| Study (author, year, journal) | Disease/biological context | Proposed FBXL16 action (stabilizes vs degrades) | Direct target(s)/partner(s) | Key evidence types | Quantitative/statistical highlights | URL/DOI | Publication date (month/year) |
|---|---|---|---|---|---|---|---|
| Qu et al., 2024, *Biomarker Research* | Alzheimer’s disease; APP/PSEN and 3×Tg-AD mouse models; neuronal cell lines | Promotes ubiquitination-dependent **degradation** of APP | APP; broader interactome included 141 FBXL16-associated proteins, with proteomics highlighting USP17 family members, HSPA5, PSMD4, PRDX1/2, VIM, TXN, CTSD, LTF (pqac-00000000, pqac-00000002) | Flag-FBXL16 IP followed by LC-MS/MS; molecular docking; cytoplasmic colocalization; co-IP of FBXL16 with APP; MG132 and CHX assays; ubiquitination assay; stereotaxic lentiviral overexpression in hippocampus; IHC/ICC; Morris water maze and Y-maze; conditional knockout mice (pqac-00000000, pqac-00000004, pqac-00000005, pqac-00000014) | 141 interacting proteins identified; STRING/GO enrichment for ubiquitin-dependent protein catabolic process *p*=1.04E-09; GAD enrichment for cognition/aging 1.49E-06 and 1.56E-06; docking lowest-energy pose −41.228 kcal/mol; APP decreased dose-dependently with FBXL16 overexpression; behavioral and histologic improvements reported with *P*<0.05 or *P*<0.01 vs controls; APP levels significantly higher in FBXL16-cko mice (pqac-00000000, pqac-00000005, pqac-00000014) | https://doi.org/10.1186/s40364-024-00691-w | Nov 2024 |
| Morel & Long, 2024, *Molecular Oncology* | KRAS-mutant lung adenocarcinoma; drug resistance to sotorasib | **Stabilizes** IRS1 and upregulates IRS1/AKT signaling | IRS1; signaling outputs pAKT and pS6K/S6; IRS1 interaction requires LRR domain and both F-box/LRR needed for stabilization/signaling (pqac-00000001, pqac-00000008) | siRNA knockdown; stable overexpression; proteomic mass spectrometry; CHX chase; western blotting; soft-agar transformation; TMA/IHC; CPTAC data mining; growth and migration assays; drug-sensitivity assays with sotorasib (pqac-00000001, pqac-00000008, pqac-00000013, pqac-00000018) | FBXL16 vs IRS1 correlation in LUAD cell lines: *r*=0.93, *R*²=0.86, *P*<0.001; in LUAD patient samples (*N*=102): *r*=0.6, *R*²=0.36, *P*<0.001; IRS1 upregulated in KRAS-mutant CPTAC LUAD (KRAS WT *N*=77 vs mutant *N*=33); IRS1 half-life in A549 changed from 5.5 h to 0.9 h after FBXL16 knockdown; in NL-20 from 1.8 h to 8 h with FBXL16 overexpression; overexpression increased IRS1 half-life 4.4-fold; significance annotated as *P*<0.05, **P*<0.01, ***P*<0.001 (pqac-00000001, pqac-00000013, pqac-00000018) | https://doi.org/10.1002/1878-0261.13554 | Jan 2024 |
| Yao et al., 2024, *Respiratory Research* | COPD; fibroblast transdifferentiation/myofibroblast activation; cigarette smoke mouse model | FBXL16 is functionally **suppressed** by miR-1307-5p; reduced FBXL16 permits HIF1α-axis activation and fibroblast transdifferentiation | FBXL16 as a direct miR-1307-5p target; study title and abstract place FBXL16 in an FBXL16/HIF1α axis, but gathered evidence here directly supports miRNA→FBXL16 targeting rather than a direct FBXL16–HIF1α binding assay (pqac-00000010) | In silico seed prediction; luciferase reporter with WT vs mutant FBXL16 3′UTR; qPCR in MRC-5 cells; primary fibroblasts from COPD patients; chronic cigarette smoke mouse experiments; BALF inflammatory-cell analysis; lung pathology and pulmonary function readouts (pqac-00000010) | miR-1307-5p increased in COPD blood and lung tissues (*n*=6/group) and in COPD-derived primary lung fibroblasts; two seed matches predicted in FBXL16 3′UTR; miR-1307-5p agomir significantly repressed FBXL16 mRNA and WT 3′UTR luciferase but not mutant reporter; statistical framework reported as *t*-test/ANOVA with *P*<0.05 and *P*<0.01 thresholds (pqac-00000010) | https://doi.org/10.1186/s12931-024-03007-6 | Oct 2024 |
| Shah, 2022, journal not specified in gathered evidence | ER-positive breast cancer; fulvestrant response; endocrine resistance | **Stabilizes** ERα by decreasing polyubiquitination and antagonizing degradation; also reported to stabilize c-MYC, SRC-3, β-catenin; separate reported context suggests degradation of HIF1α in TNBC, but mechanism unresolved | ERα; FBXO45 antagonized in estradiol-induced ERα degradation; broader reported oncoproteins c-MYC, SRC-3, β-catenin; F-box motif mediates SKP1 interaction, but no detectable CUL1 interaction in gathered evidence (pqac-00000006, pqac-00000007, pqac-00000009, pqac-00000012) | Correlative tumor expression analyses; knockdown and overexpression; ERα half-life/stability assays; ubiquitination assays; ERE-luciferase transcription assay; evaluation of ERα S118 phosphorylation; fulvestrant-sensitivity experiments; mutant ERα-Y537S studies (pqac-00000007, pqac-00000011, pqac-00000012) | FBXL16 altered in ~14% of invasive breast carcinomas and ~9% of lung adenocarcinomas; FBXL16 mRNA significantly higher in ER+ luminal A/B tumors vs normal tissue (one-way ANOVA *p*<0.01); silencing reduced ERα protein and phospho-S118 and increased fulvestrant responsiveness; no additional numeric effect sizes available in gathered evidence (pqac-00000006, pqac-00000009, pqac-00000011) | URL/DOI not available in gathered evidence | 2022 |


*Table: This table summarizes experimentally supported FBXL16 actions, targets, and methods across the studies retrieved in this chat. It highlights where evidence is strongest for substrate degradation or stabilization, and where conclusions remain more indirect.*