| Finding/Claim | System (cell line/organism) | Assay/Method | Key quantitative result(s) | Interpretation/Function | Source (first author year journal) with URL | Evidence Context ID(s) |
|---|---|---|---|---|---|---|
| TXNDC11 is an ER-resident PDI-family protein with five predicted Trx domains, a single TM segment, and a luminal region; only Trx5 contains the canonical active-site motif important for function | HeLa, KBM7 human cells | Forward genetic screens, homology modeling, immunofluorescence, EndoH sensitivity, rescue with active-site mutants | Five predicted Trx domains; Trx5 contains **CGFC** (canonical CXXC), Trx1 contains **CXXS**; Trx5 mutant abolishes rescue whereas Trx1 mutant does not | Establishes correct human TXNDC11 identity and supports a redox-active ER oxidoreductase role in glycoprotein ERAD | Timms 2016 *Nature Communications* — https://doi.org/10.1038/ncomms11786 | (pqac-00000011, pqac-00000013, pqac-00000027) |
| TXNDC11 Trx5 has reductase-like redox properties | Recombinant human Trx5 domain | AMS shift assay / redox titration | Estimated reduction potential of isolated Trx5 disulfide: **~−234 mV** | Supports classification of TXNDC11 as a **disulfide reductase** rather than oxidase in ERAD | Timms 2016 *Nature Communications* — https://doi.org/10.1038/ncomms11786 | (pqac-00000013, pqac-00000027) |
| TXNDC11 is required preferentially for glycoprotein ERAD rather than non-glycosylated substrate degradation | Human knockout/knockdown cell systems (including GFP-HLA-A2, CD3δ-YFP, NHK-mCherry ERAD substrates) | CRISPR/haploid screens, degradation assays, rescue experiments | Screen concordance reported as **>70%** overall; TXNDC11 depletion impairs degradation of multiple **glycoprotein** ERAD substrates but not a non-glycosylated variant | Places TXNDC11 specifically in **glycoprotein ERAD** | Timms 2016 *Nature Communications* — https://doi.org/10.1038/ncomms11786 | (pqac-00000010, pqac-00000013) |
| Human TXNDC11 contains a TMD, five Trx-like domains, coiled-coil region, and multiple potential N-glycosylation sites | Human TXNDC11 schematic / transfected mammalian cells | Domain mapping, immunoblotting, co-IP | Domain map shows **TMD + 5 Trx domains + coiled coil**; multiple potential N-glycosylation sites indicated | Confirms the literature matches UniProt Q6PKC3 domain architecture | George 2020 *eLife* — https://doi.org/10.7554/eLife.53455 | (pqac-00000009, pqac-00000010, pqac-00000012, pqac-00000023, pqac-00000028) |
| EDEM2 is stably disulfide-bonded to TXNDC11 through EDEM2 C558 and TXNDC11 C692 in Trx5 | Human HCT116-derived experimental system | Non-reducing SDS-PAGE, co-IP, cysteine mutagenesis | Covalent linkage requires **EDEM2 C558** and **TXNDC11 C692**; loss of this bond abolishes high-molecular-weight complex | Defines the key **EDEM2–TXNDC11 ERAD complex** and links TXNDC11 active-site chemistry to EDEM2 function | George 2020 *eLife* — https://doi.org/10.7554/eLife.53455 | (pqac-00000008, pqac-00000009, pqac-00000012, pqac-00000023, pqac-00000028) |
| Purified EDEM2–TXNDC11 complex catalyzes the first glycoprotein ERAD mannose-trimming step in vitro | Purified proteins / transfected mammalian cells | In vitro glycan conversion assay | Complex converts **PA-M9 → PA-M8B**; disulfide linkage is stated to be **essential** for EDEM2-mediated mannose trimming | TXNDC11 functions as the PDI-family partner enabling **initiating mannose trimming** in gpERAD | George 2020 *eLife* — https://doi.org/10.7554/eLife.53455 | (pqac-00000008, pqac-00000009, pqac-00000012, pqac-00000023) |
| Alternative translation initiation affects TXNDC11 membrane association/topology | Human cells expressing M1A/M58A mutants | Mutational analysis and fractionation/solubility comparison | **M1A** mutant is at least partly soluble; **M58A** remains transmembrane | Suggests the N-terminal hydrophobic region can act as a **signal anchor/weak signal peptide**, influencing ER membrane anchoring | George 2020 *eLife* — https://doi.org/10.7554/eLife.53455 | (pqac-00000008, pqac-00000010) |
| TXNDC11/EFP1 localizes to the ER and is an N-glycosylated glycoprotein | REF52.2 and CHO cells; rat ortholog highly similar to human TXNDC11 | GFP/Myc localization with PDI co-staining; Endo H sensitivity; western blot | Two EFP1 species at approximately **136 kDa** and **155 kDa**; **155-kDa** form is Endo H-sensitive high-mannose glycoform | Supports ER residency and lumenal glycoprotein maturation state for TXNDC11/EFP1 | Appel 2009 *Cell Health and Cytoskeleton* / DOI-linked report — https://doi.org/10.2147/chc.s5137 | (pqac-00000003, pqac-00000004, pqac-00000006) |
