Affinage

FBXL5

F-box/LRR-repeat protein 5 · UniProt Q9UKA1

Length
691 aa
Mass
78.6 kDa
Annotated
2026-06-09
53 papers in source corpus 21 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FBXL5 is the substrate-recognition subunit of an SCF (SKP1-CUL1-RBX1) E3 ubiquitin ligase that functions as the master iron/oxygen sensor controlling cellular and systemic iron homeostasis (PMID:21907140, PMID:23135277). It detects iron and oxygen through two redox-sensitive metal centers: an N-terminal hemerythrin-like α-helical bundle harboring a diiron center whose iron occupancy and redox state govern accessibility of a degradation sequence and thereby FBXL5's own stability, and a C-terminal [2Fe2S] cluster whose oxygen-maintained oxidized state organizes the substrate-binding loop (PMID:32126207, PMID:22253436, PMID:22648410, PMID:28131773). When iron and oxygen are replete, stabilized FBXL5 recruits, polyubiquitinates, and targets the iron-regulatory proteins IRP2 and IRP1 for proteasomal degradation, with the oxidized [2Fe2S] cluster sterically dislodging IRP2 from iron-responsive-element RNA—explaining hypoxia- and iron-limitation-induced IRP2 stabilization (PMID:32126207, PMID:22253436, PMID:22648410). Genetically, unrestrained IRP2 activity is the decisive output of FBXL5 loss: Fbxl5-null embryonic lethality and iron overload are rescued by deletion of IRP2 but not IRP1, and FBXL5-dependent iron control is required for hematopoietic stem cell self-renewal and neural progenitor homeostasis (PMID:21907140, PMID:23135277, PMID:28714470, PMID:28069738). FBXL5 abundance is itself set upstream by HERC2-mediated ubiquitination and by oxygen-dependent association with the CIA-targeting complex (MMS19/FAM96B/CIAO1) that links it to Fe-S cluster assembly (PMID:24778179, PMID:31229404). Beyond iron regulation, FBXL5 directs phosphorylation-gated degradation of additional substrates, including nuclear Snail1 in EMT control, hSSB1 in the DNA damage response, cortactin in cell migration, and CITED2 to modulate HIF-1α transactivation (PMID:24157836, PMID:24867096, PMID:25249620, PMID:25956243).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2007 Low

    First evidence that FBXL5 acts as a substrate-targeting E3 component identified a physical partner and ubiquitination target, establishing it as a functional ubiquitin ligase subunit.

    Evidence Co-IP, in vitro binding, colocalization, and ubiquitination assays with p150Glued in cells

    PMID:17532294

    Open questions at the time
    • Single Co-IP from a single lab with limited mechanistic follow-up
    • No demonstration of SCF complex assembly or physiological consequence
  2. 2011 High

    Genetic epistasis defined FBXL5's primary in vivo role by showing it degrades IRP2 to restrain iron accumulation, placing it upstream of IRP2 in iron homeostasis.

    Evidence Fbxl5−/− × Irp2−/− double-knockout mice, immunoblotting, tissue iron measurements

    PMID:21907140

    Open questions at the time
    • Did not resolve how FBXL5 senses iron molecularly
    • Tissue- and cell-type-specific roles not yet dissected
  3. 2012 High

    Structural and physiological work established the iron/oxygen-sensing mechanism: an N-terminal hemerythrin-like diiron domain controls FBXL5 stability, and FBXL5 is required for cellular and systemic iron homeostasis.

    Evidence X-ray crystallography, spectroscopy, mutagenesis, plus conditional/constitutive knockout mice with iron and gene-expression readouts

    PMID:22253436 PMID:22648410 PMID:23135277

    Open questions at the time
    • Did not explain how oxygen sensing distinct from iron sensing is transmitted to substrate recruitment
    • Mechanism of the C-terminal substrate domain unresolved
  4. 2013 Medium

    Identification of nuclear Snail1 as a substrate extended FBXL5 beyond iron biology to EMT regulation and linked its activity to iron- and irradiation-responsive stress signaling.

