Affinage

FES

Tyrosine-protein kinase Fes/Fps · UniProt P07332

Length
822 aa
Mass
93.5 kDa
Annotated
2026-04-28
100 papers in source corpus 10 papers cited in narrative 10 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FES is a non-receptor protein-tyrosine kinase that transduces signals downstream of cytokine and growth factor receptors in myeloid, hematopoietic, and neuronal cells, functioning in innate immunity, myelopoiesis, semaphorin-mediated axon guidance, and suppression of cell migration and tumorigenesis. Its SH2 domain recognizes a phospho-Tyr-hydrophilic-hydrophilic-hydrophobic motif and, together with an N-terminal domain, mediates binding to substrates including BCR, plexinA1, CRMP2, and CRAM; phosphorylation of BCR couples FES to RAS/GRB-2 signaling, while phosphorylation of plexinA1 complex components drives semaphorin 3A-induced growth cone collapse (PMID:7511210, PMID:7529874, PMID:12093729). FES is an essential effector downstream of oncogenic KIT (D816V) in mast cell neoplasia, and its kinase-inactivating somatic mutations accelerate epithelial tumor onset, establishing a context-dependent tumor suppressor role (PMID:17595334, PMID:15867340). Loss of FES promotes monocyte and smooth muscle cell migration through altered phosphorylation of migration-regulatory proteins, and Fes-null mice on an ApoE-deficient background develop larger atherosclerotic plaques, linking FES to coronary artery disease risk at 15q26.1 (PMID:36321446).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 1994 High

    Defining the substrate-recognition code of FES: the SH2 domain was shown to select a phospho-Tyr-hydrophilic-hydrophilic-hydrophobic motif, placing FES in group I SH2 domains and predicting its binding partners.

    Evidence Degenerate phosphopeptide library screening with recombinant SH2 domains

    PMID:7511210

    Open questions at the time
    • No in vivo validation that the motif dictates physiological substrate selection
    • Contribution of non-SH2 domains to substrate recognition not addressed
  2. 1995 High

    Identification of BCR as a direct FES substrate linked FES kinase activity to RAS signaling: FES phosphorylates BCR via both its SH2 and a novel N-terminal domain, inducing BCR–GRB-2/SOS complex formation, and the N-terminal domain is required for v-fps transforming activity.

    Evidence Co-expression in Sf-9 cells, reciprocal co-immunoprecipitation, deletion mutagenesis, in vivo phosphorylation assays

    PMID:7529874

    Open questions at the time
    • Whether endogenous FES-BCR interaction occurs at physiological expression levels
    • Downstream RAS pathway activation not directly measured
  3. 1996 High

    Kinetic dissection of the FES catalytic mechanism revealed that both phosphoryl group transfer and product release are rate-limiting, establishing that FES kinase operates via a rapid-equilibrium random mechanism.

    Evidence Viscosometric kinetic analysis and coupled enzyme assays with purified GST-kinase domain fusion protein

    PMID:8634284

    Open questions at the time
    • Kinetics measured with peptide substrates; behavior with full-length protein substrates unknown
    • No structural basis for the dual rate-limiting steps
  4. 1998 Medium

    Activated v-Fps was shown to trans-phosphorylate and constitutively activate the PDGF-β receptor, requiring both v-Fps kinase activity and a functional PDGF receptor for cellular transformation, revealing a mechanism of receptor tyrosine kinase hijacking by an intracellular kinase.

    Evidence Co-expression, immunoprecipitation, kinase-inactive mutants, soft agar colony formation assay

    PMID:9620549

    Open questions at the time
    • Relevance to wild-type (non-oncogenic) FES–PDGFR interaction unclear
    • Mechanism of initial FES–PDGFR physical association not defined
    • Single-lab observation
  5. 2002 High

    Two parallel studies established FES function in vivo: (1) in axon guidance, FES interacts with and phosphorylates plexinA1, CRAM, and CRMP2 downstream of semaphorin 3A, driving growth cone collapse; (2) Fes-null mice display heightened LPS sensitivity and modest myelopoietic defects rescuable by a transgene, placing FES as a regulator of innate immunity.

