Affinage

FBXL2

F-box/LRR-repeat protein 2 · UniProt Q9UKC9

Length
423 aa
Mass
47.1 kDa
Annotated
2026-06-09
26 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FBXL2 is the substrate-recognition subunit of an SCF-type E3 ubiquitin ligase (SCF-FBXL2) that controls the abundance of a broad set of cell-cycle, signaling, and inflammatory proteins by directing them to proteasomal degradation (PMID:28614300, PMID:22323446). A defining mechanistic feature is that FBXL2 frequently engages substrates through their calmodulin-binding (IQ) motifs rather than classical phosphodegrons, and calmodulin competes for these motifs to protect substrates from degradation, as shown for cyclin D2, cyclin D3, and CCTα (PMID:22323446, PMID:22020328, PMID:21343341). FBXL2 activity additionally requires geranylgeranylation-dependent membrane localization, and disrupting this localization pharmacologically (e.g. GGTi-2418) blocks degradation of membrane-associated substrates including IP3R3, EGFR, and HER2 (PMID:28614300, PMID:34635651, PMID:41612000). Through these activities FBXL2 limits ER-to-mitochondria Ca2+ transfer by degrading IP3R3 (PMID:28614300), restrains proliferation by destabilizing cyclins D2/D3 and the transcription factors FoxM1, E47, and T-bet (PMID:22323446, PMID:22020328, PMID:26790640, PMID:36113884, PMID:36460773), regulates cytokinesis via Aurora B turnover (PMID:23928698), and dampens inflammation by degrading NLRP3, pro-IL-1β, TRAF2, and TRAF6 (PMID:26674878, PMID:37004285, PMID:28378753). FBXL2 itself is a tightly regulated target: it is destabilized by FBXO3- and Smurf1-mediated ubiquitination and by O-GlcNAcylation, while substrate access is gated by competing partners such as PTEN (for IP3R3), Grp94 (for EGFR), and FUNDC1 (via the F-box domain) (PMID:26674878, PMID:31679690, PMID:32938669, PMID:34635651, PMID:33450386). Its expression is transcriptionally driven by SP1 and Nrf2 and suppressed by TNF-α/JNK signaling (PMID:32205409, PMID:40010729).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2011 High

    Established that FBXL2 acts as an SCF substrate receptor using a non-canonical recognition mode — binding calmodulin-binding IQ motifs rather than phosphodegrons — by showing it degrades cyclin D3 and the lipid-synthesis enzyme CCTα with calmodulin acting as a competitive protector.

    Evidence Ectopic expression/RNAi, in vitro ubiquitination, calmodulin competition assays, domain mapping, Golgi fractionation, and xenograft/murine models

    PMID:21343341 PMID:22020328 PMID:22024926

    Open questions at the time
    • Structural basis of IQ-motif recognition by the FBXL2 LRR domain not resolved
    • Generality of calmodulin competition across all substrates untested
  2. 2012 High

    Extended the calmodulin-competition model to cyclin D2, demonstrating FBXL2 controls G0 arrest and apoptosis and linking its activity to leukemia biology.

    Evidence Ectopic FBXL2, RNAi, ubiquitination and calmodulin competition assays, cell-cycle analysis, patient sample analysis

    PMID:22323446

    Open questions at the time
    • In vivo requirement for cyclin D2 turnover not established
    • Relative contribution of D2 vs D3 to arrest unclear
  3. 2013 High

    Resolved how FBXL2 sustains growth-factor signaling and how it regulates mitosis: it selectively degrades the free p85β pool of PI(3)K to promote p110-IRS1 coupling, and it degrades Aurora B at the midbody during cytokinesis.

    Evidence Affinity-MS, in vitro ubiquitylation, phospho-mutant analysis, lysine-to-arginine mutagenesis of Aurora B, IRS1 binding and autophagy readouts, xenograft with activator BC-1258

    PMID:23604317 PMID:23928698

    Open questions at the time
    • How Tyr655 phosphorylation gates p85β binding structurally not defined
    • Coordination of Aurora B degradation timing with mitotic exit unresolved
  4. 2015 Medium

    Defined upstream control of FBXL2 itself by showing FBXO3 ubiquitinates and degrades FBXL2, with epistatic consequences for TRAF2 stability and AMPA receptor trafficking in neuropathic pain.

