Affinage

FBXO31

F-box only protein 31 · UniProt Q5XUX0

Length
539 aa
Mass
60.7 kDa
Annotated
2026-06-09
42 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FBXO31 is the substrate-recognition subunit of an SCF (SKP1–CUL1–RBX1) E3 ubiquitin ligase that enforces cell-cycle checkpoints and genome stability by targeting cell-cycle and signaling regulators for K48-linked polyubiquitination and proteasomal degradation (PMID:16357137, PMID:19412162). Its best-defined role is in the DNA-damage response: γ-irradiation triggers ATM-mediated phosphorylation of FBXO31, causing its accumulation and the degradation of cyclin D1 to impose G1 arrest (PMID:19412162), and FBXO31 likewise directs degradation of MDM2 to stabilize p53 and arrest growth after genotoxic stress (PMID:26124108). FBXO31 also restrains cell-cycle progression at additional points by degrading the licensing factor Cdt1 in G2 to block re-replication (PMID:24828503), FOXM1 at the G2/M transition to preserve genomic stability (PMID:27568981), and by keeping cyclin A low during G1 to prevent premature replication and double-strand breaks (PMID:31413110). A crystal structure of the SKP1–FBXO31 complex bound to a phosphorylated cyclin D1 C-terminal peptide showed that FBXO31 uses a unique two-β-barrel substrate-binding domain in which the free C-terminal carboxylate of cyclin D1 inserts into a cavity of the C-terminal β-barrel, and SCF-FBXO31 can ubiquitinate cyclin D1 independently of phosphorylation (PMID:29279382); this β-barrel pocket was later shown to act as a reader of C-terminal amide-bearing proteins (CTAPs), recruiting chemically damaged amidated proteins to the SCF for degradation as a protein-quality-control surveillance mechanism, with a dominant neurodevelopmental disorder mutation reversing this substrate specificity (PMID:39880951). FBXO31 levels are tightly controlled: APC/C (CDH1/CDC20) degrades FBXO31 via a D-box following AKT-mediated Ser33 phosphorylation, while DNA-damage-induced ATM phosphorylation at Ser278 disrupts this recognition to permit FBXO31 accumulation (PMID:29343641), and FBXO46 maintains basal FBXO31 levels through an RXXR-motif-dependent reciprocal feedback loop (PMID:30171069). Beyond the checkpoint network, FBXO31 degrades a broad set of substrates—including MKK6 to dampen p38 MAPK and apoptosis (PMID:24936062), DUSP6 to tune ERK/PI3K-AKT signaling in prostate tumors (PMID:34686346), Snail1 to suppress EMT (PMID:29117943), c-Myc (PMID:34706096), GPX4 and ABL2 to sensitize cancer cells to ferroptosis (PMID:36269678, PMID:42170439), SIRT2 (PMID:38216561), and OGT to control O-GlcNAcylation homeostasis (PMID:39894887)—and it controls neuronal morphogenesis by degrading the polarity protein Par6c at the centrosome to specify axon identity and migration in the developing cerebellum (PMID:23469015). Its C-terminal amide recognition pocket has been engineered to support targeted protein degradation using amidated chemical recruiters (PMID:41963263).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2005 Medium

    Established FBXO31 as a genuine SCF E3 ligase subunit with cell-cycle inhibitory function, setting the framework for all subsequent substrate work.

    Evidence Co-IP showing association with Skp1/Roc-1/Cullin-1 plus ectopic expression causing G1 arrest in breast cancer cells

    PMID:16357137

    Open questions at the time
    • No substrate identified at this stage
    • Mechanism of G1 arrest unknown
  2. 2009 High

    Defined the first FBXO31 substrate and linked it to the DNA-damage checkpoint, answering how FBXO31 enforces G1 arrest.

    Evidence Co-IP, F-box deletion, RNAi epistasis, proteasome assays, ATM dependency in a γ-irradiation model targeting cyclin D1

    PMID:19412162

    Open questions at the time
    • Structural basis of cyclin D1 recognition not yet defined
    • ATM phosphorylation site on FBXO31 not mapped
  3. 2013 Medium

    Extended FBXO31 function to neuronal development, showing it acts at the centrosome to specify axon identity via degradation of a polarity factor.