    Evidence Co-IP, COS-7 morphology assay, DRG neuron collapse assay (plexin study); gene-targeted knockout mice, LPS challenge, transgene rescue, macrophage signaling assays (innate immunity study)

    PMID:11909942 PMID:12093729

    Open questions at the time
    • Identity of downstream phospho-targets mediating LPS sensitivity unknown
    • Neuropilin-1's inhibitory mechanism on FES–plexinA1 interaction is not molecularly resolved
    • No conditional KO to separate hematopoietic from non-hematopoietic phenotypes
  6. 2005 High

    The unexpected tumor suppressor role of FES was established: somatic colorectal cancer mutations inactivate rather than activate kinase activity, and loss of Fes accelerates breast tumor onset in a mouse model, with transgene rescue confirming specificity.

    Evidence Biochemical kinase assays of cancer-derived mutants, transgenic/knockout mouse mammary cancer model

    PMID:15867340

    Open questions at the time
    • Downstream effectors mediating tumor suppression not identified
    • Whether FES tumor suppressor function is tissue-restricted beyond breast and colon is unknown
  7. 2007 High

    FES was identified as a required signaling effector downstream of oncogenic KIT(D816V): KIT phosphorylates FES, and FES knockdown specifically reduces proliferation of KIT-mutant cells, a phenotype not shared by the paralog FER.

    Evidence RNAi knockdown, phosphotyrosine immunoblotting, proliferation assay with GM-CSF rescue in human and murine cells

    PMID:17595334

    Open questions at the time
    • Direct FES substrates mediating KIT-driven proliferation not identified
    • Therapeutic relevance of targeting FES in KIT-mutant malignancies not tested
  8. 2022 High

    FES was linked to atherosclerosis risk: the 15q26.1 CAD risk genotype reduces FES expression, FES loss promotes monocyte and smooth muscle cell migration through altered phosphorylation of migration-regulatory proteins, and Fes knockout in ApoE-null mice increases plaque size.

    Evidence CRISPR genome editing of risk locus, siRNA knockdown, phosphoproteomics, Fes knockout mouse atherosclerosis model

    PMID:36321446

    Open questions at the time
    • Specific phospho-substrates causally responsible for migration phenotype not validated individually
    • Whether kinase activity versus scaffolding drives the anti-migratory function is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis for FES autoinhibition and activation via its F-BAR/FX domains remains incompletely resolved, and the full repertoire of direct physiological substrates across tissues has not been systematically mapped.
  • No high-resolution full-length FES structure available
  • Systematic substrate identification (e.g., analog-sensitive kinase approach) not performed
  • Conditional tissue-specific knockout studies are lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5
Localization
GO:0005829 cytosol 2
Pathway
R-HSA-168256 Immune System 2 R-HSA-1266738 Developmental Biology 1
Partners
BCRCRAMCRMP2GRB2KITNRP1PLXNA1

