| 2021 |
FBXO9 interacts with p53 and promotes its ubiquitination and degradation, thereby decreasing p53 protein stability; zoledronic acid suppresses FBXO9 expression, stabilizing p53 and inducing osteoclast ferroptosis. |
Co-immunoprecipitation, knockdown/overexpression functional assays, CCK-8 viability assay, ferroptosis marker measurement (Fe2+, ROS, MDA, GPX4, GSH) |
PeerJ |
Medium |
35003915
|
| 2019 |
FBXO9 is the substrate recognition component of an SCF E3 ubiquitin ligase; its loss in AML leads to increased proteasome activity and more aggressive leukemia in an inv(16) mouse model, indicating FBXO9 normally restrains proteasome activity. |
CRISPR/Cas9 conditional knockout mouse model, quantitative mass spectrometry of primary tumors, in vitro proteasome activity assay, bortezomib sensitivity assay |
Cancers |
High |
31684170
|
| 2020 |
Fbxo9, acting downstream of Sox10, functions as a substrate receptor of an SCF-type ubiquitin ligase that binds Neurog2 through its F-box motif and promotes Neurog2 ubiquitination and proteasomal destabilization, thereby directing neural crest progenitors toward glial rather than neuronal fate. |
Co-immunoprecipitation (Fbxo9–Neurog2 interaction), overexpression and knockdown in avian trunk neural crest, epistasis analysis with Sox10, transcriptional profiling, ubiquitination assay |
Proceedings of the National Academy of Sciences of the United States of America |
High |
32029586
|
| 2024 |
FBXO9, as part of the SKP1-cullin-1-RBX1 ubiquitin ligase complex, ubiquitinates the V-ATPase catalytic subunit ATP6V1A; this ubiquitination promotes ATP6V1A interaction with the cytoplasmic chaperone HSPA8 and its sequestration in the cytoplasm, thereby inhibiting functional V-ATPase assembly, reducing vesicular acidification, and suppressing pro-metastatic Wnt signaling in lung cancer cells. |
Mass spectrometry-based protein interaction studies, co-immunoprecipitation, immunoblot, CRISPR-Cas9 knockout, shRNA knockdown, migration/clonogenic/tumor sphere assays, in vivo mouse metastasis model, V-ATPase inhibitor treatment |
Experimental hematology & oncology |
High |
38486234
|
| 2022 |
FBXO9 targets FBXW7 for ubiquitination and degradation; ZNF143 acts as a direct upstream transcription factor of FBXO9, forming a ZNF143-FBXO9-FBXW7 regulatory axis that promotes HCC cell proliferation and metastasis. |
Loss- and gain-of-function experiments in vitro and in vivo, co-immunoprecipitation, ubiquitination assay, ChIP or reporter assay for ZNF143 as transcriptional regulator, drug sensitivity assay |
Frontiers in oncology |
Medium |
35847937
|
| 2025 |
The SCF-FBXO9-CRL1 E3 ligase complex recognizes YAP through a conserved degron motif and facilitates K48-linked polyubiquitination at lysine K76, promoting proteasomal degradation; GSK-3β-mediated phosphorylation of YAP at Ser338 and Thr342 is required for FBXO9 recognition, and Akt kinase modulates this axis by controlling GSK-3β phosphorylation status. |
Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), site-directed mutagenesis of YAP K76 and phosphosites, pharmacological inhibition of Akt/GSK-3β, chemosensitivity assays in cancer models |
The Journal of biological chemistry |
High |
40902979
|
| 2024 |
FBXO9 targets DPPA5 (a pluripotency-associated protein) for ubiquitylation and proteasomal degradation; FBXO9 silencing decreases DPPA5 degradation and facilitates induction of cellular reprogramming to pluripotency. |
RNAi screen during cellular reprogramming, FBXO9 silencing with functional pluripotency readouts, proteasomal degradation assay for DPPA5 |
Stem cells (Dayton, Ohio) |
Medium |
38227647
|
| 2026 |
FBXO9 directly binds PD-L1 protein and promotes its ubiquitination and degradation, thereby impeding PD-L1 maturation and impairing tumor immune evasion in pancreatic cancer; FBXO9 overexpression suppresses tumor growth and promotes cytotoxic T cell activation in vivo. |
Co-immunoprecipitation (FBXO9–PD-L1 interaction), ubiquitination assay, overexpression in vivo tumor model, cytotoxic T cell activation readout |
Frontiers in immunology |
Medium |
41646985
|
| 2016 |
The Drosophila FBXO9 homologue CG5961 is required for normal neuronal tissue formation; altered expression of CG5961 in dopaminergic neurons reduces lifespan, suggesting conserved neuronal function for this F-box protein family member. |
Targeted UAS-EP overexpression and RNAi knockdown in Drosophila dopaminergic neurons and eye, lifespan analysis, protein domain conservation analysis |
Genetics and molecular research |
Low |
27173356
|