Human cDNA resource context; this review uses the official protein record and archived clone comparisons rather than treating library membership as a DZIP1L functional assay.

Mammalian full-length cDNA resource context; no DZIP1L-specific mechanism is inferred from this sequence resource.

Human gene-family sequence resource; supports sequence provenance rather than a target functional experiment.

Human GFP-DZIP1L localization uses IMAGE4940443 in hTERT-RPE1 cells. Reduced ciliogenesis follows combined DZIP1/DZIP1L depletion. The archived clone has the long-product architecture but differs at three residues from the current displayed sequence.

Curated positive human DZIP1L interactions with CBY2 and CEP76 are sequence- and record-qualified. The primary study describes systematic retesting; a separate target-specific orthogonal assay is not inferred.

The centrosomal BFG-Y2H screen and validated two-hybrid records support DZIP1L association with the 412-residue CBY2 product Q8NA61-2, not CBY1.

Endogenous human DZIP1L and SEPTIN2 coassociate, and N-terminal fragment assays localize association capacity. Patient fibroblasts can retain cilia while polycystin distribution is altered; organism and tissue differences constrain ciliogenesis claims.

Human fibroblast and RPE-1 microscopy supports localization in the distal basal-body/transition-zone region; biallelic variants in the human families establish autosomal-recessive polycystic kidney disease.

Mouse Dzip1l supports ciliary-bud formation and Cby positioning; mutant cells retain recruitment of Tctn2 and IFT components. Mouse tagged constructs in HEK293 cells remain mouse-protein assays.

A literal positive DZIP1L–CEP76 IntAct record includes a no-effect feature at DZIP1L residue 643. The selected cache has partial text, and an attempted original route is a challenge page; no uninspected variant mechanism is asserted.

Human DZIP1L–CEP76 interaction records carry three DZIP1L mutation-with-no-effect features. The general variant-screen methodology does not turn these into disruptive or negative pair results.

HuRI records support seven target-specific positive pairs, retaining the exact partner products, fragments and assay methods. Verified partner classes support selected binding refinements without transferring their activities to DZIP1L.

The CBY1-bait DZIP1L-prey record is an anti-tag co-immunoprecipitation/AP-MS spoke association. It supports the association at that scope, not an independently purified binary interaction.

Official identity, two natural products, sequence features and curated localization provide the gene-level source baseline.

Individual HPA reliability supports basal-body localization, while the other six reported compartments are uncertain.

Saved-input reconstruction verifies exact interaction participant records, current propagation paths, individual HPA reliability and natural-product/archived-clone sequence distinctions.

Stable interaction identifiers, public primary locators, source access and species/construct boundaries are mapped to the reviewed assertions.

Public locators distinguish primary human localization, independent partner-class evidence, exact interaction records, source-access limits and the project-specific binding disposition.