    Evidence Centrosomal immunofluorescence, Co-IP of Par6c, RNAi and in vivo cerebellar migration assays

    PMID:23469015

    Open questions at the time
    • Single lab
    • Whether Par6c degradation fully accounts for the axon phenotype unresolved
  4. 2014 High

    Broadened the cell-cycle role by showing FBXO31 degrades Cdt1 in G2 and MKK6 to control re-replication and stress signaling respectively.

    Evidence Co-IP, in-cell ubiquitylation assays, cell-cycle-synchronized degradation, Lys48 linkage specificity, re-replication and p38 readouts

    PMID:24828503 PMID:24936062

    Open questions at the time
    • Degrons on these substrates only partially mapped
    • Coordination of multiple substrate targeting per cell-cycle phase unclear
  5. 2015 High

    Showed FBXO31 stabilizes p53 by degrading MDM2 after damage, connecting FBXO31 to the central tumor-suppressor axis.

    Evidence Reciprocal Co-IP, ATM epistasis, RNAi, proteasome inhibition with p53/MDM2 Western blots

    PMID:26124108

    Open questions at the time
    • Relative contribution of cyclin D1 vs MDM2 degradation to arrest not quantified
  6. 2016 High

    Identified FOXM1 as a G2/M substrate and demonstrated FBXO31 has additional mitotic substrates beyond FOXM1.

    Evidence Co-IP, ubiquitination assay, double-knockdown epistasis, live-cell imaging of mitosis

    PMID:27568981

    Open questions at the time
    • Identity of the additional mitotic substrate(s) unknown
  7. 2017 High

    Solved the structural basis of substrate recognition, revealing a unique two-β-barrel domain that reads the free C-terminal carboxylate and enables phosphorylation-independent ubiquitination.

    Evidence X-ray crystallography of Skp1–FBXO31 with phospho-cyclin D1 peptide, biophysical binding, in vitro ubiquitination, mutagenesis

    PMID:29279382

    Open questions at the time
    • Generality of C-terminal-tail recognition to other substrates not yet tested at this stage
  8. 2017 Medium

    Showed FBXO31 degrades Snail1 to suppress EMT, expanding its tumor-suppressive substrate repertoire.

    Evidence Co-IP, ubiquitination assay, phospho/domain mutagenesis, EMT markers, xenograft

    PMID:29117943

    Open questions at the time
    • Single lab
    • Snail1 phosphorylation kinase not identified
  9. 2018 High

    Defined the upstream control of FBXO31 abundance, showing APC/C and FBXO46 keep it low and that ATM-dependent phosphorylation switches that off after damage.

    Evidence Co-IP, D-box/Ser33/Ser278/RXXR mutagenesis, kinase inhibition, ubiquitination assays, demonstrated FBXO46–FBXO31 negative feedback

    PMID:29343641 PMID:30171069

    Open questions at the time
    • How multiple competing degradation inputs are integrated quantitatively is unresolved
  10. 2019 Medium

    Connected FBXO31 loss directly to genomic instability through failure to restrain cyclin A in G1, and linked it to TGF-β/fibrogenesis via Smad7.

    Evidence DNA combing, γH2AX foci, flow cytometry for cyclin A; Co-IP, co-localization and ubiquitination for Smad7

    PMID:31413110 PMID:31680332

    Open questions at the time
    • Whether cyclin A is a direct FBXO31 substrate not established
    • Single labs
  11. 2022 High

    Established FBXO31 as a regulator of ERK/AKT signaling and ferroptosis, and revealed reciprocal transcriptional repression by its own substrate c-Myc.

    Evidence Co-IP, ubiquitylation assays, in vivo tumor models, pharmacological rescue (DUSP6 inhibitor), GPX4 rescue, ChIP for c-Myc at the FBXO31 promoter

    PMID:34686346 PMID:34706096 PMID:36269678

    Open questions at the time
    • Context-dependence of tumor-suppressive vs other roles across tissues unresolved
    • Some substrate findings from single labs
  12. 2025 High

    Reframed the β-barrel pocket as a quality-control reader of C-terminal amide-bearing damaged proteins, generalizing the structural recognition principle and explaining a neurodevelopmental disorder mutation.

