Affinage

MAEA

E3 ubiquitin-protein transferase MAEA · UniProt Q7L5Y9

Length
396 aa
Mass
45.3 kDa
Annotated
2026-06-10
72 papers in source corpus 13 papers cited in narrative 13 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

MAEA is a RING-domain E3 ubiquitin ligase subunit of the CTLH (yeast Gid) complex that drives K48-linked polyubiquitination and proteasomal degradation of diverse substrates to control hematopoiesis, signaling, and genome integrity (PMID:22044534, PMID:33947846, PMID:40880485). Its catalytic identity was established through the yeast ortholog Gid9, whose degenerate RING finger binds Gid2/Rmd5 and is required for polyubiquitylation and degradation of gluconeogenic enzymes (PMID:22044534). In mammalian hematopoietic stem cells, MAEA degrades the surface cytokine receptors MPL and FLT3 to limit their signaling and maintain HSC quiescence; loss of MAEA stabilizes these receptors, impairs autophagy flux, and produces a lethal myeloproliferative syndrome (PMID:33947846). MAEA also targets PHD3 (at K159, stabilizing HIF-1α), PARP1 (suppressing M2 macrophage polarization), and β-catenin (inhibiting canonical Wnt signaling and controlling head formation in embryogenesis) (PMID:36882523, PMID:39990651, PMID:36444483). Independently of its hematopoietic substrates, MAEA protects stalled replication forks and promotes homologous recombination by ubiquitylating Ku80 to enable its removal from fork ends and license RAD51 loading; disease-linked variants (R34C, E349G, Y394D, M396R) are defective in this response and cause a neurodevelopmental disorder (DIADEM) with impaired DNA repair in patient-derived cells (PMID:40880485, PMID:41420108). Beyond ubiquitin ligase activity, MAEA associates with F-actin and is essential for erythroblastic island formation and erythroblast enucleation, acting cell-autonomously in erythroblasts and, postnatally, predominantly through bone marrow macrophages (PMID:16707498, PMID:30674470); it relocalizes from the nuclear matrix to the plasma membrane during macrophage maturation, where surface expression correlates with erythroblast-binding capacity (PMID:16510120, PMID:17071116).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2006 High

    Established MAEA as a cell-autonomous determinant of erythroblastic island architecture and erythroblast enucleation, linking it physically to F-actin.

    Evidence Emp-null mouse gene inactivation with fetal liver histology, immunofluorescence, and F-actin co-association assays

    PMID:16707498

    Open questions at the time
    • Molecular basis of the MAEA–F-actin association not defined
    • No connection yet to ubiquitin ligase activity
  2. 2006 Medium

    Resolved MAEA's dynamic subcellular distribution, placing it in the nuclear matrix with nuclear actin in interphase and at the spindle/contractile ring during division.

    Evidence Nuclear fractionation, immunofluorescence, reciprocal Co-IP, and GST pull-down in a single lab

    PMID:16510120

    Open questions at the time
    • Functional consequence of mitotic relocalization untested
    • Single-lab localization data
  3. 2006 Medium

    Showed MAEA traffics to the plasma membrane during macrophage maturation, coupling its surface display to erythroblast binding.

    Evidence Fractionation, pulse-chase labeling, and macrophage–erythroid co-culture binding assay

    PMID:17071116

    Open questions at the time
    • Trafficking machinery unknown
    • Binding partner on erythroblasts not identified
  4. 2008 Medium

    Demonstrated a niche-independent, erythroid-intrinsic requirement for MAEA in erythroid proliferation and terminal differentiation.

    Evidence Fetal liver HSC transplantation into irradiated wild-type mice with CFU-E/BFU-E colony and morphology readouts

    PMID:18501646

    Open questions at the time
    • Mechanism of the intrinsic defect unresolved
    • No molecular substrate linked to the phenotype
  5. 2011 High

    Defined the molecular activity of MAEA's ortholog Gid9 as a RING-finger E3 ligase subunit of the Gid complex required for substrate polyubiquitylation.

