Table 2. Pathways Upregulated Upon OXPHOS Inhibition after 6 h Treatment^a.

monolayer		PMCTS		QMCTS
pathway	p-value	pathway	p-value	pathway	p-value
cytosolic sulfonation of small molecules	0.0012	intra-Golgi and retrograde Golgi-to-ER traffic	0.0022	respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins	6.91 × 10–6
phase II conjugation	0.0029	retrograde transport at the trans-Golgi network	0.0023	the citric acid cycle and respiratory electron transport	3.57 × 10–5
platelet degranulation	0.0033	membrane trafficking	0.0030	respiratory electron transport	6.37 × 10–5
response to elevated platelet cytosolic Ca2	0.0038	vesicle-mediated transport	0.0053	complex I biogenesis	2.35 × 10–4
complex I biogenesis	0.0086	peptide chain elongation	0.0066	RHO GTPases activate CIT	6.90 × 10–4
apoptotic execution phase	0.0093	viral mRNA translation	0.0066	prefoldin-mediated transfer of substrate to CCT/TriC	1.98 × 10–3
apoptosis	0.0113	selenocysteine synthesis	0.0070	signaling by Rho GTPases	1.99 × 10–3
programmed cell death	0.0118	eukaryotic translation termination	0.0070	cooperation of prefoldin and TriC/CCT in actin and tubulin folding	2.78 × 10–3
signaling by MST1	0.0142	eukaryotic translation elongation	0.0074	RHO GTPase effectors	3.49 × 10–3
amyloid fiber formation	0.0161	nonsense-mediated decay independent of the exon junction complex	0.0074	HIV life cycle	4.99 × 10–3

^aProteins that were upregulated with fold change >0.6 upon OXPHOS inhibition were analyzed using EnrichR.