| 2016 |
FBXO10 functions as an E3 ubiquitin ligase subunit that targets BCL2 for protein degradation in mantle cell lymphoma; loss of FBXO10 expression leads to BCL2 protein accumulation due to impaired ubiquitin-proteasome degradation. |
Protein expression analysis in MCL patient tissue microarray and cell lines; RNA-seq with BTK shRNA knockdown; BCL2 protein level assessment after FBXO10 loss |
Oncogene |
Medium |
27157620
|
| 2017 |
FBXO10 directly associates with RAGE (receptor for advanced glycation end products) to mediate its monoubiquitination at K374 and lysosomal degradation; PKCζ phosphorylates RAGE to promote this FBXO10-mediated degradation; FBXO10 depletion stabilizes RAGE and prevents ODN2006-mediated degradation. |
Co-immunoprecipitation of FBXO10 and RAGE; FBXO10 knockdown with RAGE protein stability assay; PKCζ overexpression/knockdown; identification of ubiquitination site K374 |
FASEB journal |
Medium |
28515150
|
| 2019 |
BCR stimulation induces rapid and reversible palmitoylation of the SCF-FBXO10 E3 ligase complex, causing FBXO10 relocalization from cytosol to the cell membrane, where it targets HGAL for ubiquitylation and degradation; FBXO10 recognition of HGAL is phosphorylation-independent and requires a single conserved HGAL residue H91; HGAL degradation via FBXO10 decreases BCR-induced calcium influx and phosphorylation of proximal BCR effectors, creating a negative autoregulatory feedback loop. |
Palmitoylation assay, subcellular fractionation/localization, ubiquitination assay, site-directed mutagenesis (H91), calcium influx measurements, phosphorylation assays of BCR effectors |
Leukemia |
High |
31570756
|
| 2021 |
FBXO10 promotes ubiquitination and degradation of RAGE in BV2 microglia cells; FBXO10 overexpression reduces RAGE accumulation, inhibits p38 MAPK and NF-κB signaling, and promotes M2 microglial polarization, while FBXO10 loss leads to RAGE stabilization and M1-skewed neuroinflammation. |
FBXO10 overexpression and RAGE knockdown in BV2 cells; ubiquitination assay; cytokine ELISA; in vivo CUS mouse model with viral FBXO10 overexpression; immunofluorescence for microglial phenotype |
CNS neuroscience & therapeutics |
Medium |
34492157
|
| 2024 |
FBXO10 undergoes geranylgeranyl lipid modification at cysteine 953 (C953), which is required for its trafficking to the outer mitochondrial membrane (OMM); this trafficking is orchestrated by interaction with PDE6δ (prenyl group-binding protein) and HSP90 chaperone; at the OMM, FBXO10 targets PGAM5 for polyubiquitylation and proteasomal degradation; the geranylgeranylation-deficient C953S mutant redistributes away from the OMM, fails to degrade PGAM5, and causes impaired mitochondrial ATP production, decreased membrane potential, increased fragmentation, and impaired myogenic differentiation. |
Geranylgeranylation site identification and C953S mutagenesis; subcellular fractionation and live-cell imaging; co-immunoprecipitation with PDE6δ and HSP90; comparative quantitative mass spectrometry (LFQ-MS/MS) of enriched mitochondria for substrate identification; PGAM5 ubiquitination assay; mitochondrial function assays (ATP, membrane potential); iPSC and murine myoblast differentiation assays |
Cell reports |
High |
38659932 39306844
|
| 2021 |
CRISPR/Cas9-engineered Fbxo10 loss-of-function mutations (D54K missense in FBOX domain and frameshift truncation) in mice did not increase BCL2 protein levels in B cells, nor did they increase mature B cell, germinal center B cell, or other BCL2-regulated lymphocyte subset numbers — indicating that FBXO10 does not regulate BCL2 as a sole non-redundant E3 ligase in mouse B lymphocytes. |
CRISPR/Cas9 knock-in mice with two distinct Fbxo10 mutations; Western blot for BCL2 protein; flow cytometry for lymphocyte subsets |
PloS one |
Medium |
33914737
|
| 2025 |
FBXO10 directly interacts with ACSL4 and mediates its ubiquitination and proteasomal degradation; FBXO10 silencing stabilizes ACSL4 and potentiates ferroptosis through amplified lipid peroxidation and Fe2+ accumulation in esophageal squamous cell carcinoma cells; this axis operates independently of the GPX4/SLC7A11 pathway. |
Co-immunoprecipitation and immunofluorescence colocalization of FBXO10 and ACSL4; FBXO10 silencing with ACSL4 ubiquitination and protein stability assay; ferroptosis markers (lipid peroxidation, Fe2+); in vivo xenograft with FBXO10 knockdown |
Journal of molecular histology |
Medium |
40616744
|
| 2025 |
FBXO10 directly interacts with FRMPD1 and mediates its K63-linked polyubiquitination, leading to FRMPD1 stabilization (not degradation); this post-translational stabilization of FRMPD1 promotes hepatocellular carcinoma cell proliferation. |
Co-immunoprecipitation of FBXO10 and FRMPD1; K63-linkage ubiquitination assay; FBXO10 silencing and overexpression with FRMPD1 protein level measurement; FRMPD1 rescue experiment |
Current issues in molecular biology |
Low |
40699790
|
| 2026 |
FBXO10 promotes ubiquitin-dependent degradation of RAS, thereby inactivating the RAS/ERK axis and suppressing Golgi stress and neuronal apoptosis; EZH2 represses FBXO10 expression by promoting H3K27me3 modification at the FBXO10 promoter, thus indirectly activating RAS/ERK-driven Golgi stress. |
Co-immunoprecipitation of FBXO10 and RAS; RAS ubiquitination assay; ChIP for H3K27me3 at FBXO10 promoter; FBXO10 knockdown/overexpression in H2O2-treated neuronal cell lines (HT-22, NSC34); Western blot for RAS, ERK, Golgi markers |
FASEB journal |
Medium |
41999223
|
| 2013 |
FBXO10/Fbxo10 transcription is activated via a PKC-dependent pathway: TPA activates PKCµ (an atypical PKC isoform), which signals through c-Fos/AP1 transcription factor binding to AP1-specific DNA elements in the Fbxo10 promoter; TPA induces endogenous FBXO10 mRNA and protein in Jurkat T cells with peak expression at 1.5–2.5 h. |
Luciferase reporter assays with Fbxo10 promoter constructs; PKC inhibitors; c-Fos identification as AP1 mediator; endogenous FBXO10 mRNA/protein induction by TPA in Jurkat cells |
Molecular carcinogenesis |
Medium |
24008983
|