    Evidence RING-finger mutagenesis, in vitro polyubiquitylation assays, and Gid2/Rmd5 binding studies in yeast

    PMID:22044534

    Open questions at the time
    • Mammalian substrate range not addressed
    • Direct catalytic mechanism in human cells untested
  6. 2019 High

    Localized the in vivo requirement for erythroblastic island formation to MAEA expressed in macrophages rather than erythroblasts in postnatal bone marrow.

    Evidence Lineage-specific Cre conditional knockouts (Csf1r-, CD169-, Epor-Cre), in vivo island quantification, and antibody inhibition

    PMID:30674470

    Open questions at the time
    • Apparent contrast with earlier erythroid-intrinsic findings not fully reconciled
    • Ubiquitin substrate underlying macrophage role not identified here
  7. 2021 High

    Connected MAEA's ligase activity to HSC maintenance by identifying surface cytokine receptors MPL and FLT3 as degradation targets controlling quiescence and autophagy.

    Evidence Conditional knockout mice, surface receptor flow cytometry, signaling and autophagy flux assays, and pharmacological rescue

    PMID:33947846

    Open questions at the time
    • Direct ubiquitination of MPL/FLT3 not reconstituted in vitro
    • Link between receptor degradation and autophagy flux mechanistically incomplete
  8. 2022 Medium

    Extended MAEA's substrate repertoire to β-catenin, defining a role in restraining canonical Wnt signaling during embryonic patterning.

    Evidence Xenopus gain/loss-of-function, β-catenin Western blots, ubiquitination assay with a 4KR mutant, and Wnt reporter assays

    PMID:36444483

    Open questions at the time
    • Target lysine residues on β-catenin not mapped
    • Conservation of this role in mammals untested
  9. 2023 High

    Showed MAEA mediates K48-linked degradation of PHD3 at K159 to stabilize HIF-1α and promote glioblastoma stemness and drug resistance.

    Evidence TMT proteomics, Co-IP, K48-specific ubiquitination assays, K159 mutagenesis, and xenograft tumor assays

    PMID:36882523

    Open questions at the time
    • Whether CTLH complex assembly is required for PHD3 targeting not addressed
    • Substrate selectivity determinants unknown
  10. 2025 High

    Defined a CTLH/MAEA function in genome maintenance: ubiquitylation of Ku80 to enable RAD51 loading and homologous recombination at stalled forks, with patient variants establishing disease causation.

    Evidence CRISPR knockout screens, DNA fiber and fork restart assays, RAD51 immunofluorescence, MAEA–Ku80 Co-IP and ubiquitylation, and patient-derived variant analysis across two concurrent studies

    PMID:40880485 PMID:41420108

    Open questions at the time
    • Structural basis of Ku80 recognition unresolved
    • How MAEA partitions between hematopoietic and genome-integrity roles unclear
  11. 2025 Medium

    Identified PARP1 as a MAEA degradation substrate linking the ligase to macrophage polarization and phagocytosis in gastrointestinal cancer.

    Evidence Mass spectrometry interactome, MAEA–PARP1 Co-IP, K48 ubiquitination assays, and in vitro/xenograft functional assays

    PMID:39990651

    Open questions at the time
    • Direct ubiquitination site on PARP1 not mapped
    • Single-lab study without reciprocal genetic validation

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single E3 ligase subunit coordinates its many context-specific substrates and its non-catalytic actin/membrane functions remains unresolved.
  • No unifying model of substrate selection across CTLH contexts
  • Relationship between actin-association/localization functions and ligase activity undefined
  • Structural information on MAEA substrate recognition lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 4 GO:0016874 ligase activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005634 nucleus 2 GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-162582 Signal Transduction 2 R-HSA-168256 Immune System 2 R-HSA-73894 DNA Repair 2
Complex memberships
CTLH complex (Gid complex)