    Evidence CRISPR screen, semi-synthetic chemical biology, structure-informed pocket analysis, in vitro ubiquitylation, mutagenesis, disease-mutation characterization; also OGT identified as a substrate via CRISPR screen

    PMID:39880951 PMID:39894887

    Open questions at the time
    • Endogenous physiological CTAP substrate landscape not enumerated
    • Mechanism by which the disorder mutation rewires specificity in vivo incompletely defined
  13. 2026 Medium

    Demonstrated FBXO31 can be co-opted for targeted protein degradation and identified ABL2 and SIRT2 as further substrates, broadening both its biology and its therapeutic utility.

    Evidence Ternary complex and TPD assays with amidated recruiters, F-box mutagenesis, Co-IP, ubiquitination and ferroptosis assays, tumor models; m6A/YTHDF1 control of FBXO31 translation for SIRT2

    PMID:38216561 PMID:41963263 PMID:42170439

    Open questions at the time
    • TPD work is biochemical/cellular, not validated in vivo
    • Single labs

Open questions

Synthesis pass · forward-looking unresolved questions
  • The full endogenous substrate spectrum of FBXO31 and how its expanding roles (checkpoint enforcement, protein-quality surveillance, ferroptosis, signaling) are coordinated within a given cell remain unresolved.
  • No unbiased proteome-wide substrate map reported
  • Determinants of tissue-specific substrate choice unknown
  • Whether cyclin A and cofilin-1 are direct substrates not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 7 GO:0016874 ligase activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005815 microtubule organizing center 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-73894 DNA Repair 2
Partners
CCND1CDT1CUL1FBXO46FOXM1MDM2RBX1SKP1
Complex memberships
SCF (SKP1-CUL1-RBX1-FBXO31) E3 ubiquitin ligase