    Evidence Spinal nerve ligation model, intrathecal siRNA/BC-1215, Co-IP, GluR1 trafficking and behavioral assays

    PMID:26674878

    Open questions at the time
    • Direct TRAF2 ubiquitination by FBXL2 inferred from epistasis, not reconstituted
    • In vivo complexity limits assignment of effects to FBXL2 alone
  5. 2016 Medium

    Broadened the FBXL2 substrate repertoire to transcription factors and active-zone proteins, identifying FoxM1 and RIM1α as targets controlling proliferation and presynaptic CaV2.2 signaling respectively.

    Evidence Tandem MS, Co-IP, ubiquitination assays, subcellular fractionation, electrophysiology, in vivo nerve ligation model

    PMID:26790640 PMID:27629721

    Open questions at the time
    • Recognition motifs on FoxM1 and RIM1α not mapped
    • Single-lab findings without reciprocal validation
  6. 2020 High

    Identified additional layers of FBXL2 regulation: FUNDC1 binds the F-box domain to gate IP3R3 turnover and cardiac mitochondrial Ca2+ homeostasis, and SP1 transcription (suppressed by TNF-α/JNK) drives FBXL2 expression required for myogenic differentiation.

    Evidence MS, Co-IP with F-box deletion mutants, FUNDC1-/- mouse on high-fat diet; ChIP, EMSA, promoter reporters, SP1 phospho-analysis, differentiation assays

    PMID:32205409 PMID:32938669

    Open questions at the time
    • How FUNDC1 binding stabilizes FBXL2 mechanistically unclear
    • JNK target site on SP1 not definitively mapped
  7. 2021 High

    Established competitive substrate shielding and proteostatic control as recurring themes by showing Grp94 blocks EGFR degradation by FBXL2, and Smurf1 (driven by FOSL1) degrades FBXL2 to activate Wnt/β-catenin signaling.

    Evidence Reciprocal Co-IP, proteasome inhibition, knockdown/overexpression, Wnt reporter, nebivolol treatment, xenograft models

    PMID:33450386 PMID:34635651

    Open questions at the time
    • Structural basis of Grp94-EGFR-FBXL2 competition not resolved
    • Smurf1-FBXL2 link is single-lab
  8. 2022 Medium

    Connected FBXL2 to immune and stemness regulation by demonstrating degradation of T-bet (modulated by TNF-α) in lung allograft rejection and of E47 to suppress breast cancer stem-cell traits.

    Evidence Co-IP, ubiquitination assays, dose-response transfection, orthotopic lung transplant and xenograft models, mammosphere and flow assays, nebivolol treatment

    PMID:36113884 PMID:36460773

    Open questions at the time
    • Degron determinants on T-bet and E47 not defined
    • Specificity over related bHLH/T-box factors untested
  9. 2023 Medium

    Demonstrated FBXL2 directly restrains inflammasome output by ubiquitinating and degrading NLRP3 and pro-IL-1β (but not pro-caspase-1), positioning FBXL2 stabilization (via FBXO3 inhibition) as a brake on IL-1β secretion.

    Evidence Co-IP, ubiquitination assays, MG-132 rescue, FBXL2 overexpression, BC-1215 treatment, ELISA

    PMID:37004285

    Open questions at the time
    • Substrate selectivity between NLRP3 and pro-IL-1β not dissected
    • Single-lab study
  10. 2026 High

    Resolved a clinically actionable substrate by mapping FBXL2-driven HER2 polyubiquitination at K747, showing that blocking FBXL2 membrane localization elevates surface HER2 and sensitizes HER2-low TNBC to antibody-drug conjugates.

    Evidence Co-IP, K747 site-directed mutagenesis, proteasomal degradation assays, membrane-localization inhibition, lipid nanoparticle delivery, xenograft models

    PMID:41612000

    Open questions at the time
    • Whether HER2 is recognized via an IQ-like motif unknown
    • Endogenous physiological context of HER2 regulation by FBXL2 untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how FBXL2 achieves selectivity across its unusually broad substrate range and how its membrane localization, calmodulin/calcium status, and competing partners are integrated to license degradation of specific substrates in a given cell.
  • No structure of FBXL2 bound to any substrate
  • No global rules distinguishing IQ-motif from non-IQ substrates
  • Quantitative interplay of calcium, calmodulin, and membrane targeting unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 11 GO:0016874 ligase activity 5 GO:0098772 molecular function regulator activity 4
Localization
GO:0005886 plasma membrane 3 GO:0005815 microtubule organizing center 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-168256 Immune System 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 2
Partners
CALMODULINEGFRFBXO3FUNDC1GRP94IP3R3PTENSMURF1
Complex memberships
SCF-FBXL2 (SCF-type E3 ubiquitin ligase)