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 Emp (MAEA) associates with F-actin, and this interaction is important for normal distribution of F-actin in both erythroblasts and macrophages. Emp null erythroblasts fail to extrude their nuclei even when bound by wild-type macrophages, indicating a cell-autonomous role in enucleation. Emp null fetal livers show virtually no erythroblastic islands and macrophages lack cytoplasmic projections. Targeted gene inactivation (Emp null mice), immunofluorescence microscopy, F-actin co-association assay, fetal liver histology The Journal of biological chemistry High 16707498
2006 Emp (MAEA) is present predominantly in the nuclear matrix of interphase cells, partially co-localizes with nuclear actin (confirmed by co-immunoprecipitation and GST pull-down), and during mitosis redistributes to the mitotic spindle/spindle poles and to the contractile ring during cytokinesis. Sequential nuclear fractionation, immunofluorescence microscopy, co-immunoprecipitation, GST pull-down assay Biochemical and biophysical research communications Medium 16510120
2006 During macrophage differentiation, Emp (MAEA) transitions from predominantly nuclear-matrix localization in immature macrophages to predominantly plasma-membrane localization in mature macrophages; pulse-chase experiments show nascent Emp traffics more efficiently to the plasma membrane in mature cells. Surface Emp expression on mature macrophages correlates with their capacity to bind erythroblasts. Immunofluorescence microscopy, biochemical fractionation, pulse-chase labeling, erythroid-macrophage co-culture binding assay Blood cells, molecules & diseases Medium 17071116
2008 Emp (MAEA) plays a cell-intrinsic role in the erythroid lineage: Emp-null fetal liver cells transplanted into lethally irradiated wild-type mice cause persistent anemia, extensive extramedullary erythropoiesis, increased apoptosis of erythroid precursors, and morphologically immature CFU-E-derived erythroblasts, indicating impaired erythroid proliferation and terminal differentiation independent of the niche. Fetal liver HSC transplantation into lethally irradiated wild-type mice, CFU-E/BFU-E colony assays, morphological examination Blood cells, molecules & diseases Medium 18501646
2011 Gid9 (yeast ortholog of MAEA/GID9) contains a degenerate RING finger domain and functions as an additional E3 ubiquitin ligase subunit of the Gid complex; it binds Gid2/Rmd5, and mutation of its degenerate RING finger abolishes polyubiquitylation and proteasomal degradation of gluconeogenic enzymes (fructose-1,6-bisphosphatase and two others). RING finger mutagenesis, in vitro polyubiquitylation assay, protein interaction studies (binding to Gid2/Rmd5), degradation assays in yeast FEBS letters High 22044534
2019 Maea (MAEA) expressed specifically in macrophages (not erythroblasts) is required for postnatal bone marrow erythroblastic island formation and maintenance: conditional deletion in macrophages (Csf1r-Cre or CD169-Cre) severely reduces bone marrow macrophages, erythroblasts, and in vivo island formation, whereas erythroid-lineage deletion (Epor-Cre) has no such phenotype. Spleen macrophages are unaffected by Maea deletion. Conditional (cell-type-specific Cre) knockout mouse models, in vivo erythroblastic island quantification, flow cytometry, monoclonal antibody inhibition Blood High 30674470
2021 MAEA functions as a membrane-associated E3 ubiquitin ligase subunit essential for HSC maintenance: Maea deletion in mice severely impairs HSC quiescence and causes lethal myeloproliferative syndrome. Mechanistically, MAEA promotes ubiquitin-mediated degradation of cytokine receptors MPL and FLT3 at the cell surface; loss of Maea stabilizes these receptors, prolonging their intracellular signaling. This is associated with impaired autophagy flux in HSCs. Receptor kinase inhibitors or autophagy-inducing compounds rescue the functional defects of Maea-deficient HSCs. Conditional knockout mice, flow cytometry (receptor surface expression), intracellular signaling assays, autophagy flux assays, pharmacological rescue (kinase inhibitors, autophagy inducers) Nature communications High 33947846