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 FBXO31 is a component of an SCF ubiquitin ligase complex, associating with Skp1, Roc-1, and Cullin-1, and its ectopic expression induces G1 cell cycle arrest in breast cancer cell lines. Co-immunoprecipitation (association with Skp1, Roc-1, Cullin-1); ectopic expression with cell cycle analysis by flow cytometry Cancer Research Medium 16357137
2009 FBXO31 directly binds cyclin D1 and mediates its proteasomal degradation, requiring the F-box motif of FBXO31 and phosphorylation of cyclin D1 at Thr286, resulting in G1 arrest. DNA damage (gamma-irradiation) induces FBXO31 accumulation through ATM-mediated phosphorylation of FBXO31, and FBXO31 knockdown prevents efficient G1 arrest after DNA damage. Co-immunoprecipitation, RNAi knockdown, ectopic expression, proteasome inhibitor assays, domain mutagenesis (F-box deletion), ATM kinase epistasis, gamma-irradiation DNA damage model Nature High 19412162
2013 FBXO31-SCF localizes to the centrosome and regulates neuronal morphogenesis, axonal identity, dendrite growth, and neuronal migration in developing cerebellar cortex. FBXO31 interacts with and targets the polarity protein Par6c for proteasomal degradation to control axon (but not dendrite) growth. Centrosomal localization (immunofluorescence), Co-immunoprecipitation, RNAi knockdown in cerebellar neurons, in vivo migration assays in cerebellar cortex PLoS One Medium 23469015
2014 FBXO31 interacts with Cdt1 (DNA replication licensing factor) and mediates its ubiquitylation and proteasomal degradation specifically during G2 phase, independently of previously described Cdt1 proteolysis pathways (CRL4-Cdt2 and SCF-Skp2), preventing re-replication. Targeting is mediated through the N-terminus of Cdt1. Co-immunoprecipitation, ubiquitylation assay, cell cycle-synchronized degradation assay, RNAi knockdown with re-replication readout (flow cytometry) Journal of Biological Chemistry High 24828503
2014 FBXO31 (as part of SCF complex) binds MKK6 and mediates its Lys48-linked polyubiquitination and proteasomal degradation, thereby negatively regulating p38 MAPK signaling and protecting cells from stress-induced apoptosis. Co-immunoprecipitation, ubiquitin linkage-specific assay (Lys48), RNAi knockdown, ectopic expression with p38 activation readout Journal of Biological Chemistry Medium 24936062
2015 FBXO31 directs MDM2 degradation following genotoxic stress: ATM phosphorylates both FBXO31 (increasing its levels) and MDM2 (enabling recognition); FBXO31 then interacts with MDM2 and promotes its proteasomal degradation, resulting in elevated p53 levels and growth arrest. FBXO31 depletion prevents MDM2 degradation and p53 accumulation after DNA damage. Co-immunoprecipitation, RNAi knockdown, ATM kinase inhibition/epistasis, proteasome inhibitor assays, Western blot for p53/MDM2 levels PNAS High 26124108
2016 FBXO31 interacts with and ubiquitinates FOXM1 specifically during the G2/M transition, promoting its degradation. Loss of FBXO31 leads to increased FOXM1 levels, spindle checkpoint activation, lagging chromosomes, and anaphase bridges; co-depletion of FOXM1 rescues genomic instability but not the mitotic delay, indicating FBXO31 has additional mitotic substrates. Co-immunoprecipitation, ubiquitination assay, RNAi double knockdown epistasis, flow cytometry, live-cell imaging for mitotic progression Oncogene High 27568981
2017 Crystal structures of Skp1-FBXO31 complex alone and bound to phosphorylated cyclin D1 C-terminal peptide revealed that FBXO31 possesses a unique substrate-binding domain with two β-barrel motifs, and cyclin D1 binds by inserting its free C-terminal carboxylate tail into a cavity of the C-terminal β-barrel. Biophysical and functional studies showed SCFFBXO31 can ubiquitinate cyclin D1 in a phosphorylation-independent manner. X-ray crystallography, biophysical binding assays, in vitro ubiquitination assay, mutagenesis PNAS High 29279382