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2017 FBXL2 (as the substrate-recognition subunit of SCF-FBXL2 ubiquitin ligase) binds IP3R3 and targets it for ubiquitin-, p97- and proteasome-mediated degradation, limiting Ca2+ release from the ER into mitochondria. PTEN competes with FBXL2 for IP3R3 binding, counteracting this degradation to promote Ca2+-dependent apoptosis. Loss of PTEN accelerates FBXL2-dependent IP3R3 degradation, and FBXL2 localization (and thus activity) requires geranylgeranylation. Co-immunoprecipitation, knock-in FBXL2-insensitive IP3R3 mutant clones, FBXL2 knockdown, Ca2+ flux assays, xenograft models, GGTi-2418 (geranylgeranyl transferase inhibitor) treatment Nature High 28614300
2013 FBXL2 interacts specifically with the pool of p85β PI(3)K regulatory subunit that is free of p110 catalytic subunits and targets it for ubiquitylation and proteasomal degradation, dependent on p85β's CaaX motif. Phosphorylation of p85β on Tyr655 inhibits its binding to FBXL2, while dephosphorylation by PTPL1 stimulates binding and degradation. FBXL2-mediated p85β degradation promotes p110 association with IRS1 and sustains PI(3)K signaling; loss of this degradation inhibits PI(3)K and promotes autophagy. Affinity purification/mass spectrometry of FBXL2 interactors, Co-IP, in vitro ubiquitylation assay, phospho-mutant analysis, IRS1 binding assays, autophagy readouts Nature cell biology High 23604317
2012 SCF-FBXL2 ubiquitinates and destabilizes cyclin D2, leading to G0 phase arrest and apoptosis. FBXL2 recognizes a calmodulin-binding motif within cyclin D2 (not a phosphodegron). Calmodulin competes with FBXL2 for occupancy of this motif, protecting cyclin D2 from degradation. Ectopic FBXL2 expression, RNAi knockdown, ubiquitination assay, cell cycle analysis, calmodulin competition assay, leukemia patient sample analysis Blood High 22323446
2011 SCF-FBXL2 mediates polyubiquitination and proteasomal degradation of cyclin D3, causing G2/M-phase arrest, supernumerary centrosomes, and apoptosis in lung cancer cells. FBXL2 recognizes a calmodulin-binding motif in cyclin D3 (not a phosphodegron); calmodulin competes with FBXL2 for this site, protecting cyclin D3. Both cyclin D3 and FBXL2 colocalize within the centrosome. Ectopic expression and RNAi, ubiquitination assay, cell cycle and centrosome analysis, co-localization imaging, calmodulin competition assay, xenograft tumor assay Oncogene High 22020328
2011 During Pseudomonas aeruginosa infection, FBXL2 is activated by calcium influx and localizes to the Golgi complex, where it monoubiquitinates and degrades CCTα (the rate-limiting enzyme for phosphatidylcholine synthesis) via binding to the IQ motif of CCTα through its C-terminus. Calmodulin traffics to the Golgi, binds FBXL2 (residues 80–90) via its C-terminus, and competes with FBXL2 for occupancy of the CCTα IQ motif, antagonizing FBXL2 activity. Co-IP, domain-mapping mutagenesis, calcium influx assays, Golgi fractionation/localization, RNAi knockdown, calmodulin gene transfer in murine pneumonia model Molecular and cellular biology High 21343341
2013 SCF-FBXL2 mediates ubiquitination and proteasomal degradation of Aurora B kinase within the midbody during cytokinesis. Key ubiquitin acceptor lysines K102, K103, and K207 on Aurora B were identified; a triple K→R mutant resists SCF-FBXL2-directed polyubiquitination and causes anaphase delay and apoptosis when overexpressed. Ubiquitination assay, lysine-to-arginine mutagenesis of Aurora B, overexpression and knockdown, mitotic arrest/apoptosis assays, xenograft tumor model with small-molecule FBXL2 activator BC-1258 Cell death & disease High 23928698
