PN placement:Mitochondrial proteostasis|Organelle-specific protein degradation|mitoCPR pathway ; PN-node mapping: group(mitoCPR)=no_mapping; class(Organelle-specific protein degradation)=mapped/ok GO:0035694 (mitochondrial protein catabolic process, new_to_goa); branch=no_mapping.
Consistency: Consistent. Deep research, notes, review YAML agree ATAD1/Msp1 is a hexameric OMM AAA+ extractase/dislocase that removes mislocalized tail-anchored proteins (PEX26/GOS28) and the BH3-only protein BIM, for rerouting or degradation. Review core = GO:0140567 (membrane protein dislocase) + GO:0140570 (extraction of mislocalized protein from mitochondrial OM). The PN class is degradation-centric; ATAD1's sharper mechanism is extraction, but degradation is a real downstream outcome.
PN story / NEW pressure: PN projects GO:0035694 (mitochondrial protein catabolic process), absent from ATAD1 GOA. The review accepted it as NEW (TAS) — notably GO:0140570 is NOT a subclass of GO:0035694 (verified via OLS: GO:0140570 sits under establishment-of-protein-localization, not catabolic process), so the two are orthogonal, not redundant. Adding GO:0035694 is defensible (degradation outcome supported by PMID:24843043) though broader/less mechanistic than GO:0140570. Conclude: ADD already done in-review (accepted NEW); both terms real and complementary.
Mapping strategy:ATAD1 mildly supports the class mapping. GO:0035694 is broader than the gene's specific GO:0140570 but, unlike TOMM20-type rejections, it is a distinct degradation axis the review judged worth a conservative NEW. mitoCPR leaf no_mapping is appropriate (human mitoCPR poorly defined). Node status/scope fine.
Evidence alignment: PN row carries no reference titles. Review anchors on PMID:24843043 (extraction/degradation of TA proteins) plus new human primaries (PMID:36409067 BIM; PMID:35550246 cryo-EM) — all reinforce the dislocase core. No citation conflicts.
Verdict: Consistent; PN GO:0035694 is real, complementary to GO:0140570, and already added as NEW. No edits warranted.