    Evidence shRNA, Co-IP, ubiquitination assay, subcellular fractionation, and localization imaging

    PMID:24157836

    Open questions at the time
    • Single lab
    • Spatial paradox of nuclear ubiquitination with cytosolic degradation not fully resolved
  5. 2014 Medium

    FBXL5's own turnover was shown to be governed by HERC2, defining an upstream layer that sets sensor abundance, while phosphorylation-gated degradation of cortactin and hSSB1 revealed substrate selection coupled to ERK and ATM signaling.

    Evidence Interactome MS, Co-IP, RNAi, iron measurements (HERC2); Co-IP, ubiquitination, and phosphosite mutagenesis (cortactin, hSSB1)

    PMID:24778179 PMID:24867096 PMID:25249620

    Open questions at the time
    • Each substrate characterized in a single lab
    • How phosphorylation switches gate FBXL5 recruitment mechanistically unknown
  6. 2015 Medium

    FBXL5-mediated degradation of CITED2 connected the ligase to HIF-1α transcriptional output, broadening its role in oxygen-responsive gene regulation.

    Evidence Co-IP, RNAi, overexpression, FRET/BRET, and reporter assays

    PMID:25956243

    Open questions at the time
    • Single lab
    • In vivo relevance of the FBXL5-CITED2-HIF axis not established here
  7. 2017 High

    Tissue-level studies and CIA crosstalk established FBXL5 as essential for stem cell and progenitor iron control and linked it functionally to Fe-S cluster assembly through both IRP1 and IRP2.

    Evidence Conditional knockouts in HSCs and neural progenitors with IRP2-suppression rescue; siRNA, IRP1 phosphosite mutants, and polyubiquitination assays for CIA crosstalk

    PMID:28069738 PMID:28714470 PMID:28768766

    Open questions at the time
    • mTOR as downstream effector in NSPCs inferred pharmacologically
    • Molecular coupling between CIA status and FBXL5 activity not fully defined
  8. 2019 Medium

    Oxygen-dependent association of FBXL5 with the CIA-targeting complex (MMS19/FAM96B/CIAO1) provided a mechanism linking ambient oxygen to FBXL5-mediated IRP degradation.

    Evidence Co-IP, mass spectrometry, and IRP degradation assays under varied O2

    PMID:31229404

    Open questions at the time
    • Single lab
    • Structural basis of the oxygen-dependent interaction not determined
  9. 2020 High

    A cryo-EM structure of the IRP2-FBXL5-SKP1 complex resolved the C-terminal [2Fe2S] cluster as the oxygen-sensing module that organizes the substrate-binding loop and dislodges IRP2 from IRE-RNA, completing the dual-sensor mechanism.

    Evidence Cryo-EM, in vitro ubiquitination, mutagenesis, EPR spectroscopy

    PMID:32126207

    Open questions at the time
    • Structure of the full SCF holocomplex on substrate not solved
    • Integration of N-terminal diiron and C-terminal [2Fe2S] signals into one stability/activity output not structurally unified
  10. 2021 Medium

    A negative-control study showed IRP2 can be activated by Fe-S cluster deficiency at tissue O2 levels independently of FBXL5, delimiting the boundary of the FBXL5-dependent regulatory axis.

    Evidence ISC inhibition, IRP RNA-binding assays, IRP1/IRP2 double knockout, FBXL5 knockdown, ferroptosis assays

    PMID:34039609

    Open questions at the time
    • FBXL5-independent IRP2 activation mechanism not identified
    • Physiological contexts where each pathway dominates unclear
  11. 2023 Medium

    Translational and disease-context studies expanded FBXL5 regulation and substrate scope, showing G3BP1-mediated suppression of FBXL5 translation drives ferroptosis, and identifying TFEB and oocyte CITED2 as functionally relevant targets.