2011 SCF-FBXL2 impairs cell proliferation by mediating cyclin D3 polyubiquitination and degradation; cyclin D3 and FBXL2 colocalize at the centrosome. FBXL2 overexpression disrupts cyclin D3 association with centrosomal assembly proteins Aurora A, Plk4, and CDK11. Ectopic expression and RNAi, ubiquitination assay, co-localization imaging, co-immunoprecipitation of cyclin D3 with centrosomal proteins Cell cycle (Georgetown, Tex.) Medium 22024926
2015 Fbxo3 promotes Fbxl2 ubiquitination and degradation; this relieves Fbxl2-mediated ubiquitination of TRAF2, leading to TRAF2 accumulation, TNIK activation, GluR1 phosphorylation, and trafficking of GluR1-containing AMPA receptors to the plasma membrane in dorsal horn neurons, contributing to neuropathic allodynia. Spinal nerve ligation rat model, intrathecal siRNA/inhibitor (BC-1215) injection, co-immunoprecipitation, GluR1 trafficking assays, behavioral allodynia measurement The Journal of neuroscience Medium 26674878
2016 Fbxo3 inhibits Fbxl2-mediated ubiquitination and degradation of the active zone protein RIM1α in the spinal dorsal horn. Deubiquitinated RIM1α accumulates in synaptic plasma membranes, directly binds CaV2.2, and increases presynaptic CaV2.2 expression, driving neuropathic allodynia. Spinal nerve ligation rat model, intrathecal BC-1215 (Fbxo3 inhibitor), siRNA knockdown of Fbxl2 and RIM1α, co-immunoprecipitation, subcellular fractionation, electrophysiology (sEPSC) The Journal of neuroscience Medium 27629721
2016 FBXL2 interacts with the transcription factor FoxM1 and promotes its ubiquitination and proteasomal degradation in gastric cancer cells, thereby reducing expression of FoxM1 downstream targets Cdc25B and p27 and inhibiting cell proliferation and invasion. Tandem mass spectrometry, co-immunoprecipitation, ubiquitination assay, ectopic expression and knockdown, cell proliferation/invasion assays FEBS letters Medium 26790640
2019 O-GlcNAcylation promotes FBXL2 ubiquitination and degradation (FBXL2 is itself a target of ubiquitin-mediated degradation), leading to stabilization of FOXM1 (an FBXL2 ubiquitination substrate) and cancer cell proliferation. The O-GlcNAcase inhibitor Thiamet G reduces FBXL2-FOXM1 interaction and FOXM1 ubiquitination. Co-immunoprecipitation, ubiquitination assay, pharmacological O-GlcNAcylation manipulation, western blot, cell proliferation assays Biochemical and biophysical research communications Medium 31679690
2020 FUNDC1 interacts with FBXL2 via FBXL2's F-box domain; loss of FUNDC1 accelerates FBXL2 degradation and decelerates IP3R3 degradation, leading to mitochondrial Ca2+ overload. The FUNDC1-FBXL2 interaction thus functions as a gatekeeper for IP3R3 protein levels and mitochondrial Ca2+ homeostasis in the heart. Mass spectrometry, co-immunoprecipitation, FUNDC1-/- mouse model on high-fat diet, truncated F-box deletion mutants, FBXL2 overexpression/transfection, IP3R3 inhibition Science advances High 32938669
2021 FBXL2 targets EGFR (and TKI-resistant EGFR mutants) for proteasomal degradation. Grp94 (glucose-regulated protein 94) protects EGFR from this degradation by blocking FBXL2 binding to EGFR. Disruption of FBXL2 membrane localization (by GGTi-2418) or upregulation of FBXL2 expression (by nebivolol) reduces EGFR levels and inhibits NSCLC growth. Co-IP, proteasome inhibitor experiments, FBXL2 knockdown/overexpression, Grp94 manipulation, nebivolol treatment, xenograft models Nature communications High 34635651
2021 Smurf1 ubiquitinates and degrades FBXL2; loss of FBXL2 leads to activation of Wnt/β-catenin signaling, promoting colorectal cancer progression. FOSL1 drives this pathway by upregulating Smurf1. Co-IP, ubiquitination assay, FBXL2 and Smurf1 knockdown/overexpression, Wnt/β-catenin reporter, xenograft metastasis assay Pharmacological research Medium 33450386