2017 FBXO31 interacts with Snail1 (SNAI1) and mediates its ubiquitin- and proteasome-dependent degradation in gastric cancer cells, suppressing EMT. The F-box domain of FBXO31 and phosphorylation of Snail1 are required for the interaction. Co-immunoprecipitation, ubiquitination assay, ectopic expression/knockdown with EMT markers, domain/phosphorylation mutagenesis, mouse xenograft model Molecular Cancer Research Medium 29117943
2018 APC/C (with coactivators CDH1 and CDC20) degrades FBXO31 via a D-box motif in a cell-cycle-regulated manner, maintaining low basal FBXO31 levels. AKT phosphorylates FBXO31 at Ser33 to enable APC/C-mediated degradation, while ATM phosphorylation of FBXO31 at Ser278 following DNA damage disrupts interaction with CDH1/CDC20, preventing FBXO31 degradation and allowing its levels to rise. Co-immunoprecipitation, site-directed mutagenesis (Ser33, Ser278, D-box), kinase inhibition, RNAi knockdown, cell-cycle synchronization, ubiquitination assay PNAS High 29343641
2018 The SCF-E3 ligase FBXO46 recognizes an RXXR motif at the C-terminus of FBXO31 and directs its polyubiquitination and proteasomal degradation to maintain basal FBXO31 levels in unstressed cells, preventing premature senescence. Following DNA damage, ATM phosphorylates FBXO46 at Ser21/Ser67, leading to FBXO46 degradation via FBXO31 (negative feedback loop). Co-immunoprecipitation, molecular docking, RXXR motif mutagenesis, RNAi knockdown, ubiquitination assay, ATM kinase inhibitor Journal of Biological Chemistry High 30171069
2019 FBXO31 interacts with Smad7 (negative regulator of TGF-β/Smad signaling) and enhances its ubiquitination, promoting fibrogenesis in hepatic stellate cells. FBXO31 and Smad7 co-localize in HSC-T6 cells and in mouse liver fibrosis tissues. Co-immunoprecipitation, immunofluorescence co-localization, ubiquitination assay, ectopic expression/knockdown with α-SMA and Col-1 readouts Journal of Cellular Biochemistry Medium 31680332
2019 FBXO31 is essential for maintaining low cyclin A levels during G1 phase. Stable FBXO31 knockdown causes atypical cyclin A accumulation in G1, leading to premature DNA replication, compromised MCM loading, replication from fewer origins, and DNA double-strand breaks, resulting in genomic instability. Flow cytometry, Western blot, immunofluorescence, RNAi stable knockdown, DNA combing for replication origin analysis, γH2AX foci for DSBs Journal of Biological Chemistry Medium 31413110
2021 CRL1FBXO31 promotes ubiquitylation-mediated degradation of DUSP6, a dual-specificity phosphatase that inactivates ERK1/2. FBXO31 depletion stabilizes DUSP6, suppresses ERK signaling, and activates PI3K-AKT signaling, promoting prostate tumor development. Pharmacological inhibition of DUSP6 rescues the tumor-promoting effects of FBXO31 loss. Co-immunoprecipitation, ubiquitylation assay, RNAi knockdown, mouse orthotopic tumor model, DUSP6 inhibitor (BCI) treatment Cell Reports High 34686346
2022 FBXO31 interacts with and promotes ubiquitination and proteasomal degradation of GPX4, sensitizing cholangiocarcinoma cancer stem cell-like cells to cisplatin-induced ferroptosis. GPX4 overexpression reverses FBXO31-promoted ferroptosis. Co-immunoprecipitation, ubiquitination assay, ectopic expression/knockdown, ferroptosis assay, GPX4 rescue experiment, in vivo tumor model Liver International Medium 36269678
