PMID:23478265, DOI 10.1128/MCB.01603-12, was independently inspected as indexed text from the author PDF. Methods use human full-length 662-aa DDX3X and engineered fragments, recombinant IKKε/IRF3, HEK293T/A549 cells and Sendai virus. Results/Figures 5–6 distinguish IKKε activation from IRF3 recruitment: “DDX3, but not the S102A mutant, interacts directly with IRF3.” The S102A mutant retains IKKε binding and activation but loses IRF3 association/phosphorylation and reporter enhancement; S102D supports the phosphorylation-dependent recruitment interpretation. The higher-order kinase arrangement in the final model is not an experimentally resolved architecture. No DDX3X kinase activity is inferred. The normal publication cache remains abstract-only; failed direct downloads and the successful indexed original access are both preserved.
PMID:29222110, original DOI 10.1242/jcs.207316, uses human DDX3X/CK1ε, a cytoplasmic FRET kinase sensor, DDX3X depletion, kinase inhibitors/dead-kinase controls, purified full-length protein and residues 414–582, and CK1-derived peptide assays. The Figure 3 caption supports the kinase-stimulation interpretation; its short exact quotation is attached to that activity in the review YAML. RNA inhibits the DDX3X–CK1 interaction/kinase stimulation, whereas CK1 phosphorylation reduces DDX3X ATPase activity in the tested system. Modeling of binding orientation is distinct from the ELISA, thermal-shift and biolayer-interferometry observations. Methods specify full-length protein purified from HEK293T cells and bacterial fragments; these constructs do not establish natural short-isoform functional equivalence.
PMID:23413191, DOI 10.1126/science.1231499, remains abstract-only after bounded publisher/supplement/repository attempts. Its actual abstract explicitly reports Wnt-dependent CK1ε binding/stimulation, Dishevelled phosphorylation, mammalian cells and Xenopus/Caenorhabditis developmental effects. This supports the established kinase-regulatory/Wnt function with the later mechanistic evidence, but does not recover its membrane-localization assay. The two signaling activities complement RNA helicase and auxiliary translation-initiation roles; they are not new annotation proposals because their specific MF/BP terms are already seeded.
PMID:21589879(https://doi.org/10.1371/journal.pone.0017169), Methods (protein expression/purification and enzyme assays), Results and Figures 2–7, examines recombinant human full-length DDX3X, isolated domains and mutants. RNA unwinding, ATP hydrolysis and RNA-binding results support the helicase function. The positive DNA assay used an 18/38-nucleotide substrate with a 5′ extension; the tested 3′ extension did not support the same activity. An overhang preference does not establish processive directional translocation. The paper contains inconsistent numbering of its DADA substitution between sections; no unverified residue coordinate is asserted here.
PMID:41587182, editorial correction, complete correction text and revised figure captions, replaces the purification image in Figure 2A, clarifies TLC splices, corrects lane numbering and changes Figure 4F ordering. The notice reports that available original/repeat data support the explanations, but original images for Figures 2D, 3E, 4B–D, 4G–H, 6A–B and 7 and quantitative data for Figures 2–5 and 7 are unavailable. Thus resolved presentation corrections and unresolved data-verification limits must be distinguished. The article is not retracted and the notice does not explicitly reject unwinding. Independently supported RNA chemistry remains central; the source-specific DNA result is retained as non-core with an explicit verification limitation. The original publication cache remains unchanged. Figure captions and correction text were read; figure pixels and the correction’s underlying-data attachment were not independently inspected.
PMID:29037760(https://pmc.ncbi.nlm.nih.gov/articles/PMC5693625/), Methods and biochemical Results, uses full-length tag-cleaved DDX3X and tests a 16-base-pair DNA duplex with a 25-nucleotide 3′ extension. The negative DNA result does not directly reproduce the earlier positive 5′-extended substrate. PMID:31300642(https://pubmed.ncbi.nlm.nih.gov/31300642/), structural and biochemical Methods/Results, instead uses an engineered human 132–607 core. Neither construct is the naturally shorter 646-residue product. DNA unwinding is therefore not a separate physiological core, and the two substrate conditions are preserved rather than presented as an exact replication conflict.
PMID:22323517(https://pubmed.ncbi.nlm.nih.gov/22323517/), interaction and translation-reconstitution Results/Methods, supports an auxiliary initiation-factor role and mature 80S joining. eIF2 association is RNA-dependent; eIF3 association survives RNA removal and is supported by purified-component experiments. Detection through eIF3C identifies the complex rather than an isolated eIF3C interface. Functional joining is demonstrated, while a specific bridging geometry and an ATPase requirement for that joining step are not established by this source. GO:0042256 includes joining mature ribosomal subunits; the annotation does not claim pre-rRNA biogenesis.