Evidence

Reading pass · 10 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 The SH2 domain of fps/fes recognizes a specific phosphotyrosine motif: phospho-Tyr-hydrophilic-hydrophilic-hydrophobic, as determined by screening a degenerate phosphopeptide library. The fps/fes SH2 domain falls into group I (Phe/Tyr at beta D5 position), which defines this binding specificity. Degenerate phosphopeptide library screening Molecular and cellular biology High 7511210
1995 FES/FPS tyrosine kinase directly phosphorylates BCR on tyrosine residues, forming a stable BCR-FES protein complex. Complex formation requires the SH2 domain of FES and a novel N-terminal binding domain (first 347 aa) of FES. Tyrosine phosphorylation of BCR by FES induces BCR association with GRB-2/SOS (the RAS guanine nucleotide exchange factor complex), linking FES to RAS signaling. Deletion of the BCR-binding N-terminal domain from v-fps abolished transforming activity. Co-expression in Sf-9 cells, co-immunoprecipitation, deletion mutagenesis, in vivo phosphorylation assays Molecular and cellular biology High 7529874
1996 The kinase domain of v-fps (the activated avian homolog of fes) phosphorylates tyrosine-containing peptide substrates; rate-determining steps include both phosphoryl group transfer (~40–100 s⁻¹) and product release (~17–22 s⁻¹), with peptide substrates in rapid equilibrium with the enzyme. Viscosometric kinetic analysis, coupled enzyme assay, competitive inhibition studies with kinase domain fusion protein (GST-kin) Biochemistry High 8634284
1998 v-Fps (activated fes oncogene product) induces tyrosine phosphorylation of the PDGF beta receptor within minutes of kinase activation, requiring the kinase activity of v-Fps. Sustained v-Fps expression causes downregulation of PDGF receptor mRNA (~4–8-fold) and protein (>100-fold). Transformation requires both v-fps expression and a wild-type (kinase-active) PDGF receptor, indicating that constitutive PDGF receptor activation by v-Fps tyrosine phosphorylation drives the proliferative signal. Co-expression, immunoprecipitation, kinase-inactive mutants, soft agar colony formation assay Oncogene Medium 9620549
2002 FES tyrosine kinase is present in the CRMP-CRAM complex and interacts with plexinA1 (PlexA1), phosphorylating PlexA1, CRAM, and CRMP2 on tyrosine residues. NP-1 (neuropilin-1) negatively regulates PlexA1 activation by FES under resting conditions. Semaphorin3A (Sema3A) enhances association of FES with PlexA1 and FES-mediated phosphorylation. Co-expression of FES with PlexA1 induces COS-7 cell contraction (active PlexA1 morphology), and kinase-negative FES mutants suppress Sema3A-induced growth cone collapse in DRG neurons. Co-immunoprecipitation, co-expression in COS-7 cells, kinase-negative dominant-negative mutants, DRG neuron growth cone collapse assay The EMBO journal High 12093729
2002 fps/fes-null mice are more sensitive to lipopolysaccharide (LPS)-induced endotoxicity, confirming a role for Fps/Fes in regulating the innate immune response. Fps/Fes-null mice show slightly reduced bone marrow myeloid progenitors and circulating mature myeloid cells, indicating involvement but non-essentiality in myelopoiesis. These phenotypes were rescued by a fps/fes transgene. Bone marrow-derived Fps/Fes-null macrophages show no defects in GM-CSF-, IL-6-, or IL-3-induced Stat3/Stat5A activation, or LPS-induced IκB degradation, p38, Jnk, Erk, or Akt activation. Fps/fes knockout mouse (gene targeting), LPS challenge, transgene rescue, bone marrow macrophage signaling assays Molecular and cellular biology High 11909942
2005 Three of four somatic fps/fes mutations found in colorectal cancers result in kinase inactivation (not activation) of Fps/Fes, and fps/fes null or kinase-inactivating mutations accelerate tumor onset in a mouse breast epithelial cancer model, while a fps/fes transgene restores normal tumor onset kinetics, suggesting a tumor suppressor role for Fps/Fes in epithelial cells. Biochemical kinase activity assays of mutants, transgenic/knockout mouse breast cancer model, structural modeling Cancer research High 15867340
2007 FES is phosphorylated on tyrosine residues in cells carrying KIT(D816V) mutation in a KIT-dependent manner. RNAi-mediated reduction of FES expression decreases cell proliferation in human and murine cells harboring KIT(D816V) or KIT(D814Y), but not when the related fer gene is targeted. Reduced growth from FES knockdown is rescued by GM-CSF. Signaling downstream of KIT(D816V) is altered in FES-deficient cells, placing FES as an essential effector downstream of activated KIT. RNA interference knockdown, phosphotyrosine immunoblotting, cell proliferation assay, cytokine rescue, signaling pathway analysis Blood High 17595334
2012 The N-terminal F-BAR and FX domains of FES/FER kinases regulate subcellular localization and kinase activation. FES kinase activity is enhanced upon ligand binding to its SH2 domain, which can lead to further phosphorylation of ligand-associated proteins. In mast cells, SH2 ligands of FES include the KIT receptor PTK and the high-affinity IgE receptor (FcεRI), triggering rapid FES activation and signaling to regulators of the actin cytoskeleton and membrane trafficking. Domain characterization, co-immunoprecipitation, kinase activity assays, mast cell signaling studies Frontiers in bioscience (Landmark edition) Medium 22201778
2022 CRISPR-engineered monocytic cell lines with the 15q26.1 CAD risk genotype show reduced FES expression. siRNA-mediated knockdown of FES promotes migration of monocytes and vascular smooth muscle cells. Phosphoproteomics after FES knockdown revealed altered phosphorylation of proteins regulating cell migration. Fes knockout in apolipoprotein E-deficient mice fed a high-fat diet increased atherosclerotic plaque size and within-plaque monocyte/macrophage and smooth muscle cell content. CRISPR genome editing, siRNA knockdown, phosphoproteomics, single-cell RNA-seq, Fes knockout mouse atherosclerosis model Circulation research High 36321446