    Evidence 35S labeling/RIP and in vivo kidney injury (G3BP1); Co-IP/ubiquitination/siRNA in HepG2 (TFEB); oocyte siRNA, ROS, spindle imaging, in vitro ubiquitination (CITED2)

    PMID:37462473 PMID:37743009 PMID:38118197

    Open questions at the time
    • TFEB and YAP1 substrate findings rest on single Co-IP/ubiquitination studies
    • Whether these substrates depend on FBXL5's iron-sensing state is untested
  12. 2026 Low

    FBXL5 was implicated in tumor suppression via Galectin-3-enhanced degradation of YAP1, extending its substrate repertoire to Hippo-pathway control.

    Evidence Co-IP, ubiquitination assay, xenograft model, proliferation assays

    PMID:42093989

    Open questions at the time
    • Single lab with limited mechanistic detail
    • Degron and recruitment determinants for YAP1 unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the N-terminal diiron and C-terminal [2Fe2S] sensors are jointly integrated to set both FBXL5 stability and substrate selectivity across its many non-IRP targets remains unresolved.
  • No unified structural model coupling both metal centers to substrate choice
  • Whether non-IRP substrates are regulated by iron/oxygen state is untested
  • Tissue-specific substrate prioritization unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0140299 molecular sensor activity 3 GO:0016740 transferase activity 2 GO:0140313 molecular sequestering activity 1
Localization
GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953897 Cellular responses to stimuli 2
Partners
CITED2CORTACTINHERC2HSSB1IRP1IRP2SKP1SNAIL1
Complex memberships
SCF (SKP1-CUL1-RBX1-FBXL5) E3 ubiquitin ligase