2022 Xenopus laevis Maea (ortholog of MAEA) ubiquitinates β-catenin and promotes its degradation via the ubiquitin/proteasome system, thereby inhibiting canonical Wnt signaling target genes (nodal3.1, sia1) and controlling head formation during early embryogenesis. Maea.S ubiquitinated a β-catenin-4KR mutant (with four known ubiquitination lysines mutated to arginine), indicating it targets previously unknown lysine residues. mRNA injection (gain-of-function), morpholino knockdown, Western blot for β-catenin protein levels, ubiquitination assay, reporter gene assay for Wnt target genes Development, growth & differentiation Medium 36444483
2023 MAEA (E3 ubiquitin ligase) promotes K48-linked polyubiquitination and proteasomal degradation of PHD3 at lysine K159, leading to stabilization of HIF-1α and upregulation of CD133, which promotes stemness and temozolomide resistance in glioblastoma cells. Tandem mass tag proteomics, co-immunoprecipitation, ubiquitination assay with K48-linkage specificity, site-directed mutagenesis (K159 in PHD3), Western blot for HIF-1α/CD133, in vivo xenograft tumor growth assay Oncogene High 36882523
2025 MAEA, as a core component of the CTLH E3 ubiquitin ligase complex, is required for homologous recombination repair of stalled replication forks. Loss of MAEA impairs RAD51 recruitment at stalled replication forks, increases sensitivity to replication stress-inducing agents, and causes excessive degradation of nascent DNA strands. Mechanistically, MAEA associates with Ku80 and mediates its ubiquitylation, enabling Ku80 removal from replication fork ends to facilitate RAD51 loading. Disease-linked MAEA variants (R34C, E349G, Y394D, M396R) are defective in this replication stress response. CRISPR-Cas9 knockout screen, replication fork protection assays (DNA fiber assay), RAD51 recruitment assay (immunofluorescence at stalled forks), co-immunoprecipitation (MAEA-Ku80 interaction), ubiquitylation assay for Ku80, functional assays with patient-derived cell lines and variant mutagenesis Science advances High 40880485
2025 MAEA (CTLH complex subunit) is a critical regulator of homologous recombination and the replication stress response; MAEA dysfunction reduces efficiency of RAD51 loading at DNA damage sites, impairing HR-dependent repair and replication fork restart/protection. Eight patients with MAEA variants present a neurodevelopmental disorder (DIADEM) with defective DNA repair in patient-derived cell lines. CRISPR-Cas9 knockout screen (camptothecin), HR repair assays, replication fork restart assays, RAD51 loading assays, patient-derived cell line analysis EMBO molecular medicine High 41420108
2025 MAEA mediates K48-linked ubiquitination and proteasomal degradation of PARP1, suppresses M2 macrophage polarization, and enhances macrophage phagocytic activity in gastrointestinal cancer; MAEA and PARP1 inhibitor veliparib show enhanced combined efficacy in vivo. Mass spectrometry (interactome identification), co-immunoprecipitation (MAEA-PARP1), K48-linked ubiquitination assay, loss/gain-of-function in vitro and xenograft in vivo, macrophage polarization and phagocytosis assays International journal of biological sciences Medium 39990651
2017 MAEA overexpression in primary mouse hepatocytes attenuates expression of gluconeogenesis genes and suppresses HNF-4α mRNA expression, suggesting MAEA negatively regulates hepatic gluconeogenesis. Adenovirus vector-mediated MAEA overexpression in primary mouse hepatocytes, RT-PCR for gluconeogenesis gene expression, blood glucose and insulin measurement in mice Biochemistry and biophysics reports Low 28955747

