| Year | Citation (first author) | Publication (journal/preprint) | URL | What it shows about EMC9 (identity, localization, paralog status) | Key quantitative/data points | Notes/limitations |
|---|---|---|---|---|---|---|
| 2019 | Chitwood et al. | *Trends in Cell Biology* (review) | https://doi.org/10.1016/j.tcb.2019.01.007 | Defines human EMC9 (FAM158A) as one of the cytosolic EMC subunits; EMC8 and EMC9 are paralogs with ~40% sequence identity; mammalian EMC contains EMC8/9 as metazoan-specific component(s) (pqac-00000004) | EMC8 ~24 kDa; EMC9 ~23 kDa; purified mammalian EMC estimated at ~250–300 kDa with ~1 copy of each subunit (pqac-00000004) | Review, not EMC9-specific primary experiment; summarizes broader EMC field rather than direct EMC9 perturbation |
| 2019 | Tian et al. | *Cell Reports* | https://doi.org/10.1016/j.celrep.2019.08.006 | Places EMC9 among the soluble/cytosolic EMC subunits in mammalian cells, supporting peripheral localization on the cytosolic face of the ER-associated complex (pqac-00000016) | Quantitative proteomics identified 36 EMC-dependent and 171 EMC-independent transmembrane proteins in EMC-deficient cells; mechanistic theme: EMC dependence tracks with polar/charged TMD features (pqac-00000016) | Focuses on EMC4/EMC6-deficient models and client classes; does not directly test EMC9-specific knockout phenotypes |
| 2020 | O'Donnell et al. | *eLife* | https://doi.org/10.7554/eLife.57887 | Provides direct structural/biochemical context for EMC9: EMC9 is a cytosolic EMC subunit, ~44% identical to EMC8 in mammals, forms a stable 1:1 complex with EMC2, and likely occupies the cytosolic vestibule leading to the insertase pathway (pqac-00000006, pqac-00000008, pqac-00000015) | EMC2·EMC9 complex measured at expected 59 kDa; EMC8 monomer ~23 kDa; no ternary EMC2·EMC8·EMC9 complex formed in reconstitution; full EMC cryo-EM map at 6.4 Å used to place EMC2·EMC9 (pqac-00000006, pqac-00000015) | Key primary source for EMC9 architecture, but could not resolve whether EMC8 and EMC9 coexist in one 10-subunit EMC or substitute in alternative 9-subunit complexes |
| 2020 | Volkmar & Christianson | *Journal of Cell Science* (review) | https://doi.org/10.1242/jcs.243519 | Interprets EMC9, EMC8, and EMC2 as lacking ER-targeting signals/TMDs and therefore forming the cytoplasmic interface of EMC; classifies EMC9 among peripheral, non-core subunits (pqac-00000002, pqac-00000007, pqac-00000009) | EMC9 length noted as ~208 aa; depletion of peripheral subunits such as EMC9 generally reported to have mild/no major effect on overall EMC stability versus core subunits (pqac-00000002) | Review-level synthesis; statements about stability are generalized across subunits and not from EMC9-only perturbation |
| 2022 | Bai & Li | *The FEBS Journal* (review) | https://doi.org/10.1111/febs.15786 | Summarizes cryo-EM structures showing that an aqueous subunit, either EMC8 or EMC9, sits atop EMC2 in the human EMC cytosolic region, reinforcing EMC9’s role as the EMC8 paralog in the cytosolic module (pqac-00000003) | Synthesizes four recent cryo-EM studies; no new EMC9-specific quantitative perturbation data in the review excerpt (pqac-00000003) | Review; useful for structural consensus but not direct EMC9 experimentation |
| 2022 | Hegde | *Annual Review of Biochemistry* (review) | https://doi.org/10.1146/annurev-biochem-032620-104553 | Presents current mechanistic understanding: EMC2, EMC8, and EMC9 are cytosolic; EMC8/9-containing cytosolic cradle likely participates in early membrane-protein engagement before insertion/folding (pqac-00000003) | Review emphasizes EMC as a nine-protein complex built around a conserved EMC3-EMC6 core and discusses insertase plus later folding/assembly roles (pqac-00000003) | Broad EMC review; informative for functional model but limited EMC9-specific experimental granularity |
| 2023 | Chen et al. | *Nature* | https://doi.org/10.1038/s41586-023-06175-5 | Shows the EMC cytoplasmic “Cyto dock” can bind CaVβ through EMC2 and EMC8 regions in a human EMC-client structure, demonstrating a client-binding role for the cytosolic module closely related to EMC9’s paralogous position in alternative complexes (pqac-00000011, pqac-00000012, pqac-00000017) | Human EMC–CaV1.2–CaVβ3 complex solved at ~3.4 Å; assembled CaV1.2–CaVβ3–CaVα2δ-1 at ~3.3 Å; EMC–client complex ~0.6 MDa (pqac-00000012) | Structure directly visualizes EMC2/EMC8 rather than EMC2/EMC9, so EMC9 involvement is inferred by paralogy/alternative complex composition rather than directly observed |
| 2023 | Marquez et al. | *genesis* | https://doi.org/10.1002/dvg.23520 | Most relevant recent disease-focused source: links damaging EMC9 variants to congenital anomalies and supports non-redundant developmental importance of EMC9 despite similarity to EMC8; Xenopus CRISPR depletion implicates EMC9 in neural crest, craniofacial, neuromuscular, and WNT-related biology (pqac-00000005, pqac-00000013, pqac-00000014) | Table 1 summarizes mutations in EMC9/EMC10 across 18 individuals from 10 families; sox10 assay n=60/condition over 3 replicates; craniofacial cartilage assay n=60/condition; motility assay control n=30 and emc9-depleted n=30; pooled immunoblots used n=30/stage/condition (pqac-00000013) | Combines EMC9 and EMC10 in some analyses and uses Xenopus rather than human cell mechanistic assays; strong developmental evidence but limited biochemical dissection of EMC9-specific molecular action |
| 2024 | Open Targets platform | Database/knowledgebase | https://platform.opentargets.org/target/ENSG00000100908 | Indicates no well-supported disease-target evidence currently curated specifically for human EMC9 despite recognition as a target entry; supports conclusion that clinical annotation remains sparse and emerging (pqac-00000000) | Returned one generic “genetic disorder” association row with evidence score 0 and no supporting evidence rows (pqac-00000000) | Useful as a negative/coverage signal rather than mechanistic evidence; database evidence can lag primary literature |
| 2026* | Stanton et al. | *bioRxiv* preprint | https://doi.org/10.64898/2026.01.14.699575 | Suggests EMC8- and EMC9-containing EMC complexes can be functionally distinct, with EMC8-specific binding to CaVβ and developmental non-redundancy of EMC9 cited from prior work (pqac-00000001, pqac-00000003) | Reports tissue-varying EMC8:EMC9 expression ratios and argues EMC9 loss is not redundant developmentally (pqac-00000001) | *Outside requested 2019–2024 focus*; preprint and later than requested, so should be used cautiously and mainly as forward-looking context |


*Table: This table summarizes the most useful sources for functional annotation of human EMC9, emphasizing recent structural, mechanistic, and disease-related evidence. It highlights where EMC9 is directly studied versus where conclusions are inferred from the broader EMC or EMC8/EMC9 paralog context.*