| Evidence type | Finding | Molecular partners/substrates | Biological context (cell type/tissue/disease) | Key quantitative/statistical data | Publication (with year) | URL/DOI | Citation context ID |
|---|---|---|---|---|---|---|---|
| Primary | Human FBXW12 functions as an SCF-family E3 ligase subunit that binds IL-22R and promotes its ubiquitination and degradation | IL-22R/IL-22RA1; SKP1; CUL1 | Human epithelial cells; Beas-2B and HeLa; mucosal/airway epithelial signaling | IL-22R half-life shortened from ~6 h to ~2 h with FBXW12 overexpression; representative statistics include *p*<0.05, n=4 in degradation assays | Franz et al. (2015) | https://doi.org/10.1155/2015/912713 | (pqac-00000021, pqac-00000026) |
| Primary | FBXW12 knockdown increases IL-22R abundance and enhances downstream IL-22 signaling | IL-22R; STAT3; ERK; JNK | HeLa epithelial cells; IL-22-responsive epithelial signaling | Relative p-STAT3 densitometry values reported as 0, 0.75, 1.5, 2.25 under assay conditions; IL-22 at 60 ng/mL for 60 min in signaling assays | Franz et al. (2015) | https://doi.org/10.1155/2015/912713 | (pqac-00000023, pqac-00000027) |
| Primary | FBXW12 behaves as an epithelial growth suppressor; depletion promotes proliferation and cell-cycle progression | FBXW12-linked IL-22R/STAT3/MAPK axis | HeLa epithelial cells | Control cell-cycle distribution approximately 80% G0/G1, 14% S, 4% G2/M; growth differences significant at 24 h and 40 h by ANOVA (*p*<0.05), 5 replicates/group | Franz et al. (2015) | https://doi.org/10.1155/2015/912713 | (pqac-00000022, pqac-00000025) |
| Review | FBXW12 degrades IL-22R and restricts lung epithelial proliferation; silencing FBXW12 is proposed as a therapeutic strategy for infection-induced epithelial damage | IL-22R | Infectious disease / lung epithelium / IL-22 biology | No new quantitative data reported in the review excerpt | Zhang et al. (2023) | https://doi.org/10.3390/pathogens12020176 | (pqac-00000009, pqac-00000028) |
| Review | FBXW12 is among F-box genes with high transcript levels in human testis, suggesting possible spermatogenesis-related roles, but direct mechanisms remain unresolved | Not specified for FBXW12 in excerpt | Human testis / spermatogenesis / male infertility context | Qualitative expression statement only; no numeric values in excerpt | Xuan et al. (2024) | https://doi.org/10.1186/s13619-024-00196-9 | (pqac-00000007) |
| Bioinformatic/annotation | FBXW12 maps to UniProt Q6X9E4 and is annotated as an E3 CRL adaptor with F-box and WD-repeat domains, supporting classification as an FBXW substrate receptor | F-box domain; WD repeats | Human protein annotation / domain architecture | Length reported as 394 aa in table entry | Poirson et al. (2017) | https://doi.org/10.1111/febs.14193 | (pqac-00000004, pqac-00000012) |
| Review (circRNA, not linear protein) | circ-FBXW12 is overexpressed in diabetic nephropathy models; its knockdown reduces proliferation, oxidative stress, and ECM production via the miR-31-5p/LIN28B axis | circ-FBXW12; miR-31-5p; LIN28B | Human mesangial cells / diabetic nephropathy | Epidemiology in review: ~1 in 3 people with diabetes in the USA have DN; globally DN occurs in 30–40% of patients with diabetes | Basudkar et al. (2023) | https://doi.org/10.1515/dine-2023-0007 | (pqac-00000006, pqac-00000029) |


*Table: This table summarizes direct and indirect evidence relevant to human FBXW12 (UniProt Q6X9E4), emphasizing experimentally supported function, pathway context, domain annotation, and translational implications. It distinguishes evidence on the linear FBXW12 protein from circ-FBXW12 literature to avoid gene-product conflation.*