Human gene identity and expression study; cached abstract identifies the human orthologue, 198-residue coding sequence and tissue expression. This is a NAS source, not the direct human enzyme assay. Later PMID:12651944 supplies biochemical support.

Human AICDA-deficiency paper; cached abstract explicitly reports loss of class switching and hypermutation and giant germinal centers. Direct catalytic participation is grounded separately in enzyme studies, not inferred only from patient necessity.

Cached full Methods/Results inspected. Human AID-GFP is expressed in mouse NIH3T3 cells; export inhibition reveals nuclear accumulation. Human protein and mouse cell host are distinguished.

Cached full text inspected. Human AID interacts with the PKA holoenzyme and is phosphorylated; mouse B-cell rescue assays test function. Direct binary binding to each subunit is not resolved, and AID is not assigned kinase activity.

Cached abstract and primary PubMed identity inspected; original full Results remain unavailable. CTNNBL1 interaction and AID-mutant phenotypes support antibody diversification; independent human studies corroborate enzyme chemistry and localization. DT40 knockout evidence is explicitly avian.

Cached abstract and original Nature record inspected; full Results not recovered. Active import and retention are explicitly reported. Individual karyopherin and self-binding panels remain curator-sourced, with later independent human evidence used where noted.

Full primary PMC2781619 Methods/Results/Discussion read externally; local cache is abstract-only. Replication-factory localization concerns SLIP-GC, while AID depletion rescues damage and apoptosis. This supports an AID-dependent damage mechanism, not an identified AID replication-regulatory step.

Cached full text inspected. Human Ramos AID-associated fractions contain RNA-exosome proteins; mouse B-cell and human transfection experiments complement the biochemistry. The authors explicitly leave direct versus indirect association unresolved; AID is not established as a canonical exosome core subunit.

Cached full Results/Methods inspected. Includes AID despite the spliceosomal title: human-cell AID localization variants and karyopherin binding, plus chicken DT40 CTNNBL1-loss experiments. Cargo association is not nuclear-transport-receptor activity.

Cached abstract plus indexed primary PMC3088758 Results/Methods inspected with independent consultation. Human ORF constructs include AID; HEK293 overexpression affects hydroxymethylated reporters, while adult mouse physiological loss-of-function centers on Tet1/Apobec1. The paper does not establish purified AID 5hmC chemistry and explicitly allows other intermediates.

Cached full Results/Methods inspected. Human and mouse constructs, mouse CH12 switching and human BL2 reporter mutation are distinct. The BL2 assay uses truncated AID-ER; the conclusion that Spt6 is dispensable for SHM does not deny AID participation.

Normal cache has full-text sections but omits Results. Indexed primary PMC3230223 Figure 6 supplies tagged human-cell co-immunoprecipitations, endogenous mouse P19 association and purified-protein interaction. TDG glycosylase chemistry is measured; the proposed coupled AID deamination mechanism is not a measured standalone demethylase reaction.

Cached abstract inspected. It distinguishes positive DNAJA1 and DNAJA2 in-vitro interactions from the DNAJA1-specific cellular stabilization phenotype. HSPA8 pair details were not recovered; no denial of that curator interaction and no chaperone activity assigned to the AID client.

Cached abstract establishes the solubility-based screen, independent interaction verification and RNF126-mediated AID ubiquitylation. Supports specific ligase binding, not an E3 activity of AID. Detailed native-context consequences remain outside the accessed abstract.

Cached abstract supports AID/UNG-dependent HBV cccDNA degradation and core-protein recruitment in hepatocytes. HBV is a DNA virus; this cannot by itself establish the distinct retroviral RNA-replication process.

Cached abstract directly identifies human patient EBV-transformed B cells and engineered Ramos cells. Decreased nuclear AID accompanies CTNNBL1 M466V and reduced SHM. This is positive human localization/function support without treating every mutant effect as a separate AID activity.

Primary PubMed identity and indexed original JBC Results verified. Purified mouse GST-AID converts free cytidine; the original RNA-editing family name is not proof of an endogenous AID RNA target.

Human Ramos-derived GST-AID expressed in Sf9 deaminates free nucleosides and DNA-bound cytosine; RNA removal changes DNA-substrate access in these assays.

Primary PubMed and indexed PMC4426339 verified. Mouse switch-RNA/AID experiments support structured RNA binding and targeting; human patient genetics motivates the study but does not turn those assays into direct human measurements.

Engineered human AID constructs oligomerize on G4 DNA, with interface mutations affecting class-switching rescue; this does not establish a fixed native homodimer.

Primary PubMed/PMC2665220 full Methods/Results inspected. Human AID is explicitly among eight tested vertebrate proteins. L1/MusD restriction is mobile-element evidence; it does not alone establish infectious retrovirus restriction.

Primary PubMed and indexed PMC3568302 Results verified. The first Results section explicitly identifies the unfused construct as human AID; subsequent RNA panels continue the AID/GFP comparison, with separate human/mouse AID-ER assays identified as such. Encapsidated RNA C-to-U changes have polymerase/RNase-H and immunoprecipitation controls. Endogenous human BL2 assays independently support antiviral activity. This is contextual viral RNA editing, not a demonstrated physiological immunoglobulin RNA target.