| EFP1/TXNDC11 shows thioredoxin/PDI-like catalytic activity in insulin reduction assay | Recombinant rat EFP1 ortholog (informative for human ortholog) | Insulin disulfide reduction assay | Assay conditions: **3.9 µM EFP1**, **0.13 mM insulin**, **0.33 mM DTT**, **120 µL** final volume; activity slower than *E. coli* thioredoxin; mean of **3 independent experiments** | Demonstrates intrinsic **disulfide-reductase** activity consistent with PDI family membership | Appel 2009 *Cell Health and Cytoskeleton* / DOI-linked report — https://doi.org/10.2147/chc.s5137 | (pqac-00000002, pqac-00000003, pqac-00000004, pqac-00000006) |
| EFP1/TXNDC11 interacts with Par-4 and modulates ER-stress-linked apoptosis | CHO/NIH3T3 and related cell systems; rat ortholog study | Pull-down, dot blot, co-IP, apoptosis assays with ER stressors and Par-4 siRNA | Par-4 knockdown reduced apoptosis induced by **ionomycin (p = 0.0043)** and **thapsigargin (p = 0.0019)**; apoptosis scoring used **5 independent experiments** with **100–200 cells/condition** | Supports a role in **ER-stress response** and cell-fate decisions, though based on ortholog data | Appel 2009 *Cell Health and Cytoskeleton* / DOI-linked report — https://doi.org/10.2147/chc.s5137 | (pqac-00000001, pqac-00000002, pqac-00000006) |
| Endogenous EDEM2 is post-transcriptionally stabilized by TXNDC11; TXNDC11 deficiency lowers EDEM2 protein | HEK293 human cells | CRISPR-deficient cell lines; western blot; RT-PCR | In SEL1L-deficient cells, TXNDC11 previously increased by **~1.5-fold**; in **TXNDC11-deficient** cells, EDEM2 protein was **markedly decreased** despite lack of corresponding mRNA reduction | Indicates TXNDC11 is important for **EDEM2 protein stability/maintenance** in the ERAD pathway | Murase 2023 *BPB Reports* — https://doi.org/10.1248/bpbreports.6.6_193 | (pqac-00000020, pqac-00000022) |
| Reductive stress destabilizes both EDEM2 and TXNDC11 proteins; EDEM2 decrease is proteasome- and SEL1L-sensitive | HEK293 human cells | DTT treatment ± MG132 or SEL1L deficiency | **1 mM DTT** decreased EDEM2 and TXNDC11 protein **time-dependently**; decrease in EDEM2 after DTT was **partially suppressed by MG132 (10 µM)** and largely absent in **SEL1L-deficient** cells | Suggests EDEM2 stability depends on disulfide-linked state with TXNDC11 and that free/cleaved EDEM2 can enter **SEL1L-mediated ERAD** | Murase 2023 *BPB Reports* — https://doi.org/10.1248/bpbreports.6.6_193 | (pqac-00000020, pqac-00000021, pqac-00000022) |
| High TXNDC11 expression is associated with higher-grade glioma and poor prognosis | Human glioma clinical cohort | IHC, Kaplan–Meier survival, Cox regression | **n = 86** cases; **20 WHO grade II**, **66 WHO grade III–IV**; high TXNDC11 associated with high grade (**p < 0.001**) and shorter survival (**p < 0.001**); univariate HR **0.248** (95% CI **0.117–0.524**, **p < 0.001**); multivariate HR **0.334** (95% CI **0.153–0.729**, **p = 0.006**) | TXNDC11 is a potential **prognostic biomarker** in glioma | Chen 2023 *International Journal of Molecular Sciences* — https://doi.org/10.3390/ijms241713367 | (pqac-00000016, pqac-00000018) |
| TXNDC11 promotes glioblastoma growth, invasion/migration, and temozolomide resistance; knockdown improves survival in vivo | GBM8401 and U87 cells; orthotopic xenograft model | siRNA/overexpression, proliferation and apoptosis assays, TMZ sensitivity, in vivo imaging | Knockdown reduced xenograft fluorescence at **day 14 (p < 0.01)** and **day 21 (p < 0.001)**; survival **25.50 ± 0.812 days** vs **20.75 ± 0.978 days** (**p = 0.006**); animal groups **n = 12** each | Supports TXNDC11 as a candidate **oncogenic dependency / therapeutic target** in glioblastoma | Chen 2023 *International Journal of Molecular Sciences* — https://doi.org/10.3390/ijms241713367 | (pqac-00000016, pqac-00000019) |


*Table: This table summarizes experimentally supported TXNDC11 findings across foundational mechanistic studies and recent translational work. It emphasizes quantitative results, domain/function evidence, and disease relevance for rapid incorporation into a functional annotation report.*