Source papers

Stage 0 corpus · 72 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Absence of erythroblast macrophage protein (Emp) leads to failure of erythroblast nuclear extrusion. The Journal of biological chemistry 122 16707498
2004 Endothelial microparticles (EMP) bind and activate monocytes: elevated EMP-monocyte conjugates in multiple sclerosis. Frontiers in bioscience : a journal and virtual library 109 15353343
2008 Iron-regulated biofilm formation in Staphylococcus aureus Newman requires ica and the secreted protein Emp. Infection and immunity 89 18268030
1987 Transport of an Mr approximately 300,000 Plasmodium falciparum protein (Pf EMP 2) from the intraerythrocytic asexual parasite to the cytoplasmic face of the host cell membrane. The Journal of cell biology 88 2437128
2010 A randomized phase II trial of personalized peptide vaccine plus low dose estramustine phosphate (EMP) versus standard dose EMP in patients with castration resistant prostate cancer. Cancer immunology, immunotherapy : CII 82 20146063
2017 EMP1, EMP 2, and EMP3 as novel therapeutic targets in human cancer. Biochimica et biophysica acta. Reviews on cancer 76 28408326
2005 sae is essential for expression of the staphylococcal adhesins Eap and Emp. Microbiology (Reading, England) 68 15941988
2012 Exponential megapriming PCR (EMP) cloning--seamless DNA insertion into any target plasmid without sequence constraints. PloS one 61 23300917
2000 Structure and biological activities of eumenine mastoparan-AF (EMP-AF), a new mast cell degranulating peptide in the venom of the solitary wasp (Anterhynchium flavomarginatum micado). Toxicon : official journal of the International Society on Toxinology 56 10775751
1996 The metabolic pathway collection from EMP: the enzymes and metabolic pathways database. Nucleic acids research 52 8594593
2019 Maea expressed by macrophages, but not erythroblasts, maintains postnatal murine bone marrow erythroblastic islands. Blood 49 30674470
2018 AGE/RAGE-Induced EMP Release via the NOX-Derived ROS Pathway. Journal of diabetes research 46 29744367
2011 Gid9, a second RING finger protein contributes to the ubiquitin ligase activity of the Gid complex required for catabolite degradation. FEBS letters 40 22044534
2021 MAEA is an E3 ubiquitin ligase promoting autophagy and maintenance of haematopoietic stem cells. Nature communications 39 33947846
2024 Epithelial-mesenchymal plasticity (EMP) in wound healing: Exploring EMT mechanisms, regulatory network, and therapeutic opportunities. Heliyon 30 39108889
2016 Role of the Emp Pilus Subunits of Enterococcus faecium in Biofilm Formation, Adherence to Host Extracellular Matrix Components, and Experimental Infection. Infection and immunity 30 26930703
2012 EMP-1 promotes tumorigenesis of NSCLC through PI3K/AKT pathway. Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban 28 23271282
2013 Claudins reign: The claudin/EMP/PMP22/γ channel protein family in C. elegans. Tissue barriers 27 24665403
2015 Relationships between the use of Embden Meyerhof pathway (EMP) or Phosphoketolase pathway (PKP) and lactate production capabilities of diverse Lactobacillus reuteri strains. Journal of microbiology (Seoul, Korea) 26 26428921
2005 EMP-1 is a junctional protein in a liver stem cell line and in the liver. Biochemical and biophysical research communications 25 16036215
2010 Mechanisms involved in the blood-testis barrier increased permeability induced by EMP. Toxicology 24 20633596
2017 The Staphylococcus aureus extracellular matrix protein (Emp) has a fibrous structure and binds to different extracellular matrices. Scientific reports 22 29057978
2008 Requirement for erythroblast-macrophage protein (Emp) in definitive erythropoiesis. Blood cells, molecules & diseases 21 18501646
2021 68Ga-EMP-100 PET/CT-a novel ligand for visualizing c-MET expression in metastatic renal cell carcinoma-first in-human biodistribution and imaging results. European journal of nuclear medicine and molecular imaging 20 34708249