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 Specific motifs recognized by the SH2 domains of Csk, 3BP2, fps/fes, GRB-2, HCP, SHC, Syk, and Vav. Molecular and cellular biology 840 7511210
2003 An interaction between frataxin and Isu1/Nfs1 that is crucial for Fe/S cluster synthesis on Isu1. EMBO reports 282 12947415
2003 The role of Fe-S proteins in sensing and regulation in bacteria. Current opinion in microbiology 280 12732309
2008 Fe-S cluster assembly pathways in bacteria. Microbiology and molecular biology reviews : MMBR 259 18322036
2010 Human frataxin is an allosteric switch that activates the Fe-S cluster biosynthetic complex. Biochemistry 231 20873749
2010 Structural basis for Fe-S cluster assembly and tRNA thiolation mediated by IscS protein-protein interactions. PLoS biology 216 20404999
2002 Closing in on the biological functions of Fps/Fes and Fer. Nature reviews. Molecular cell biology 201 11994747
2005 The Nfs1 interacting protein Isd11 has an essential role in Fe/S cluster biogenesis in mitochondria. The EMBO journal 188 16341090
2015 Emerging critical roles of Fe-S clusters in DNA replication and repair. Biochimica et biophysica acta 182 25655665
2009 Nanostructured FeS as a mimic peroxidase for biocatalysis and biosensing. Chemistry (Weinheim an der Bergstrasse, Germany) 164 19267381
2005 In vitro characterization of salmochelin and enterobactin trilactone hydrolases IroD, IroE, and Fes. Journal of the American Chemical Society 154 16076215
2009 Iron-sulfur (Fe/S) protein biogenesis: phylogenomic and genetic studies of A-type carriers. PLoS genetics 146 19478995
1997 Superoxide-driven aconitase FE-S center cycling. Bioscience reports 144 9171919
2017 Structure of human Fe-S assembly subcomplex reveals unexpected cysteine desulfurase architecture and acyl-ACP-ISD11 interactions. Proceedings of the National Academy of Sciences of the United States of America 126 28634302
2010 Frataxin and mitochondrial FeS cluster biogenesis. The Journal of biological chemistry 126 20522547
2014 Interplay between oxygen and Fe-S cluster biogenesis: insights from the Suf pathway. Biochemistry 117 25153801
1985 The structure of the human c-fes/fps proto-oncogene. The EMBO journal 113 4065096
2003 Ssq1, a mitochondrial Hsp70 involved in iron-sulfur (Fe/S) center biogenesis. Similarities to and differences from its bacterial counterpart. The Journal of biological chemistry 109 12756240
2020 Outlining the Complex Pathway of Mammalian Fe-S Cluster Biogenesis. Trends in biochemical sciences 106 32311335
2004 The yeast scaffold proteins Isu1p and Isu2p are required inside mitochondria for maturation of cytosolic Fe/S proteins. Molecular and cellular biology 101 15143178
2002 Involvement of Fes/Fps tyrosine kinase in semaphorin3A signaling. The EMBO journal 98 12093729
2014 Mössbauer spectroscopy of Fe/S proteins. Biochimica et biophysica acta 95 25498248
2014 Alternative FeS cluster ligands: tuning redox potentials and chemistry. Current opinion in chemical biology 94 24463764
2013 Two Fe-S clusters catalyze sulfur insertion by radical-SAM methylthiotransferases. Nature chemical biology 94 23542644
2012 Glutathione complexed Fe-S centers. Journal of the American Chemical Society 91 22687047
2014 Mammalian Fe-S cluster biogenesis and its implication in disease. Biochimie 89 24440636
