2026-10-03. PAINT no-IBA backlog. Provider: affinage (gates clear).
69 residues, neural-enriched, binds the type II regulatory subunits of PKA (RIIα/PRKAR2A,
RIIβ/PRKAR2B) through a predicted amphipathic helix — the AKAP binding mode — but with no targeting
domain. So it occupies the docking site AKAPs need, and expressed AKAIN1 blocks AKAP-mediated PKA
localization:
One paper, abstract only. The authors' "endogenous disruptor peptide" framing is a proposal: the
displacement result is from expression, and the endogenous-protein work used a FLAG knock-in in
mouse Neuro2a cells.
affinage's gates only certify precision, so I searched PubMed independently (AKAIN1, C18orf42).
Three other hits, none functional: PMID:36672701 lists AKAIN1 among ten Alzheimer's entorhinal-cortex
DEGs (cited, LOW); PMID:29275994 never mentions AKAIN1 in its full text; PMID:32799782 is AKIP1,
a different gene caught by name similarity. So affinage did not miss a decisive paper this time.
GO:0051018 PKA binding (IDA + IEA) → MODIFY to GO:0034237 PKA regulatory subunit binding.
The paper specifies RII. GO:0034237 is a direct child of GO:0051018 with no children (checked
via OLS ancestors/children, not inferred from labels). Comparator check: AKAP1, AKAP5 and AKAP11 —
RII-binding amphipathic-helix proteins — carry GO:0034237; AKAP7 carries only GO:0051018. So the
specific term is the established one, not universal. A refinement, not a dispute.
GO:0008104 intracellular protein localization (IDA) → ACCEPT, and the reason matters. I
considered MODIFY to GO:1903828 negative regulation of protein localization, since AKAIN1
disrupts PKA localization. But the mouse ortholog (G3UWD5), curated by MGI from the same
paper, keeps this very term and separately carries GO:0031333 negative regulation of
protein-containing complex assembly (IDA). The full-text readers represent this as two statements.
Collapsing them would overrule a choice whose basis I cannot see. The human-side absence of
GO:0031333 is recorded as a CURATION knowledge gap instead of being added as NEW — the
endogenous work was in a mouse line, which may be exactly why human was not given it.
GO:0005829 cytosol (IEA, Ensembl Compara) → ACCEPT. Its source, mouse Akain1, carries cytosol
by IDA from the same paper.
GO:0005515 protein binding with ROPN1 (HuRI) → REMOVE per policy — but flagged. ROPN1 carries
InterPro IPR047844, "Ropporin, dimerization/docking domain", and ropporins are AKAP-associated
sperm proteins. An RII-binding amphipathic helix hitting a docking-domain protein is the shape of
interaction AKAIN1 is known for. Raised as a question, not asserted from a Y2H hit.
set -- $pair does not split in zsh, so $1 held bothGO_REF:0000120 is "…Multiple IEA Methods",