| Context | Finding | Quantitative/statistics | Application/implementation | Supporting citation IDs |
|---|---|---|---|---|
| Paraneoplastic anti-Hu autoimmunity cohort | Anti-Hu paraneoplastic neurological disorder sera/CSF show reactivity to neuronal ELAVL proteins (including ELAVL3/HuC), but the dominant mapped response in this dataset is concentrated on shared nELAVL epitopes and is largely ELAVL4-biased rather than ELAVL3-specific. | Anti-Hu cohort **n=44**; anti-Yo comparator **n=36**; **38%** of anti-Hu patients enriched nELAVL peptides; **76** anti-Hu samples total (32 paired serum/CSF, 2 CSF, 10 serum); **19** samples with significant nELAVL enrichment; **20** unique nELAVL peptides; **>80%** of enriched peptides mapped to ELAVL4; **0/50** healthy control sera showed significant nELAVL enrichment. | Supports laboratory use of **PhIP-Seq/high-resolution epitope mapping** for paraneoplastic antibody characterization and differential diagnosis; high control specificity in this dataset supports translational diagnostic value. | (pqac-00000016, pqac-00000018, pqac-00000019) |
| Anti-Hu epitope definition | The immunodominant anti-Hu/nELAVL antibody signature maps to a short region near the exon 6/7a junction and centers on a recurring motif shared across nELAVL proteins, including ELAVL3. | Dominant **17-residue** signature; deep mutational scanning identified a preferred **RLDxLL** motif; **34/36 (94%)** significant peptides in motif reanalysis shared **RLDxxLL**. | Enables **epitope-level assay design**, mechanistic interpretation of anti-Hu serology, and refined antigen mapping beyond whole-protein tests. | (pqac-00000016, pqac-00000017, pqac-00000020, pqac-00000022, pqac-00000023) |
| Central tolerance / antigenicity context | The anti-Hu signature region is linked to thymic exon exclusion and predicted MHC-I presentation, consistent with a mechanism for autoreactivity against nELAVL proteins. | In human thymic epithelial cell amplicon sequencing, exon 7a-containing reads were **<0.5%**; human TEC libraries averaged **~1 million 125-nt paired-end reads** each, in triplicate. | Relevant to **mechanistic interpretation** of paraneoplastic autoimmunity and may guide future biomarker/epitope validation studies. | (pqac-00000017, pqac-00000020) |
| ALS/FTLD neuropathology | Human neurodegenerative disease tissue shows ELAVL3/HuC nuclear depletion and abnormal cytoplasmic pathology, supporting ELAVL3 disruption as a neuropathological marker in ALS/FTLD-spectrum disease. | Prior anterior horn motor neuron study: **nearly 75%** of neurons showed total loss of nuclear ELAVL3. | Potential **neuropathology biomarker** and disease-stratification feature in ALS/FTLD research workflows; supports ELAVL3 immunostaining as a readout of RNA-binding protein dysfunction. | (pqac-00000024, pqac-00000025, pqac-00000027) |
| FTLD-Tau overlap | ELAVL3 nuclear loss is not restricted to TDP-43 proteinopathy and also appears in tauopathy-associated FTLD cells with phosphorylated aggregates. | Majority of FTLD-Tau cases **4/5** showed related ELAVL3 nuclear loss in cells with phosphorylated aggregates. | Suggests ELAVL3 depletion may be a **shared marker across proteinopathies**, broadening relevance beyond classic TDP-43 ALS/FTLD. | (pqac-00000024, pqac-00000025) |
| Human ALS model relevance | ELAVL3 abnormalities may occur early in disease-linked cellular models and have been proposed as earlier or complementary markers relative to TDP-43 abnormalities. | Review-level summary indicates ELAVL3 abnormalities were reported as **more common/earlier** than TDP-43 abnormalities in cited patient/model studies, but no explicit n or effect size was provided in the extracted text. | Supports investigation of ELAVL3 as an **early biomarker or therapeutic focus** in ALS research, though quantitative validation is still needed. | (pqac-00000027) |
| Open Targets disease association | ELAVL3 has curated disease-target associations in Open Targets spanning neurodevelopmental and neurologic phenotypes. | Neurodegenerative disease score **0.4831**; Cannabis use **0.1452**; generalised epilepsy **0.0978**; autism spectrum disorder **0.0924**; generalized epilepsy with febrile seizures-plus **0.0874**; evidence count **5** for each listed disease in the retrieved summary. | Useful for **target prioritization**, disease landscaping, and hypothesis generation; these are association scores, not proof of causality. | (pqac-00000000) |


*Table: This table summarizes clinically relevant ELAVL3/HuC evidence from the retrieved literature and databases, including anti-Hu paraneoplastic autoimmunity metrics, neuropathology findings in ALS/FTLD, and Open Targets disease associations. It is useful for connecting molecular annotation to diagnostic and translational contexts.*