2022 c-Myc suppresses FBXO31 transcription by binding its promoter (shown by ChIP), while FBXO31 reciprocally interacts with c-Myc and directs its polyubiquitination via the SCF complex and proteasomal degradation in a phosphorylation-independent manner, inhibiting ovarian cancer growth. Chromatin immunoprecipitation (c-Myc at FBXO31 promoter), Co-immunoprecipitation, ubiquitination assay, ectopic expression/knockdown, in vitro and in vivo tumor growth assays International Journal of Cancer Medium 34706096
2024 FBXO31 promotes proteasome-dependent degradation of SIRT2 by interacting with its sirtuin-type domain, and this is regulated upstream by METTL3-mediated m6A modification of FBXO31 mRNA, enhancing FBXO31 translation in a YTHDF1-dependent manner. Co-immunoprecipitation, ubiquitination assay, protein half-life assay, domain mapping (sirtuin-type domain of SIRT2), m6A RNA modification analysis, YTHDF1 knockdown Cell Death & Disease Medium 38216561
2025 FBXO31 is a reader of C-terminal amide-bearing proteins (CTAPs), recognizing their C-terminal amide modification via a conserved binding pocket in its β-barrel domain. FBXO31 recruits CTAPs to the SCF ubiquitin ligase for ubiquitylation and proteasomal degradation, enabling surveillance of chemically damaged proteins. A dominant neurodevelopmental disorder mutation reverses substrate specificity such that non-amidated neo-substrates are now degraded. CRISPR screen to identify FBXO31, semi-synthetic chemical biology approach, crystal structure-informed binding pocket analysis, in vitro ubiquitylation, mutagenesis of binding pocket residues, cellular degradation assays Nature High 39880951
2025 FBXO31 mediates ubiquitination and proteasomal degradation of OGT (O-GlcNAc transferase), thereby regulating O-GlcNAcylation homeostasis in endometrial cancer cells. CRISPR screen, Co-immunoprecipitation, ubiquitination assay, ectopic expression/knockdown, endometrial organoid models, mouse tumor model Nature Communications Medium 39894887
2025 FBXO31 phosphorylation at Thr37 and Ser523 contributes to FBXO31 protein stabilization, as shown by identification of five phosphorylation sites (Thr28, Thr37, Ser33, Ser400, Ser523) by LC-MS/MS in HEK293T cells, with mutagenesis demonstrating differential effects on protein turnover. LC-MS/MS phosphoproteomics, site-directed mutagenesis, cycloheximide chase assay, Western blot, flow cytometry Advanced Biology Medium 40847744
2026 FBXO31 can be exploited as a TPD-competent E3 ligase using C-terminal amide-bearing degrons (amidated Ala-Phe motif as chemical recruiter), forming ternary complexes with neo-substrates (FKBP12, multiple kinases, BRD2/3/4) for targeted degradation. Key residues in FBXO31 required for recruiter engagement were identified. Ternary complex formation assay, targeted protein degradation assays, mutagenesis of FBXO31 residues, biochemical degradation assays for multiple substrates Journal of the American Chemical Society Medium 41963263
2026 FBXO31 interacts with ABL2 via its F-box motif, promotes ABL2 ubiquitination and proteasomal degradation, and thereby induces xCT-mediated ferroptosis and inhibits progression in triple-negative breast cancer. Co-immunoprecipitation, ubiquitination assay, F-box domain mutagenesis, ectopic expression/knockdown, ferroptosis assay, rescue experiments, mouse tumor model American Journal of Translational Research Medium 42170439
2021 FBXO31 binds cofilin-1 (shown by mass spectrometry and co-immunoprecipitation), and FBXO31-mediated Taxol chemoresistance in esophageal squamous cell carcinoma is at least partly dependent on cofilin-1, as cofilin-1 knockdown in FBXO31-overexpressing cells reversed FBXO31-induced suppression of apoptosis. Mass spectrometry, co-immunoprecipitation, RNAi knockdown epistasis, apoptosis assay (FACS/TUNEL), in vivo xenograft Biochemical and Biophysical Research Communications Low 34839191