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2020 The C-terminal substrate-binding domain of FBXL5 harbors a [2Fe2S] iron-sulfur cluster in the oxidized state. A cryo-EM structure of the IRP2-FBXL5-SKP1 complex revealed that this cluster organizes the FBXL5 C-terminal loop responsible for recruiting IRP2. IRP2 binding to FBXL5 depends on the oxidized state of the [2Fe2S] cluster maintained by ambient oxygen, explaining hypoxia-induced IRP2 stabilization. FBXL5 also sterically dislodges IRP2 from iron-responsive element RNA to facilitate its turnover. Cryo-EM structure determination, in vitro ubiquitination assay, mutagenesis, EPR spectroscopy Molecular cell High 32126207
2012 The N-terminal domain of FBXL5 adopts a hemerythrin-like α-helical bundle fold containing an unusual diiron center. This domain senses iron and oxygen availability by distinct mechanisms: iron limitation causes substantive structural changes in the domain, whereas oxygen depletion does not produce the same conformational changes. The domain controls accessibility of a degradation sequence required for proteasomal degradation of FBXL5 itself. X-ray crystallography, biochemical assays, mutagenesis, spectroscopy The Journal of biological chemistry High 22253436 22648410
2011 FBXL5 mediates iron-dependent proteasomal degradation of IRP2 in vivo. Fbxl5-null mice die in utero with excessive iron accumulation; embryonic lethality is rescued by simultaneous deletion of IRP2 but not IRP1, establishing that unrestrained IRP2 activity is the primary cause of death and placing FBXL5 upstream of IRP2 in iron homeostasis. Genetic epistasis (Fbxl5−/− × Irp2−/− double knockout mice), immunoblotting, tissue iron measurements Cell metabolism High 21907140
2012 FBXL5 is required for maintenance of cellular and systemic iron homeostasis in vivo. FBXL5-null mice fail to sense increased cellular iron, show constitutive IRP2 accumulation and misexpression of IRP2 target genes, and die during embryogenesis; viability is restored by IRP2 but not IRP1 deletion. Heterozygous mice show increased intestinal iron absorption via enhanced duodenal IRP2 responsiveness and upregulation of DMT-1. Conditional and constitutive knockout mice, genetic epistasis, gene expression analysis, hematological measurements The Journal of biological chemistry High 23135277
2014 HERC2, a large HECT-type E3 ubiquitin ligase, interacts with FBXL5 and targets it for ubiquitin-dependent proteasomal degradation, controlling FBXL5 basal turnover. Inhibition of HERC2-FBXL5 interaction or HERC2 depletion stabilizes FBXL5, leading to decreased intracellular ferrous iron. Proteomics/mass spectrometry interactome, Co-IP, RNA interference, ferrous iron measurements The Journal of biological chemistry Medium 24778179
2019 FBXL5 interacts with the CIA-targeting complex (composed of MMS19, FAM96B, and CIAO1) in an oxygen-dependent manner. This interaction, robust at 21% O2 but severely diminished at 1% O2, promotes FBXL5-mediated degradation of IRPs and links IRP-dependent iron homeostasis with Fe-S cluster assembly machinery. Co-IP, mass spectrometry, cell-based IRP degradation assays under varying O2 conditions Molecular cell Medium 31229404
2017 FBXL5 promotes IRP1 polyubiquitination and degradation when cytosolic iron-sulfur (Fe-S) cluster assembly (CIA) is impaired. FBXL5 and CIA act synergistically through both IRP1 and IRP2 to control iron metabolism. IRP1 Ser-138 phosphorylation is required for iron rescue when CIA is inhibited. A negative feedback loop exists whereby elevated IRP expression induces FBXL5 protein levels. siRNA knockdown, IRP1 phosphorylation-site mutants, polyubiquitination assays, cell viability assays The Journal of biological chemistry Medium 28768766
2013 FBXL5 is localized in the nucleus where it interacts with the transcription factor Snail1, promotes its polyubiquitination, impairs Snail1 DNA binding, and reduces Snail1 protein stability. Although polyubiquitination occurs in the nucleus, Snail1 is degraded in the cytosol. Lats2 phosphorylation of Snail1 prevents nuclear export but not FBXL5-mediated polyubiquitination. FBXL5 is downregulated by iron depletion and γ-irradiation, explaining Snail1 stabilization under these stresses. shRNA screening, co-immunoprecipitation, ubiquitination assay, subcellular fractionation, nuclear localization imaging Nucleic acids research Medium 24157836
2014 FBXL5 interacts with cortactin and targets it for ERK-dependent ubiquitylation and proteasomal degradation. ERK-mediated serine phosphorylation of cortactin at S405/S418 is required for FBXL5-induced degradation; the cortactinS405A/S418A phospho-null mutant resists FBXL5-induced degradation and shows enhanced gastric cancer cell migration. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis, cell migration assays Tumour biology Medium 24867096
