopodial stalling and vesicle runs stall first, transport is actin-motor dependent rather than lipid-docking dependent.
Evidence: Causality plan defined — Granger causality between vesicle position and filopodial extension is the decisive analysis, since co-localization alone cannot distinguish motor-driven cargo from a passive ride; the Xenopus lipid study supplies an analytical template.
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