Generated RARA-deep-research-falcon.md and used it to complete the initialized
GO review.
Core synthesis: RARA/RARalpha is a retinoic-acid-binding nuclear receptor
transcription factor. The Falcon report summarizes the central mechanism as
[file:human/RARA/RARA-deep-research-falcon.md "RARA encodes RARα, a
ligand-activated nuclear receptor that functions as a sequence-specific
DNA-binding transcription factor."] RARA binds retinoic acid response elements
as an RXR heterodimer [file:human/RARA/RARA-deep-research-falcon.md "RARα binds
RAREs primarily as an RXR heterodimer."] and acts through a ligand-dependent
corepressor/coactivator switch [file:human/RARA/RARA-deep-research-falcon.md
"RARα supports a canonical nuclear-receptor cofactor “switch” mechanism"].
Core annotations retained as ACCEPT include nuclear receptor activity, retinoic
acid binding, RARE/RNA polymerase II cis-regulatory DNA binding, retinoic acid
receptor signaling, positive and negative regulation of RNA polymerase II
transcription, nucleus/chromatin localization, and RNA polymerase II
transcription regulator complex.
Broad developmental, immune, proliferation, apoptotic-cell-clearance, estrogen
response, and retinoid response terms were generally kept as non-core when the
evidence supported them. The main caveat is that many RA-treated cell phenotypes
are downstream programs rather than direct RARA DNA-bound functions
[file:human/RARA/RARA-deep-research-falcon.md "many transcriptomic or phenotypic
outcomes in RA-treated cells reflect indirect downstream programs"].
Several terms were removed or marked over-annotated:
protein binding rows were marked over-annotated because the informative