2014 FBXL5 directly interacts with hSSB1 (single-stranded DNA-binding protein 1) and targets it for SCF-mediated ubiquitination and degradation. ATM-mediated phosphorylation of hSSB1 at T117 prevents FBXL5-induced degradation. FBXL5 overexpression abrogates ATM signaling, DNA damage checkpoint activation, and increases radio- and chemo-sensitivity. Co-immunoprecipitation, ubiquitination assay, phosphorylation-site mutagenesis, DNA damage assays Nucleic acids research Medium 25249620
2015 FBXL5 directly interacts with CITED2 and promotes its ubiquitination-dependent proteasomal degradation. FBXL5 depletion increases CITED2 levels; FBXL5 overexpression decreases CITED2 levels, impairs CITED2 interaction with the CH1 domain of p300, and enables transcriptional activity of the HIF-1α N-terminal transactivation domain. Co-immunoprecipitation, RNA interference, overexpression, FRET/BRET assay in living cells, reporter assay Archives of biochemistry and biophysics Medium 25956243
2007 FBXL5 interacts with p150Glued (dynactin subunit) both in vitro and in vivo, co-localizes with it in the cytoplasm with peri-nuclear enrichment, and promotes its poly-ubiquitination and protein turnover. Co-immunoprecipitation, in vitro binding assay, immunofluorescence colocalization, overexpression ubiquitination assay Biochemical and biophysical research communications Low 17532294
2017 FBXL5-mediated regulation of cellular iron homeostasis is required for hematopoietic stem cell (HSC) self-renewal. Conditional deletion of Fbxl5 in mouse HSCs causes cellular iron overload, reduced HSC number, and stem cell exhaustion upon bone marrow transplantation. Suppression of IRP2 accumulation in FBXL5-deficient HSCs restores stem cell function. Conditional knockout mice, bone marrow transplantation, transcriptomic analysis, genetic epistasis (IRP2 suppression) Nature communications High 28714470
2017 Brain-specific deletion of FBXL5 in nestin-expressing neural stem progenitor cells (NSPCs) leads to IRP2 stabilization, iron accumulation, ROS generation, and aberrant NSPC and astroglia proliferation in the cerebral cortex. Pharmacological manipulation implicated mTOR signaling as the downstream effector of FBXL5 deficiency. Conditional knockout mice (nestin-Cre), iron measurements, ROS assays, mTOR pathway inhibition Molecular and cellular biology Medium 28069738
2017 Redox state of the FBXL5 diiron center governs its conformation and stability. EPR, direct electrochemistry, SRCD, and fluorescence spectroscopy showed that redox reactions at the diiron center are accompanied by conformational changes and iron release, which are mechanistically linked to FBXL5 stability and its function as an iron/oxygen sensor. EPR spectroscopy, direct electrochemistry, SRCD, fluorescence emission spectroscopy, redox kinetics Archives of biochemistry and biophysics Medium 28131773
2021 At tissue-level O2 concentrations, ISC deficiency can activate IRP2 and promote ferroptosis sensitivity independently of IRP1, FBXL5, and changes in IRP2 protein level. IRP2 responds to Fe-S cluster synthesis suppression via a previously unidentified mechanism that does not involve FBXL5-mediated degradation. ISC synthesis inhibition, IRP RNA-binding assays, IRP1/IRP2 double knockout, FBXL5 knockdown, ferroptosis assays Science advances Medium 34039609
2023 FBXL5 promotes ubiquitination and proteasomal degradation of TFEB (transcription factor EB). In alcoholic fatty liver disease, FBXL5 is upregulated and its interaction with TFEB promotes TFEB degradation, contributing to lipid accumulation; TFEB knockdown reverses the effect of FBXL5 inhibition. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, overexpression in HepG2 cells Cellular signalling Low 37743009
2023 FBXL5 mRNA translation is suppressed by the RNA-binding protein G3BP1, which stabilizes IRP2 by binding to and suppressing FBXL5 mRNA translation. Sodium arsenite intoxication activates this G3BP1-FBXL5-IRP2 axis, elevating labile iron and triggering ferroptosis. 35S-methionine labeling, RIP assay, siRNA knockdown, ferroptosis assays, mouse kidney injury model Journal of hazardous materials Medium 38118197
2023 FBXL5 is required for redox homeostasis and spindle assembly during mouse oocyte meiotic maturation. Fbxl5 silencing caused meiotic failure, overproduction of ROS, and abnormal accumulation of CITED2. An in vitro ubiquitination assay confirmed that FBXL5 directly interacts with CITED2 and mediates its proteasomal degradation in oocytes. siRNA knockdown in mouse oocytes, ROS assay, immunofluorescence spindle imaging, in vitro ubiquitination assay, Co-IP FASEB journal Medium 37462473
2026 FBXL5 promotes YAP1 protein degradation through the ubiquitin-proteasome pathway without altering YAP1 transcript levels. Galectin-3 (Gal-3) binds FBXL5 and enhances its expression, increasing YAP1 degradation and restraining colorectal cancer growth in vivo. Co-immunoprecipitation, ubiquitination assay, xenograft mouse model, cell proliferation assay Frontiers in immunology Low 42093989