2022 FBXL2 polyubiquitinates the transcription factor T-bet and co-immunoprecipitates with T-bet; ectopic FBXL2 expression reduces T-bet protein in a dose-dependent manner. TNF-α negatively regulates both FBXL2 mRNA and protein levels, providing cross-regulation of FBXL2 and T-bet during lung allograft rejection. Co-immunoprecipitation/pulldown, ubiquitination assay, FBXL2 transfection with dose-response, orthotopic lung transplant mouse model, immunohistochemistry, costimulation blockade treatment Journal of immunology Medium 36113884
2022 FBXL2 targets transcription factor E47 for polyubiquitin- and proteasome-mediated degradation, inhibiting breast cancer stem cell stemness (CD44high/CD24low subpopulation, mammosphere formation) and overcoming paclitaxel resistance. Nebivolol (a β1 receptor inhibitor) activates FBXL2 expression to achieve this effect. Co-IP, ubiquitination assay, ectopic expression and knockdown, flow cytometry, mammosphere assay, in vivo xenograft, nebivolol treatment Oncogene Medium 36460773
2023 FBXL2 binds to and ubiquitinates both NLRP3 and pro-IL-1β (but not pro-caspase-1), targeting them for proteasome-mediated degradation. BC-1215 (an FBXO3 inhibitor that prevents FBXL2 ubiquitination/degradation) upregulates FBXL2 levels and thereby reduces NLRP3 and pro-IL-1β protein levels, suppressing ATP-induced IL-1β secretion. Co-immunoprecipitation, ubiquitination assay, proteasome inhibitor (MG-132) rescue, FBXL2 overexpression, BC-1215 pharmacological treatment, western blot and ELISA Biochemical and biophysical research communications Medium 37004285
2020 TNF-α suppresses Fbxl2 mRNA expression in skeletal myoblasts by activating JNK-mediated phosphorylation of SP1, which impairs SP1 binding to the Fbxl2 core promoter (localized to bp -160 to +42). SP1 transcriptional activation of Fbxl2 is required for myogenic differentiation; FBXL2 knockdown in myoblasts activates MAP kinases and NF-κB, promotes proliferation, and impairs myotube formation. Chromatin immunoprecipitation, gel shift (EMSA), promoter reporter assays, SP1 phospho-site analysis, RNAi knockdown, myogenic differentiation assays, mRNA stability measurement Molecular and cellular biology Medium 32205409
2017 FBXL2-mediated ubiquitination and degradation of TRAF6 is implicated in LIPUS-mediated protection against polyethylene debris-induced periprosthetic inflammatory loosening; LIPUS strengthens this FBXL2-TRAF6 ubiquitination pathway. Gene overexpression and siRNA in RAW264.7 macrophages, western blot for FBXL2 and TRAF6 levels, inflammatory cytokine measurement, LIPUS treatment Scientific reports Low 28378753
2026 FBXL2 promotes HER2 polyubiquitination at lysine K747 and proteasomal degradation, reducing HER2 surface expression. Blocking FBXL2 membrane localization with GGTi-2418 or ketoconazole elevates HER2 expression on the plasma membrane of HER2-IHC 0 TNBC cells, sensitizing them to trastuzumab deruxtecan. Co-IP, site-directed mutagenesis (K747 ubiquitination site), proteasomal degradation assays, FBXL2 membrane localization inhibition, lipid nanoparticle delivery, xenograft models Nature cancer High 41612000
2025 Nrf2 transcriptionally upregulates FBXL2 expression; FBXL2 promotes NLRP3 ubiquitination-mediated degradation and suppresses pyroptosis. High glucose treatment decreases Nrf2 and FBXL2 and enhances NLRP3-mediated pyroptosis; scutellarin reverses this by increasing Nrf2/FBXL2. Dual-luciferase reporter assay (Nrf2 binding to FBXL2 promoter), immunoprecipitation for ubiquitination, western blotting, Nrf2 knockdown, FBXL2 knockdown, NLRP3 activation rescue Endocrine journal Medium 40010729