1981 onc sequences (v-fes) of Snyder-Theilen feline sarcoma virus are derived from noncontiguous regions of a cat cellular gene (c-fes). Nature 85 6259536
2011 Oxygen-tolerant [NiFe]-hydrogenases: the individual and collective importance of supernumerary cysteines at the proximal Fe-S cluster. Journal of the American Chemical Society 83 21916508
2006 Iron-responsive degradation of iron-regulatory protein 1 does not require the Fe-S cluster. The EMBO journal 81 16424901
2006 Mrs3p, Mrs4p, and frataxin provide iron for Fe-S cluster synthesis in mitochondria. The Journal of biological chemistry 80 16769722
1997 Analysis of blood clearance and labeled metabolites for the estrogen receptor tracer [F-18]-16 alpha-fluoroestradiol (FES). Nuclear medicine and biology 75 9257333
2020 Fe-S cluster biogenesis by the bacterial Suf pathway. Biochimica et biophysica acta. Molecular cell research 74 32822728
1990 Myeloid expression of the human c-fps/fes proto-oncogene in transgenic mice. Molecular and cellular biology 73 2188092
2015 How Is Fe-S Cluster Formation Regulated? Annual review of microbiology 72 26488283
1997 Bovine-heart NADH:ubiquinone oxidoreductase is a monomer with 8 Fe-S clusters and 2 FMN groups. Biochimica et biophysica acta 69 9030258
1996 Isolation and propagation of yolk-sac-derived endothelial cells from a hypervascular transgenic mouse expressing a gain-of-function fps/fes proto-oncogene. In vitro cellular & developmental biology. Animal 61 8792159
2015 Fe/S protein assembly gene IBA57 mutation causes hereditary spastic paraplegia. Neurology 60 25609768
1998 The c-Fes family of protein-tyrosine kinases. Critical reviews in oncogenesis 59 9754447
2018 Mitochondrial complex III Rieske Fe-S protein processing and assembly. Cell cycle (Georgetown, Tex.) 58 29243944
2014 Recent advances in the Suf Fe-S cluster biogenesis pathway: Beyond the Proteobacteria. Biochimica et biophysica acta 58 25447545
2014 TtcA a new tRNA-thioltransferase with an Fe-S cluster. Nucleic acids research 56 24914049
2011 Effect of mitochondrial complex I inhibition on Fe-S cluster protein activity. Biochemical and biophysical research communications 56 21570952
1995 Tyrosine phosphorylation of BCR by FPS/FES protein-tyrosine kinases induces association of BCR with GRB-2/SOS. Molecular and cellular biology 55 7529874
2016 Roles of Fe-S proteins: from cofactor synthesis to iron homeostasis to protein synthesis. Current opinion in genetics & development 54 27061491
2011 Fe-S clusters, fragile sentinels of the cell. Current opinion in microbiology 53 21288764
2021 Two stripe rust effectors impair wheat resistance by suppressing import of host Fe-S protein into chloroplasts. Plant physiology 51 34890460
2012 Interaction of J-protein co-chaperone Jac1 with Fe-S scaffold Isu is indispensable in vivo and conserved in evolution. Journal of molecular biology 51 22306468
2012 Persulfide formation on mitochondrial cysteine desulfurase: enzyme activation by a eukaryote-specific interacting protein and Fe-S cluster synthesis. The Biochemical journal 48 22928949
2002 Enhanced endotoxin sensitivity in fps/fes-null mice with minimal defects in hematopoietic homeostasis. Molecular and cellular biology 46 11909942
1983 Transforming genes of avian (v-fps) and mammalian (v-fes) retroviruses correspond to a common cellular locus. Virology 46 6301150
2006 RNA silencing of mitochondrial m-Nfs1 reduces Fe-S enzyme activity both in mitochondria and cytosol of mammalian cells. The Journal of biological chemistry 45 16787928