2016 Production of the Bioactive Compounds Violacein and Indolmycin Is Conditional in a maeA Mutant of Pseudoalteromonas luteoviolacea S4054 Lacking the Malic Enzyme. Frontiers in microbiology 19 27695447
1998 Androgen antagonistic effect of estramustine phosphate (EMP) metabolites on wild-type and mutated androgen receptor. Biochemical pharmacology 18 10076535
2011 Effect of Electromagnetic Pulses (EMP) on associative learning in mice and a preliminary study of mechanism. International journal of radiation biology 17 21929296
2010 Final report on low-dose estramustine phosphate (EMP) monotherapy and very low-dose EMP therapy combined with LH-RH agonist for previously untreated advanced prostate cancer. Aktuelle Urologie 17 20094950
2006 Emp is a component of the nuclear matrix of mammalian cells and undergoes dynamic rearrangements during cell division. Biochemical and biophysical research communications 17 16510120
2023 E3 ligase MAEA-mediated ubiquitination and degradation of PHD3 promotes glioblastoma progression. Oncogene 16 36882523
2007 Extramedullary plasmacytoma (EMP): Report of a case manifested as a mediastinal mass and multiple pulmonary nodules and review of literature. World journal of surgical oncology 16 17963517
1992 Stimulation of growth by both androgen and estrogen of the EMP-K1 transplantable tumor with androgen and estrogen receptors from human extramammary Paget's disease in nude mice. Journal of the National Cancer Institute 15 1312178
2006 Changing pattern of the subcellular distribution of erythroblast macrophage protein (Emp) during macrophage differentiation. Blood cells, molecules & diseases 13 17071116
2007 Expression of TM4SF10, a Claudin/EMP/PMP22 family cell junction protein, during mouse kidney development and podocyte differentiation. Developmental dynamics : an official publication of the American Association of Anatomists 12 17195181
2017 Erythroblast macrophage protein (Emp): Past, present, and future. European journal of haematology 11 29032607
2013 Impact of expression of EMP enzymes on glucose metabolism in Zymomonas mobilis. Applied biochemistry and biotechnology 10 23613118
2007 Mapping the transcription start points of the Staphylococcus aureus eap, emp, and vwb promoters reveals a conserved octanucleotide sequence that is essential for expression of these genes. Journal of bacteriology 10 17965149
1995 [Extramedullary plasmocytoma (EMP) of the head and neck: a series of 22 cases]. Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale 10 8711997
2017 Adenovirus vector-mediated macrophage erythroblast attacher (MAEA) overexpression in primary mouse hepatocytes attenuates hepatic gluconeogenesis. Biochemistry and biophysics reports 9 28955747
2015 [Endothelial microparticles (EMP) in physiology and pathology]. Postepy higieny i medycyny doswiadczalnej (Online) 9 26400879
2015 Influence of irradiation on release of endothelial microparticles (EMP) in vitro. Clinical hemorheology and microcirculation 8 26410868
2021 Expression of epithelial membrane protein (EMP) 1, EMP 2, and EMP 3 in thyroid cancer. Histology and histopathology 7 34617578
2017 Sirt6 mRNA-incorporated endothelial microparticles (EMPs) attenuates DM patient-derived EMP-induced endothelial dysfunction. Oncotarget 7 29371988
2010 The effects of electromagnetic pulses (EMP) on the bioactivity of insulin and a preliminary study of mechanism. International journal of radiation biology 7 20070212
2002 [Effect of EMP-1 gene on human esophageal cancer cell line]. Ai zheng = Aizheng = Chinese journal of cancer 7 12451984
2000 Plasminogen activator inhibitor-1 fused with erythropoietin (EPO) mimetic peptide (EMP) enhances the EPO activity of EMP. The journal of peptide research : official journal of the American Peptide Society 7 10961539
2024 Epigenetic Regulation of EMP/EMT-Dependent Fibrosis. International journal of molecular sciences 6 38474021