Source papers

Stage 0 corpus · 53 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 AP1-mediated multidrug resistance in Saccharomyces cerevisiae requires FLR1 encoding a transporter of the major facilitator superfamily. The Journal of biological chemistry 162 9235926
2021 Iron-sulfur cluster deficiency can be sensed by IRP2 and regulates iron homeostasis and sensitivity to ferroptosis independent of IRP1 and FBXL5. Science advances 158 34039609
2020 FBXL5 Regulates IRP2 Stability in Iron Homeostasis via an Oxygen-Responsive [2Fe2S] Cluster. Molecular cell 145 32126207
2011 The FBXL5-IRP2 axis is integral to control of iron metabolism in vivo. Cell metabolism 142 21907140
2001 Multiple Yap1p-binding sites mediate induction of the yeast major facilitator FLR1 gene in response to drugs, oxidants, and alkylating agents. The Journal of biological chemistry 86 11056165
2013 Nuclear ubiquitination by FBXL5 modulates Snail1 DNA binding and stability. Nucleic acids research 85 24157836
2017 iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling. Journal of experimental & clinical cancer research : CR 71 28399926
1999 FLR1 gene (ORF YBR008c) is required for benomyl and methotrexate resistance in Saccharomyces cerevisiae and its benomyl-induced expression is dependent on pdr3 transcriptional regulator. Yeast (Chichester, England) 70 10572257
2017 Essential role of FBXL5-mediated cellular iron homeostasis in maintenance of hematopoietic stem cells. Nature communications 65 28714470
2015 FBXL5 inhibits metastasis of gastric cancer through suppressing Snail1. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 63 25832584
2012 Structural and molecular characterization of iron-sensing hemerythrin-like domain within F-box and leucine-rich repeat protein 5 (FBXL5). The Journal of biological chemistry 57 22253436
2007 Yeast adaptation to mancozeb involves the up-regulation of FLR1 under the coordinate control of Yap1, Rpn4, Pdr3, and Yrr1. Biochemical and biophysical research communications 52 18086556
2014 HERC2 targets the iron regulator FBXL5 for degradation and modulates iron metabolism. The Journal of biological chemistry 48 24778179
2014 F-box and leucine-rich repeat protein 5 (FBXL5): sensing intracellular iron and oxygen. Journal of inorganic biochemistry 39 24508277
2018 Regulation of cellular iron metabolism: Iron-dependent degradation of IRP by SCFFBXL5 ubiquitin ligase. Free radical biology & medicine 36 30218771
2014 FBXL5-mediated degradation of single-stranded DNA-binding protein hSSB1 controls DNA damage response. Nucleic acids research 35 25249620
2019 An Oxygen-Dependent Interaction between FBXL5 and the CIA-Targeting Complex Regulates Iron Homeostasis. Molecular cell 34 31229404
2017 A synergistic role of IRP1 and FBXL5 proteins in coordinating iron metabolism during cell proliferation. The Journal of biological chemistry 34 28768766
2001 Transcriptional activation of FLR1 gene during Saccharomyces cerevisiae adaptation to growth with benomyl: role of Yap1p and Pdr3p. Biochemical and biophysical research communications 34 11162502
2012 Hemerythrin-like domain within F-box and leucine-rich repeat protein 5 (FBXL5) communicates cellular iron and oxygen availability by distinct mechanisms. The Journal of biological chemistry 32 22648410
2012 F-box and leucine-rich repeat protein 5 (FBXL5) is required for maintenance of cellular and systemic iron homeostasis. The Journal of biological chemistry 31 23135277
2018 miR-1306-3p targets FBXL5 to promote metastasis of hepatocellular carcinoma through suppressing snail degradation. Biochemical and biophysical research communications 26 30219228
2015 FBXL5 modulates HIF-1α transcriptional activity by degradation of CITED2. Archives of biochemistry and biophysics 26 25956243
2014 FBXL5 targets cortactin for ubiquitination-mediated destruction to regulate gastric cancer cell migration. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 25 24867096
2020 How Oxidation of a Unique Iron-Sulfur Cluster in FBXL5 Regulates IRP2 Levels and Promotes Regulation of Iron Metabolism Proteins. Molecular cell 24 32243827
2016 FBXL5 attenuates RhoGDI2-induced cisplatin resistance in gastric cancer cells. European review for medical and pharmacological sciences 23 27383304