2019 The SUF system: an ABC ATPase-dependent protein complex with a role in Fe-S cluster biogenesis. Research in microbiology 42 31419582
2019 Sideroflexin 4 affects Fe-S cluster biogenesis, iron metabolism, mitochondrial respiration and heme biosynthetic enzymes. Scientific reports 42 31873120
2014 Coordinate regulation of the Suf and Isc Fe-S cluster biogenesis pathways by IscR is essential for viability of Escherichia coli. Journal of bacteriology 42 25266384
1994 c-fes expression in ontogenetic development and hematopoietic differentiation. Oncogene 42 8108116
2022 16α-18F-fluoro-17β-Fluoroestradiol (FES): Clinical Applications for Patients With Breast Cancer. Seminars in nuclear medicine 41 35379454
2012 Mutation in the Fe-S scaffold protein Isu bypasses frataxin deletion. The Biochemical journal 41 21936771
2024 METTL17 is an Fe-S cluster checkpoint for mitochondrial translation. Molecular cell 40 38199006
2016 The DUF59 Containing Protein SufT Is Involved in the Maturation of Iron-Sulfur (FeS) Proteins during Conditions of High FeS Cofactor Demand in Staphylococcus aureus. PLoS genetics 40 27517714
2007 The tyrosine kinase FES is an essential effector of KITD816V proliferation signal. Blood 40 17595334
1989 Cardiac and neurological abnormalities in v-fps transgenic mice. Proceedings of the National Academy of Sciences of the United States of America 40 2788278
2014 Sulfur mobilization for Fe-S cluster assembly by the essential SUF pathway in the Plasmodium falciparum apicoplast and its inhibition. Antimicrobial agents and chemotherapy 39 24709262
2016 Reductive transformation of hexabromocyclododecane (HBCD) by FeS. Water research 37 27262547
2023 Oxygen toxicity causes cyclic damage by destabilizing specific Fe-S cluster-containing protein complexes. Molecular cell 36 36893757
2022 The FES Gene at the 15q26 Coronary-Artery-Disease Locus Inhibits Atherosclerosis. Circulation research 36 36321446
2019 Structural evidence for an essential Fe-S cluster in the catalytic core domain of DNA polymerase ϵ. Nucleic acids research 36 30968138
2013 Conserved hydrogen bonding networks of MitoNEET tune Fe-S cluster binding and structural stability. Biochemistry 36 23758282
2018 The ErpA/NfuA complex builds an oxidation-resistant Fe-S cluster delivery pathway. The Journal of biological chemistry 35 29626095
2015 The iron-binding CyaY and IscX proteins assist the ISC-catalyzed Fe-S biogenesis in Escherichia coli. Molecular microbiology 35 25430730
2010 Polysaccharide from fuzi (FPS) prevents hypercholesterolemia in rats. Lipids in health and disease 34 20109183
2012 FES/FER kinase signaling in hematopoietic cells and leukemias. Frontiers in bioscience (Landmark edition) 33 22201778
2020 Structural insights into Fe-S protein biogenesis by the CIA targeting complex. Nature structural & molecular biology 31 32632277
2018 TLR-activated repression of Fe-S cluster biogenesis drives a metabolic shift and alters histone and tubulin acetylation. Blood advances 31 29784770
2014 Fe-S cluster biogenesis in isolated mammalian mitochondria: coordinated use of persulfide sulfur and iron and requirements for GTP, NADH, and ATP. The Journal of biological chemistry 31 25398879
2022 Structure of the mitoribosomal small subunit with streptomycin reveals Fe-S clusters and physiological molecules. eLife 30 36480258