2023 Combined effects of EMP and RF field on emotional behavior in mice. Frontiers in public health 6 37006533
2002 EMP combination chemotherapy and low-dose monotherapy in advanced prostate cancer. Expert review of anticancer therapy 6 12113067
2025 The E3 ubiquitin ligase MAEA promotes macrophage phagocytosis and inhibits gastrointestinal cancer progression by mediating PARP1 ubiquitination and degradation. International journal of biological sciences 5 39990651
2023 Characterization of the enzyme kinetics of EMP and HMP pathway in Corynebacterium glutamicum: reference for modeling metabolic networks. Frontiers in bioengineering and biotechnology 5 38090711
2019 MAEA rs6815464 polymorphism and periodontitis in postmenopausal Japanese females: A cross-sectional study. Archives of oral biology 5 31005685
1996 [Exploration of intraspinal tumors using evoked motor potentials (EMP): correlations with data of evoked somatosensory potentials]. Neurophysiologie clinique = Clinical neurophysiology 5 8975113
2023 Fumarase activity in NAD-dependent malic enzyme, MaeA, from Escherichia coli. Biochemical and biophysical research communications 4 37634412
2023 Regulation of Embden-Meyerhof-Parnas (EMP) Pathway and Tricarboxylic Acid (TCA) Cycle Concerning Aberrant Chilling Injury Behavior in Postharvest Papaya (Carica papaya L.). International journal of molecular sciences 4 37762201
2023 Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP). Translational oncology 3 37984255
2021 Common variants in MAEA gene contributed the susceptibility to osteoporosis in Han Chinese postmenopausal women. Journal of orthopaedic surgery and research 3 33423677
2010 Differential diagnosis of acute rejection and chronic cyclosporine nephropathy after rat renal transplantation by detection of endothelial microparticles (EMP). Medical hypotheses 3 20832948
2025 Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans. Science advances 2 40880485
2024 Protein level of epithelial membrane protein (EMP) 1, EMP 2, and EMP 3 in carcinoma of unknown primary. Neoplasma 2 39556425
2023 Optimization of hydrogen production in Enterobacter aerogenes by Complex I peripheral fragments destruction and maeA overexpression. Microbial cell factories 2 37496040
2022 maea affects head formation through ß-catenin degradation during early Xenopus laevis development. Development, growth & differentiation 2 36444483
2000 [Effect of temperature on the activity of some enzymes representative of EMP pathway and TCA cycle in psychrophilic yeast]. Wei sheng wu xue bao = Acta microbiologica Sinica 2 12548764
2025 Loss of CTLH component MAEA impairs DNA repair and replication and leads to developmental delay. EMBO molecular medicine 1 41420108
2024 ZEB2 drives intra-tumor heterogeneity and skin squamous cell carcinoma formation with distinct EMP transition states. iScience 1 39555401
2023 Evaluation of [18F]AlF-EMP-105 for Molecular Imaging of C-Met. Pharmaceutics 1 37514101
2018 Multivariable quantitative relation between cell viability and the exposure parameters of 9.33 GHz RF-EMP irradiation. Electromagnetic biology and medicine 1 29902088
2018 A case study of the translocation, bioprocessing and tissue interactions of EMP following inhalation exposure. Toxicology and applied pharmacology 1 30563646
2025 Identification of MAEA protein as a potential target for chemoresistance in osteosarcoma using bioinformatics and proteomic analysis. Frontiers in oncology 0 40989695
2025 MAP4 phosphorylation induced by ARID1A loss sensitizes colorectal cancer cells to EMP. Cell death & disease 0 41360780
2023 Expression of EMP 1, 2, and 3 in Adrenal Cortical Neoplasm and Pheochromocytoma. International journal of molecular sciences 0 37629198
2018 Author Correction: The Staphylococcus aureus extracellular matrix protein (Emp) has a fibrous structure and binds to different extracellular matrices. Scientific reports 0 29802334

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