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 F-box protein FBXO31 mediates cyclin D1 degradation to induce G1 arrest after DNA damage. Nature 238 19412162
2005 FBXO31 is the chromosome 16q24.3 senescence gene, a candidate breast tumor suppressor, and a component of an SCF complex. Cancer research 74 16357137
2015 F-box protein FBXO31 directs degradation of MDM2 to facilitate p53-mediated growth arrest following genotoxic stress. Proceedings of the National Academy of Sciences of the United States of America 56 26124108
2019 Identification of miR-29c and its Target FBXO31 as a Key Regulatory Mechanism in Esophageal Cancer Chemoresistance: Functional Validation and Clinical Significance. Theranostics 54 31037126
2017 FBXO31 Suppresses Gastric Cancer EMT by Targeting Snail1 for Proteasomal Degradation. Molecular cancer research : MCR 52 29117943
2014 F-box protein FBXO31 is down-regulated in gastric cancer and negatively regulated by miR-17 and miR-20a. Oncotarget 50 25115392
2014 SCF-FBXO31 E3 ligase targets DNA replication factor Cdt1 for proteolysis in the G2 phase of cell cycle to prevent re-replication. The Journal of biological chemistry 49 24828503
2014 F-box only protein 31 (FBXO31) negatively regulates p38 mitogen-activated protein kinase (MAPK) signaling by mediating lysine 48-linked ubiquitination and degradation of mitogen-activated protein kinase kinase 6 (MKK6). The Journal of biological chemistry 47 24936062
2017 Structural basis of the phosphorylation-independent recognition of cyclin D1 by the SCFFBXO31 ubiquitin ligase. Proceedings of the National Academy of Sciences of the United States of America 44 29279382
2013 The centrosomal E3 ubiquitin ligase FBXO31-SCF regulates neuronal morphogenesis and migration. PloS one 44 23469015
2010 FBXO31 is down-regulated and may function as a tumor suppressor in hepatocellular carcinoma. Oncology reports 40 20664978
2022 FBXO31 sensitizes cancer stem cells-like cells to cisplatin by promoting ferroptosis and facilitating proteasomal degradation of GPX4 in cholangiocarcinoma. Liver international : official journal of the International Association for the Study of the Liver 33 36269678
2016 FBXO31 protects against genomic instability by capping FOXM1 levels at the G2/M transition. Oncogene 33 27568981
2014 Truncation of the E3 ubiquitin ligase component FBXO31 causes non-syndromic autosomal recessive intellectual disability in a Pakistani family. Human genetics 31 24623383
2015 FBXO31 promotes cell proliferation, metastasis and invasion in lung cancer. American journal of cancer research 30 26175949
2021 Loss of FBXO31-mediated degradation of DUSP6 dysregulates ERK and PI3K-AKT signaling and promotes prostate tumorigenesis. Cell reports 29 34686346
2016 MicroRNA-210 interacts with FBXO31 to regulate cancer proliferation cell cycle and migration in human breast cancer. OncoTargets and therapy 28 27601917
2024 FBXO31 is upregulated by METTL3 to promote pancreatic cancer progression via regulating SIRT2 ubiquitination and degradation. Cell death & disease 26 38216561
2018 Degradation of FBXO31 by APC/C is regulated by AKT- and ATM-mediated phosphorylation. Proceedings of the National Academy of Sciences of the United States of America 26 29343641
2025 C-terminal amides mark proteins for degradation via SCF-FBXO31. Nature 22 39880951
2018 A Rare Variant (rs933717) at FBXO31-MAP1LC3B in Chinese Is Associated With Systemic Lupus Erythematosus. Arthritis & rheumatology (Hoboken, N.J.) 21 29044928
2019 FBXO31 modulates activation of hepatic stellate cells and liver fibrogenesis by promoting ubiquitination of Smad7. Journal of cellular biochemistry 17 31680332
2020 F-box protein FBXO31 modulates apoptosis and epithelial-mesenchymal transition of cervical cancer via inactivation of the PI3K/AKT-mediated MDM2/p53 axis. Life sciences 16 32800832
2009 FBXO31: a new player in the ever-expanding DNA damage response orchestra. Science signaling 14 19903939
2022 Feedback-regulated transcriptional repression of FBXO31 by c-Myc triggers ovarian cancer tumorigenesis. International journal of cancer 13 34706096
2019 The tumor suppressor FBXO31 preserves genomic integrity by regulating DNA replication and segregation through precise control of cyclin A levels. The Journal of biological chemistry 13 31413110
2025 FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy. Nature communications 12 39894887
2018 The SCFFBXO46 ubiquitin ligase complex mediates degradation of the tumor suppressor FBXO31 and thereby prevents premature cellular senescence. The Journal of biological chemistry 12 30171069
2022 Apolipoprotein C3-Rich Low-Density Lipoprotein Induces Endothelial Cell Senescence via FBXO31 and Its Inhibition by Sesamol In Vitro and In Vivo. Biomedicines 11 35453604
2024 Aberrantly High FBXO31 Impairs Oocyte Quality in Premature Ovarian Insufficiency. Aging and disease 8 37611899
2021 Effects and mechanisms of FBXO31 on Taxol chemoresistance in esophageal squamous cell carcinoma. Biochemical and biophysical research communications 8 34839191
2022 Pseudophosphatase STYX is induced by Helicobacter pylori and promotes gastric cancer progression by inhibiting FBXO31 function. Cell death & disease 7 35338113
2022 FBXO31 suppresses lipogenesis and tumor progression in glioma by promoting ubiquitination and degradation of CD147. Prostaglandins & other lipid mediators 5 35940557
2021 MicroRNA-210 targets FBXO31 to inhibit tumor progression and regulates the Wnt/β-catenin signaling pathway and EMT in esophageal squamous cell carcinoma. Thoracic cancer 4 33538099
2024 MiR-3571 modulates traumatic brain injury by regulating the PI3K/AKT signaling pathway via Fbxo31. Cell biochemistry and biophysics 3 39080190
2023 KLF9‑regulated FBXO31 inhibits the progression of endometrial cancer and enhances the sensitivity of endometrial cancer cells to cisplatin. Experimental and therapeutic medicine 2 38234628
2026 SCF-FBXO31 E3 ubiquitin ligase in cancer: Molecular insights and clinical implications. Biochimica et biophysica acta. Reviews on cancer 0 41554415
2026 Harnessing FBXO31 with terminal amide-functionalized molecules for targeted protein degradation. bioRxiv : the preprint server for biology 0 41659466
2026 Harnessing FBXO31 with Terminal Amide-Functionalized Molecules for Targeted Protein Degradation. Journal of the American Chemical Society 0 41963263
2026 FBXO31-induced ABL2 ubiquitination increases cystine-glutamate antiporter-mediated ferroptosis and inhibits malignant progression in triple-negative breast cancer. American journal of translational research 0 42170439
2025 FBXO31 inhibits the stemness characteristics of CD147 (+) melanoma stem cells. Open life sciences 0 40822976
2025 Phosphorylation-Mediated Regulation of FBXO31 Stability Under Cellular Homeostasis. Advanced biology 0 40847744

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