Human K562 functional tests distinguish intact ALK4 signaling from truncated dominant-negative isoforms. G1 accumulation supports inhibition of cell-cycle progression, not promotion of the G1/S transition.

InhBP/IGSF1 association modulates the receptor complex and inhibin B antagonism. Association with an inhibin-binding protein does not demonstrate direct ALK4-inhibin binding.

Receptor-associated TRAP1/TGFBRAP1 and SMAD4 chaperoning are studied; this does not assign chaperone activity to ALK4.

Sorting-nexin receptor association study. The abstract emphasizes different type-I/type-II receptor preferences; its focus is not grounds to call the ALK4 interaction misattributed.

Direct CRIPTO-ALK4 and nodal signaling evidence; nodal coreceptor dependence must not be transferred to activin.

Mammalian reporter and coculture studies distinguish CRIPTO coreceptor and coligand functions in nodal signaling.

Biochemical ALK4/5/7 inhibition and downstream signaling are relevant to receptor kinase activity. SB-431542 inhibits all three, so drug effects alone do not uniquely identify ALK4 in every cell.

ALK4 extracellular-domain mutations and activin cross-linking are studied in the presence of ActRII. This is cooperative ligand contact by the receptor complex, not isolated high-affinity ALK4 ligand capture.

Human CRIPTO CFC-domain structure/function study directly reports ALK4 interaction independent of its EGF domain.

Myostatin uses ActRIIB together with ALK4 or ALK5 to activate SMAD2/3 and oppose BMP7-associated adipogenesis. It does not establish identical ligand specificity for ALK4 and ALK5.

Lefty antagonizes EGF-CFC-dependent nodal/Vg1 responses while activin remains coreceptor independent. Shared receptor use does not imply identical extracellular regulation.

FKBP12 recruits the inhibitory SMAD7-SMURF1 apparatus to ALK4 and controls receptor ubiquitination and signaling duration. This is inhibitory feedback, not evidence that FKBP12 is a positive activin regulator.

The accessible abstract supports TTRAP/Alk4/SMAD3 interactions and zebrafish development. The precise threonine-phosphorylation assay and kinase construct species were not independently verified; no false human-assay or misattribution claim is made.

Full text inspected: Figure 5 and discussion explicitly test ALK4 knockdown, which reduces trophoblast invasion, opposite to ALK7/nodal knockdown. The ALK7-focused title does not invalidate the ALK4 annotation.

TSC22D1 antagonizes SMAD7-dependent receptor turnover. The TGFBR1-focused abstract does not exclude additional ALK4 interaction experiments; bare binding is removed for lack of functional information, not as false.

Mouse C2C12 studies support BMP-3b/GDF10 signaling functionally facilitated by ALK4/ActRIIA and negative osteoblast differentiation. The ligand activates SMAD2/3 rather than the canonical BMP SMAD1/5/8 pathway.

HSP90 client-interaction survey supplies binding context. It does not make ALK4 a chaperone or establish an additional receptor ligand.

Variant/wild-type interaction screening context; the individual ALK4 pair was not revalidated from the abstract. No physiological SMAD4 substrate activity is inferred.

Abstract explicitly places inhibin binding at ActRII and reports failure to assemble the SKR2/ALK4-containing complex. Full publisher text was inaccessible; the direct ALK4 inhibin-binding row remains UNDECIDED.

Early cloning/sequence study includes an incomplete ALK4 cDNA and predicts kinase architecture. Later receptor biochemistry independently supports the mature human receptor function.

Receptor assembly and GS-domain mutation experiments establish type-II-to-type-I activation and downstream signal propagation; isolated ALK4 does not bind activin efficiently.

Human K562 inducible receptor experiments establish ligand-dependent complex formation and erythroid differentiation/proliferation outputs.

Mouse B-cell hybridoma study distinguishes ActRI from ActRIB and supports ActRIB-enhanced activin apoptosis. Its cellular model is explicitly not a direct human phenotype.

Primary activin receptor association study establishes transient SMAD2/3 binding and SMAD7 inhibition, linking receptor activation to transcription.

Conditional mouse Alk4 deletion and cortical interneuron experiments provide gene-specific mammalian support for the inherited nervous-system-development function.

ACVR1B is the transmembrane ALK4 receptor kinase and phosphorylates SMAD2/3 after type-II-receptor-dependent activation.