2023 A regulatory module comprising G3BP1-FBXL5-IRP2 axis determines sodium arsenite-induced ferroptosis. Journal of hazardous materials 20 38118197
2007 FBXL5 interacts with p150Glued and regulates its ubiquitination. Biochemical and biophysical research communications 20 17532294
2017 FBXL5 Inactivation in Mouse Brain Induces Aberrant Proliferation of Neural Stem Progenitor Cells. Molecular and cellular biology 19 28069738
2018 Leishmania donovani inhibits ferroportin translation by modulating FBXL5-IRP2 axis for its growth within host macrophages. Cellular microbiology 17 29470856
2010 Refining current knowledge on the yeast FLR1 regulatory network by combined experimental and computational approaches. Molecular bioSystems 17 20938527
2019 Oxidative Stress Regulated Iron Regulatory Protein IRP2 Through FBXL5-Mediated Ubiquitination-Proteasome Way in SH-SY5Y Cells. Frontiers in neuroscience 13 30760976
2022 Circular RNA Fbxl5 Regulates Cardiomyocyte Apoptosis During Ischemia Reperfusion Injury via Sponging microRNA-146a. Journal of inflammation research 10 35479829
2011 Ultradian rhythm in the intestine of Caenorhabditis elegans is controlled by the C-terminal region of the FLR-1 ion channel and the hydrophobic domain of the FLR-4 protein kinase. Genes to cells : devoted to molecular & cellular mechanisms 10 21518154
2005 Expression of FLR1 transporter requires phospholipase C and is repressed by Mediator. The Journal of biological chemistry 7 16352614
2013 The MFS-type efflux pump Flr1 induced by Yap1 promotes canthin-6-one resistance in yeast. FEBS letters 6 23912082
2011 Qualitative modelling and formal verification of the FLR1 gene mancozeb response in Saccharomyces cerevisiae. IET systems biology 5 22010757
2022 Yap1-mediated Flr1 expression reveals crosstalk between oxidative stress signaling and caffeine resistance in Saccharomyces cerevisiae. Frontiers in microbiology 3 36504777
2019 Association between Fbxl5 gene polymorphisms and partial economic traits in Jinghai Yellow chickens. Archives animal breeding 3 31807618
2025 Targeting FBXL5 to induce ferroptosis and reverse oxaliplatin resistance in iron-rich colorectal cancer. Scientific reports 2 41136490
2024 The F-box protein FBXL-5 governs vitellogenesis and lipid homeostasis in C. elegans. Frontiers in cell and developmental biology 2 38946799
2023 FBXL5 promotes lipid accumulation in alcoholic fatty liver disease by promoting the ubiquitination and degradation of TFEB. Cellular signalling 2 37743009
2017 Redox sensing molecular mechanism of an iron metabolism regulatory protein FBXL5. Archives of biochemistry and biophysics 2 28131773
2017 Influence of sodium nitroprusside on expressions of FBXL5 and IRP2 in SH-SY5Y cells. Sheng li xue bao : [Acta physiologica Sinica] 2 28638917
2011 Quantitative modeling of the Saccharomyces cerevisiae FLR1 regulatory network using an S-system formalism. Journal of bioinformatics and computational biology 2 21976379
2024 The F-box protein FBXL-5 governs vitellogenesis and lipid homeostasis in C. elegans. bioRxiv : the preprint server for biology 1 38712300
2023 Role of FBXL5 in redox homeostasis and spindle assembly during oocyte maturation in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1 37462473
2026 MFS-transporter Flr1 is a major drug-efflux transporter in Saccharomyces cerevisiae ascospores. FEMS yeast research 0 41700724
2026 The OsRALF5-FLR1 Module Regulates Rice Root Development and Provides a Target for Studying Cell-Cell Communication. Rice (New York, N.Y.) 0 41910879
2026 miR-1229-3p promotes epithelial-mesenchymal transition and metastasis of cervical cancer cells by targeting FBXL5. Hereditas 0 42015317
2026 Galectin-3 promotes FBXL5-dependent ubiquitination and degradation of YAP1 to constrain colorectal cancer growth. Frontiers in immunology 0 42093989
2026 Cardiomyocyte-specific Fbxl5 deficiency promotes iron overload-driven hypercontractility and late-onset pathological hypertrophy in mice. Journal of cardiology 0 42162863
2025 Identification and validation of TUBB, CLTA, and FBXL5 as potential diagnostic markers of postmenopausal osteoporosis. Biomolecules & biomedicine 0 40791155

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