ARNT (P27540; HIF-1 beta) is best reviewed as a nuclear bHLH-PAS transcription factor subunit. The primary evidence supports partner-specific heterodimerization and regulatory DNA binding: ARNT is a structural component of the Ah receptor XRE-binding form PMID:1317062, HIF-1 beta is an ARNT gene product that heterodimerizes with HIF-1 alpha or AHR PMID:7539918, and the AHR-ARNT heterodimer has been structurally resolved on DRE DNA PMID:28396409.
Falcon deep research completed successfully and independently summarized ARNT as a heterodimeric transcription-factor scaffold/partner rather than an enzyme or transporter [file:human/ARNT/ARNT-deep-research-falcon.md "ARNT functions primarily as a heterodimeric transcription-factor scaffold/partner, enabling DNA binding and transcriptional activation by AHR and HIF-α proteins rather than acting as an enzyme or transporter."].
For the Proteostasis PN batch, ARNT appears in the projection as a candidate new annotation to GO:1990756 ubiquitin-like ligase-substrate adaptor activity from the UPS Cul4A/Cul4B substrate adaptor group, via the source path Ubiquitin Proteasome System|E3 ubiquitin and UBL ligases|Cul4A/Cul4B substrate adaptor|AHR / ARNT / TBL3 complex|PAS [file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_annotations.tsv "ARNT ... GO:1990756 ... ubiquitin-like ligase-substrate adaptor activity ... new_to_goa"]. This projection should be treated conservatively. The narrower AHR / ARNT / TBL3 complex mapping nodes are explicitly no_mapping in the UPS mapping YAML [file:projects/PROTEOSTASIS/mappings/ubiquitin_proteasome_system.yaml "No additional direct GO mapping is needed at this node."], and the reviewed ARNT literature does not show ARNT directly recruiting substrates to a CUL4 ligase. I did not add GO:1990756 to proposed_new_terms or core_functions.
Generic protein binding annotations were re-reviewed as low-information. Where the cited paper supports AHR/HIF-family dimerization, the review recommends more specific dimerization or AHR-binding terms; large-scale or context-only interaction records were marked over-annotated. Downstream hypoxia outputs such as VEGF production, glycolytic gene induction, and erythropoietin-related phenotypes are biologically plausible ARNT/HIF consequences but should be treated as non-core or over-annotated depending on directness PMID:8756616 PMID:8089148.