2017 [Fe-S] cluster assembly in the apicoplast and its indispensability in mosquito stages of the malaria parasite. The FEBS journal 30 28695709
2015 The antimalarial drug primaquine targets Fe-S cluster proteins and yeast respiratory growth. Redox biology 30 26629948
1987 Structure of the feline c-fes/fps proto-oncogene: genesis of a retroviral oncogene. Journal of virology 30 3553615
2022 Fe-S clusters masquerading as zinc finger proteins. Journal of inorganic biochemistry 29 35247854
2018 The NMR contribution to protein-protein networking in Fe-S protein maturation. Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry 29 29569085
2010 The Fe/S cluster assembly protein Isd11 is essential for tRNA thiolation in Trypanosoma brucei. The Journal of biological chemistry 29 20442400
2020 Biosynthesis of the catalytic H-cluster of [FeFe] hydrogenase: the roles of the Fe-S maturase proteins HydE, HydF, and HydG. Chemical science 27 34123177
2021 A Review of Multiple Mitochondrial Dysfunction Syndromes, Syndromes Associated with Defective Fe-S Protein Maturation. Biomedicines 26 34440194
2014 Fe/S protein biogenesis in trypanosomes - A review. Biochimica et biophysica acta 26 25196712
2011 Iron chaperones for mitochondrial Fe-S cluster biosynthesis and ferritin iron storage. Current opinion in chemical biology 26 21288761
1996 Rate-determining steps for tyrosine phosphorylation by the kinase domain of v-fps. Biochemistry 26 8634284
2016 Glutathione-complexed [2Fe-2S] clusters function in Fe-S cluster storage and trafficking. Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry 25 27590019
2020 Inhibition of RAGE by FPS-ZM1 alleviates renal injury in spontaneously hypertensive rats. European journal of pharmacology 24 32502492
2018 Fe-S Cluster Assembly in Oxymonads and Related Protists. Molecular biology and evolution 24 30184127
2015 Frataxin Is Localized to Both the Chloroplast and Mitochondrion and Is Involved in Chloroplast Fe-S Protein Function in Arabidopsis. PloS one 24 26517126
2005 An identity crisis for fps/fes: oncogene or tumor suppressor? Cancer research 24 15867340
2021 Sulfur Administration in Fe-S Cluster Homeostasis. Antioxidants (Basel, Switzerland) 23 34829609
2016 A Regulatory Circuit Composed of a Transcription Factor, IscR, and a Regulatory RNA, RyhB, Controls Fe-S Cluster Delivery. mBio 23 27651365
2014 Epigenetic role for the conserved Fe-S cluster biogenesis protein AtDRE2 in Arabidopsis thaliana. Proceedings of the National Academy of Sciences of the United States of America 23 25197096
2005 Resolution and reconstitution of a bound Fe-S protein from the photosynthetic reaction center of Heliobacterium modesticaldum. Biochemistry 23 16026168
1998 v-fps causes transformation by inducing tyrosine phosphorylation and activation of the PDGFbeta receptor. Oncogene 23 9620549
2014 The scaffold protein IscU retains a structured conformation in the Fe-S cluster assembly complex. Chembiochem : a European journal of chemical biology 22 25044349
2018 Recent Advances in the [Fe-S] Cluster Biogenesis (SUF) Pathway Functional in the Apicoplast of Plasmodium. Trends in parasitology 21 30064903
2020 Aggregation of mutant cysteine string protein-α via Fe-S cluster binding is mitigated by iron chelators. Nature structural & molecular biology 20 32042150
2017 Fe-S Cluster Hsp70 Chaperones: The ATPase Cycle and Protein Interactions. Methods in enzymology 20 28882200