Source papers

Stage 0 corpus · 26 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 PTEN counteracts FBXL2 to promote IP3R3- and Ca2+-mediated apoptosis limiting tumour growth. Nature 208 28614300
2020 FUNDC1 interacts with FBXL2 to govern mitochondrial integrity and cardiac function through an IP3R3-dependent manner in obesity. Science advances 118 32938669
2013 FBXL2- and PTPL1-mediated degradation of p110-free p85β regulatory subunit controls the PI(3)K signalling cascade. Nature cell biology 109 23604317
2012 F-box protein FBXL2 targets cyclin D2 for ubiquitination and degradation to inhibit leukemic cell proliferation. Blood 85 22323446
2011 F-box protein FBXL2 exerts human lung tumor suppressor-like activity by ubiquitin-mediated degradation of cyclin D3 resulting in cell cycle arrest. Oncogene 66 22020328
2013 Skp-cullin-F box E3 ligase component FBXL2 ubiquitinates Aurora B to inhibit tumorigenesis. Cell death & disease 56 23928698
2021 FBXL2 counteracts Grp94 to destabilize EGFR and inhibit EGFR-driven NSCLC growth. Nature communications 54 34635651
2011 Calmodulin antagonizes a calcium-activated SCF ubiquitin E3 ligase subunit, FBXL2, to regulate surfactant homeostasis. Molecular and cellular biology 47 21343341
2015 Fbxo3-Dependent Fbxl2 Ubiquitination Mediates Neuropathic Allodynia through the TRAF2/TNIK/GluR1 Cascade. The Journal of neuroscience : the official journal of the Society for Neuroscience 35 26674878
2011 FBXL2 is a ubiquitin E3 ligase subunit that triggers mitotic arrest. Cell cycle (Georgetown, Tex.) 33 22024926
2021 FOSL1 promotes tumorigenesis in colorectal carcinoma by mediating the FBXL2/Wnt/β-catenin axis via Smurf1. Pharmacological research 32 33450386
2016 Spinal Fbxo3-Dependent Fbxl2 Ubiquitination of Active Zone Protein RIM1α Mediates Neuropathic Allodynia through CaV2.2 Activation. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 27629721
2016 F-box protein FBXL2 inhibits gastric cancer proliferation by ubiquitin-mediated degradation of forkhead box M1. FEBS letters 28 26790640
2020 MiR-346-5p promotes colorectal cancer cell proliferation in vitro and in vivo by targeting FBXL2 and activating the β-catenin signaling pathway. Life sciences 21 31953162
2017 Low-intensity pulsed ultrasound (LIPUS) prevents periprosthetic inflammatory loosening through FBXL2-TRAF6 ubiquitination pathway. Scientific reports 20 28378753
2022 FBXL2 promotes E47 protein instability to inhibit breast cancer stemness and paclitaxel resistance. Oncogene 16 36460773
2019 Circular RNA SMARCA5 inhibits gastric cancer progression through targeting the miR-346/ FBXL2 axis. RSC advances 16 35515212
2020 Tumor Necrosis Factor Alpha Regulates Skeletal Myogenesis by Inhibiting SP1 Interaction with cis-Acting Regulatory Elements within the Fbxl2 Gene Promoter. Molecular and cellular biology 15 32205409
2014 A lack of association between polymorphisms of three positional candidate genes (CLASP2 , UBP1, and FBXL2) and canine disorder of sexual development (78,XX; SRY -negative). Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation 7 24994500
2023 BC-1215 inhibits ATP-induced IL-1β secretion via the FBXL2-mediated ubiquitination and degradation of not only NLRP3, but also pro-IL-1β in LPS-primed THP-1 cells. Biochemical and biophysical research communications 6 37004285
2019 O-GlcNAcylation-mediated degradation of FBXL2 stabilizes FOXM1 to induce cancer progression. Biochemical and biophysical research communications 6 31679690
2024 Methylation regulation for FUNDC1 stability in childhood leukemia was up-regulated and facilitates metastasis and reduces ferroptosis of leukemia through mitochondrial damage by FBXL2. Open medicine (Warsaw, Poland) 3 38947217
2022 Cross-Regulation of F-Box Protein FBXL2 with T-bet and TNF-α during Acute and Chronic Lung Allograft Rejection. Journal of immunology (Baltimore, Md. : 1950) 3 36113884
2025 Scutellarin mitigates high glucose-induced pyroptosis in diabetic atherosclerosis: Role of Nrf2-FBXL2-mediated NLRP3 degradation. Endocrine journal 2 40010729
2024 FUNDC1 mediated mitochondria-dependent ferroptosis of epithelial cells in model of asthma by FBXL2/ar/GPX4 signaling pathway of SUMO1 at K136. International reviews of immunology 2 39323222
2026 Targeted inhibition of FBXL2 confers susceptibility of HER2-negative breast cancer to trastuzumab deruxtecan. Nature cancer 1 41612000

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