FAM149B1 supports normal cilium assembly, extension and protein distribution within cilia. The molecular activity connecting its cellular associations to those outputs remains unresolved. The current six source reviews are four ACCEPT, one supported non-core binding context and one UNDECIDED physical-location inference. The two assembly assertions are retained after reassessing the normal-frequency endpoint; the original source objects remain unchanged. Reference assessments retain their evidence scopes, with the PAINT note now matching the retained assembly decision. No molecular activity, target compartment or native complex is inferred merely to fill a core-function field.
Both lanes read actual original sources independently, with the following distinct scopes. Their complete assessments are retained verbatim as labeled sections in each publication's reference-review notes; the table summarizes rather than replaces them.
| Source | Direct original-evidence lane | Database/phylogenetic lane |
|---|---|---|
| Shaheen et al., 2019 — PMID:30905400 | Main clinical and functional Results, Figure 3/5 captions, supplementary transcriptome/qPCR Methods and Figure S1; actual Figure 3, Figure 5 and S1 pixels. S2 was read as a caption, not inspected as pixels. | Selected patient/construct context, functional Results, Figure 3/5 captions, supplementary Methods and S1/S2 captions; actual Figure 3 and S1 pixels. No Figure 5 pixel claim. |
| Satoda et al., 2022 — PMID:35609210 | FAM149B1 interaction and knockout/rescue Results, Figures 6/7 captions, relevant Discussion and target Methods; actual supplementary S1–S3 captions and Tables S1–S3; S2/S3 pixels. No main Figure 6/7 or video pixel reading. | Selected FAM149B1 interaction and knockout/rescue Results, Figures 6/7 captions, relevant Discussion and target Methods. Independently retrieved and viewed main Figure 7 from the actual XML graphic URL; no 2022 supplement or Figure 6 pixel claim. |
The 2019 complete publisher PDF with supplement has the article-specific PII S0002-9297(19)30063-1. Generic BioStudies mmc1/mmc3 routes returned unrelated 2025 papers and were excluded. The 2022 official main and supplement provide public locators. Its separate review-history PDF is not an additional experiment. Availability of complete originals does not imply whole-paper or all-figure reading by either lane.
Patient dermal fibroblasts in the 2019 study retain normal ciliation frequency, but their cilia are longer and bulbous, with IFT88/IFT46 tip accumulation and relatively preserved IFT122 distribution. The independent 2022 human hTERT-RPE1 knockout/rescue study corroborates elongated cilia and IFT88/ICK tip accumulation. Full-length FAM149B1-EGFP rescues length and IFT88 distribution. The engineered 1–179 fragment improves the IFT88 endpoint without correcting length. Neither 1–179 nor 180–582 restores normal length; intact full-length protein is required in the tested rescue assay. These results separate the measured outputs without defining the behavior of the natural 528-residue product.
Cilium assembly, GO:0060271, is retained for the imported experimental and phylogenetic contexts. A normal fraction of ciliated cells does not exclude defective assembly or extension of the structure. The same normal-frequency observation is already recorded in UniProt VAR_083866, alongside altered assembly and protein localization. Generalizing to its organization parent solely on that observation would discard supported specificity. Current CILK1 and IFT88 assembly annotations and their committed reviews provide consistent comparison, without transferring their established kinase or transport-machinery activities to FAM149B1. CDC14A's regulatory assignment depends on a distinct phosphatase mechanism; a comparable FAM149B1 mechanism is not demonstrated, so no regulation term is substituted.
Protein localization to cilium, GO:0061512, expressly includes maintenance at a location within the cilium and fits the protein-distribution defect and rescue without requiring defective initial entry. Actual current is_a and combined is_a/part_of ancestor responses show that neither assembly nor protein localization is an ancestor of the other. They represent distinct endpoints of one supported ciliary role; the assembly/organization parent-child pair is not duplicated in the core.
The 2019 tagged HEK293 co-immunoprecipitation and 2022 tagged HEK293T association/domain mapping support FAM149B1 association with BROMI and CCRK. They do not establish a purified binary interface or native stoichiometry. Adaptor and cargo-adaptor definitions were considered in the direct lane, but bridging, motor-cargo coupling and kinase regulation were not demonstrated. A cyclin-like CCRK role and regulation of IFT turnaround remain mechanistic hypotheses. Static tip enrichment is not a direct measurement of trafficking rate. The core therefore represents the accepted process role while leaving molecular function, location and complex unasserted. Its biological knowledge gap concerns the molecular step, not an alleged lack of ciliary biology or merely an absent ontology label.
The campaign instructions authorize retention of supported generic binding as non-core when no specific replacement is established, and prohibit new publication quotation anchors. The supported binding review remains exact; reference-only citations and precise source locators supply the evidence trail.
The actual PANTHER PTHR31997 v19 tree and MSA place human HGNC:29162/Q96BN6 leaf PTN002528684 beneath PTN002842395, with an exact 582-residue target sequence. The actual saved IBD file asserts both cilium assembly and protein localization to cilium on that node, using experimental descendant Q96BN6; no relevant NOT occurs on the target path. This was independently reconstructed in the database lane. Self-WITH is positive experimental grounding, not circularity, and donor count is not a weakness. GO_REF:0000033 describes the method. The current propagation assessment is NO_FAILURE_CORE with SUPPORTS_TRANSFER: neither the verified ancestry nor the assembly scope is rejected. A compact public PAINT evidence extract records the actual root-to-target persistent IDs, target sequence hash, two literal IBD rows, absence of path NOT assertions, public acquisition URLs and exact source hashes. These data support ancestry and imported process assertions; they do not identify the unknown molecular mechanism.
For physical location, GO_REF:0000044, SL-0066 and the official external2go mapping agree on cilium GO:0005929. Q96BN6's CC:SUBCELLULAR LOCATION uses ECO:0000305/PubMed:30905400. This positive curated inference remains acknowledged. The 2019 images show markers and IFT proteins, not FAM149B1 localization, while the 2022 Discussion reports unsuccessful distinct localization of FAM149B1 to cilia. GO:0005929 includes cytoplasmic ciliary parts, so no invented shaft-only criterion is imposed. Transient, low-abundance or base-associated pools remain possible. The exact location stays UNDECIDED; there is no universal absence or concrete source-defect claim.
The two natural products remain 582 and 528 residues, with both literal alternative-sequence edits for the latter retained. The 2019 clinical variants use NM_173348.1/NP_775483.1, but its complete co-IP insert sequence is unspecified. The 2022 methods identify human NM_173348.2 and full-length 582-residue protein plus engineered 1–179/180–582 fragments. Neither engineered fragment is the natural shorter product. Patient truncations, historical tagged constructs, RefSeq/Ensembl models and natural products are not functionally equated or retrospectively resequenced.
Both selected publication normal records declare full_text_available: true, so both author full_text_unavailable flags are false. Cache metadata, external complete-original access and actual reading remain distinct. PMID:35609210 was genuinely fetched by the direct owner, then reused byte-exact and deduplicated in integration. Seven normal sources remain preserved; only four cited/family dependencies plus the two original machine records are proposed for delivery. Unused genuine normals remain private. No source caches, reference identities/findings or prior evidence packets were rewritten. The assembly-scope revision restored the imported assembly judgments and corresponding core facet, clarified fragment-rescue wording, and added the public PAINT extract. The current follow-up only reconciles the PAINT assessment clause with that retained assembly decision; it adds no publication quotation or annotation.