PN placement:ER proteostasis|Protein transport|Transmembrane protein import|EMC complex component ; PN-node mapping: type → GO:0072546 (EMC complex); group → GO:0044743 (protein transmembrane import into intracellular organelle); class → GO:0015031 (protein transport); branch=no_mapping.
Consistency: Deep research, review YAML, and PN annotation agree on the EMC role: EMC10 is a single-pass type I lumenal/peripheral, non-catalytic EMC subunit. The review additionally documents the secreted isoform 2 (HSS1/INM02) as an extracellular angiogenic growth factor (PMID:28931551, 20680400, 19570817) and biallelic-LoF NEDD (NEDDFAS) disease — a substantial moonlighting biology entirely outside the PN node's scope. Not a contradiction, but the PN row captures only the membrane-EMC facet.
PN story / NEW pressure: PN asserts only EMC membership + import/insertion, already captured (GO:0072546 part_of; insertion/insertase terms KEEP_AS_NON_CORE). No NEW GO term needed for the PN claim. The secreted-form functions are already annotated (GO:0001938, GO:0010595, GO:0045766, GO:0005576) and correctly KEEP_AS_NON_CORE — they are not a PN/ER-proteostasis story.
Mapping strategy:EMC10 does not change the shared node mapping (EMC complex member → GO:0072546 stands). Same group-level concern as EMC7-9: GO:0044743 (lumenal import) mismatches EMC membrane-protein insertion; insertion terms are not subclasses of it. The secreted/angiogenic facet argues against treating this node as capturing all of EMC10's biology, but is out of PN scope.
Evidence alignment: Core EMC papers overlap (22119785, 29242231, 32439656, 30415835); review adds EMC10-specific secreted-isoform and disease PMIDs absent from the PN row.
Verdict: Consistent for the EMC facet; well-reviewed. Shared group→GO:0044743 mapping diverges from insertion semantics; note EMC10's secreted angiogenic moonlighting is correctly non-core and outside PN scope.