PMID:18596238(https://pubmed.ncbi.nlm.nih.gov/18596238/), Figure 2C and mRNP-selection Methods, supports association with polyadenylated mRNPs but does not establish the poly(A) tail as the contact. The inspected Figure 5/RNase and fractionation results support a peripheral 40S association without making DDX3X a constitutive ribosomal protein. Complete original and supplementary coverage was not obtained. PMID:27546789(https://pubmed.ncbi.nlm.nih.gov/27546789/), RNA-compaction Results, supports DDX3X-dependent compaction; target-specific annealing remains unresolved because the necessary supplementary assay was not recovered. LAF-1 annealing cannot substitute for a DDX3X measurement.
PMID:25468996(https://pmc.ncbi.nlm.nih.gov/articles/PMC4972397/), BioID Methods, uses E-cadherin–BirA in human MKN28 cells with control cells and perturbations. Proximity labeling does not by itself establish direct cadherin contact, and the DDX3X-specific supplementary target table was not recovered. PMID:16301996(https://pubmed.ncbi.nlm.nih.gov/16301996/) distinguishes human carcinoma expression from mouse NIH-3T3 knockdown phenotypes; PMID:21883093(https://pubmed.ncbi.nlm.nih.gov/21883093/) supports stress-granule/apoptosis context. These accessible sources do not settle the specifically intrinsic apoptotic pathway. Their positive observations are retained; uncertainty does not assert absence of the function.
PMID:31511697(https://pmc.ncbi.nlm.nih.gov/articles/PMC6980284/), NLRP3/ASC-speck Results and knockout/rescue/co-immunoprecipitation Methods, distinguishes mouse macrophage perturbations from tagged HEK293T interaction experiments. DDX3X associates with the NLRP3 NACHT region and supports inflammasome assembly in those conditions. The human ISS assignments remain ortholog inferences; no measured higher-order architecture, universal helicase requirement or short-product equivalence is asserted. PMID:28869602(https://pubmed.ncbi.nlm.nih.gov/28869602/), fractionation, imaging and mitochondrial translation experiments, supports a conditional mitochondrial association and translation effect without a resolved direct mitochondrial mechanism.
PMID:24965446(https://pubmed.ncbi.nlm.nih.gov/24965446/), Npro/DDX3 Results and stress-treatment Methods, uses sodium arsenate and reports redistribution/colocalization. These data do not demonstrate that DDX3X performs transport or retention of proteins in granules. GO:1903608 is currently obsolete because its historical usage confused colocalization with a process; both this ontology fact and the source-specific mechanistic limitation support the overannotation judgment.
PMID:22323517, original, Methods Purification of translation factors and Reconstitution of 48S and 80S initiation complexes, and Results/Figure 7F–G, distinguishes human-cell-purified FLAG-DDX3 from bacterial inclusion-body protein used only for quantification. With purified 40S, eIF3 and initiator tRNA on the HCV-derived reporter, added FLAG-DDX3 did not increase 48S assembly. Adding 60S and eIF5B (587–1220) produced more 80S complexes with FLAG-DDX3. The FLAG fraction lacked detectable eIF2/eIF3/eIF5 and ribosomal subunits and did not assemble complexes alone. This is a performed assembly contribution, supporting the auxiliary initiation-factor description; it is not just co-immunoprecipitation or necessity. The assay does not establish an ATPase requirement or the proposed physical bridge.
PMID:10074132, original, DOI 10.1128/JVI.73.4.2841-2853.1999, contains the NTPase-dNTPase activity analysis of His·CAP-Rf Methods, Figure 7 nucleotide-hydrolysis caption and Table 2 polynucleotide/substrate matrix used in this review. Selected indexed original passages were inspected; the normal publication cache remains abstract-only, direct publisher/BioC attempts failed, and figure pixels were not inspected. The human HuH-7 reporter increase is a positive expression outcome; its causal stage is not resolved into transcription versus RNA handling or translation by that observation alone.
PMID:29899501(https://pmc.ncbi.nlm.nih.gov/articles/PMC5998047/), Results TRPV4 cation channel interacts with DDX3X RNA helicase, Figure 1d–g, reports a tagged DDX3X pool at the plasma membrane after removal of excessive cytosolic signal and reduced association after TRPV4 activation. This independently corroborates the compartment assigned to PMID:23413191(https://doi.org/10.1126/science.1231499); it does not recover that earlier study’s localization assay. The IRF3 quotation above remains here because the normal PMID:23478265 cache lacks the original passage; it is not copied into cache-validated YAML.