Affinage

MEMO1

Protein MEMO1 · UniProt Q9Y316

Length
297 aa
Mass
33.7 kDa
Annotated
2026-06-10
64 papers in source corpus 28 papers cited in narrative 28 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MEMO1 is a structurally conserved, metal-binding signaling adaptor that couples receptor tyrosine kinase signaling to the cytoskeleton and to cellular redox and metal homeostasis (PMID:15156151, PMID:24917593, PMID:38640016). It was first defined as a relay downstream of ErbB2: through its vestigial class III nonheme-dioxygenase active site it directly binds the ErbB2 phospho-Tyr1227 motif, constituting a novel phosphotyrosine-recognition fold distinct from SH2 and PTB modules (PMID:18045866, PMID:21840311). Acting downstream of this and other receptors, MEMO1 controls directional cell migration by governing microtubule dynamics and leading-edge actin organization, mediated through proper localization of RhoA and its effector mDia1 and through direct binding to cofilin, whose F-actin-severing activity it enhances (PMID:18955552, PMID:19223396). This cytoskeletal role extends in vivo to radial glial process tiling in the developing neocortex, where MEMO1 stabilizes microtubules and directs CAMSAP2 minus-end distribution and polarized GPR56 trafficking (PMID:31277925). MEMO1 also functions as a metal-binding redox protein: it coordinates Cu(I) ions and exchanges them with the chaperone Atox1, binds iron in a mode resembling extradiol dioxygenases, and sustains NOX1-dependent ROS production required for tumor cell migration and metastasis (PMID:24917593, PMID:36067318, PMID:38640016). Its iron-binding activity feeds into ferroptosis sensitivity, mitochondrial iron supply, and iron-dependent control of TCA cycle metabolite flux (PMID:38640016, PMID:40278406). Beyond cancer, MEMO1 broadly tunes growth factor signaling—FGFR/FGF23-Klotho, IGF-IR/IRS1-PI3K/Akt, S1P, and VEGFR2—and is required for organismal mineral homeostasis, governing renal calcium, magnesium and vitamin D handling and skeletal and enamel mineralization (PMID:22824790, PMID:24056085, PMID:24714781, PMID:30038585, PMID:32706793, PMID:36434320, PMID:37475472, PMID:40936746). In C. elegans the orthologue inhibits BLI-3/NADPH oxidase via RHO-1, linking MEMO1 to ROS-dependent stress resistance and longevity (PMID:28085666).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2004 High

    Established MEMO1's founding identity by asking how ErbB2 chemotactic signals reach the cytoskeleton; it answered that MEMO is a required relay between ErbB2 and microtubule extension.

    Evidence ErbB2 phosphopeptide co-precipitation and knockdown migration/microtubule imaging in cells

    PMID:15156151

    Open questions at the time
    • Direct vs Shc-mediated binding to ErbB2 not resolved
    • Molecular mechanism linking MEMO to microtubules not yet defined
  2. 2007 High

    Resolved how MEMO1 recognizes phosphotyrosine; the crystal structure revealed a dioxygenase-like fold lacking enzymatic activity that binds the ErbB2 pTyr1227 peptide through its vestigial active site, defining a new phosphotyrosine-binding class.

    Evidence X-ray crystallography at 2.1 Å plus in vitro phosphopeptide binding

    PMID:18045866

    Open questions at the time
    • No metal or catalytic activity detected at this stage
    • Physiological relevance of the dioxygenase-like fold unexplained
  3. 2008 High

    Defined the downstream cytoskeletal mechanism by showing MEMO controls microtubule growth/shortening transitions via RhoA-mDia1 localization at the leading edge.

    Evidence siRNA knockdown, live microtubule imaging, RhoA/mDia1 immunofluorescence in migrating cells

    PMID:18955552

    Open questions at the time
    • Direct biochemical link between MEMO and RhoA not established
    • How MEMO positions RhoA/mDia1 to the membrane unknown
  4. 2009 High

    Identified a direct actin-regulatory partner, placing MEMO upstream of cofilin and PLCγ1 in ErbB2-driven chemotaxis.

    Evidence Yeast two-hybrid, recombinant pulldown, Co-IP, in vitro F-actin depolymerization assay, knockdown migration tracking

    PMID:19223396

    Open questions at the time
    • Structural basis of MEMO-cofilin interaction unknown
    • How cofilin and RhoA-mDia1 arms are coordinated unclear
  5. 2011 Medium

    Refined the phosphopeptide recognition by mapping the minimal ErbB2 sequence and a novel pTyr motif distinct from SH2/PTB.

    Evidence NMR/docking structural modeling and peptide-variant binding assays

    PMID:21840311

    Open questions at the time
    • Docking model not validated by co-crystal structure
    • Single-lab characterization
  6. 2012 Medium

    Extended MEMO1 beyond ErbB2 by linking it to IGF-IR signaling, showing it binds IRS1 and drives PI3K/Akt-Snail1 EMT.

    Evidence Co-IP, Western blots for Akt/Snail1, EMT marker and overexpression/knockdown assays in mammary epithelial cells

    PMID:22824790

    Open questions at the time
    • Direct vs indirect IRS1 binding not resolved
    • Single-lab finding
  7. 2013 Medium

    Connected MEMO1 to nuclear-receptor and FGFR signaling, showing it mediates extranuclear ERα function and is required for FGFR-dependent vitamin D/calcium homeostasis in vivo.

    Evidence Multiple Co-IPs (ERα, IGF1R, ERBB2, FGFR), signaling Western blots, ERα reporter, xenografts, and conditional KO mouse phenotyping

    PMID:23861392 PMID:24056085

    Open questions at the time
    • Whether ERα and FGFR effects share a common molecular mechanism unknown
    • Single-lab studies
  8. 2014 High

    Reframed MEMO1 as a copper-dependent redox protein required for NOX1-driven ROS, migration, and metastasis, and as a regulator of S1P signaling and vascular development.

    Evidence Biochemical redox/ROS assays, NOX1 activity, knockdown/overexpression, xenograft metastasis; separate MEF and HUVEC S1P rescue plus endothelial KO embryos

    PMID:24714781 PMID:24917593

    Open questions at the time
    • Direct enzymatic redox mechanism of MEMO1 not biochemically defined
    • Relationship between redox role and phosphopeptide-binding role unclear
  9. 2015 Medium

    Established cell-autonomous developmental roles in endochondral ossification through neural crest-specific deletion affecting cranial base mineralization and vascular invasion.

    Evidence ENU mutant mapping, neural crest conditional KO, histology, gene expression, micro-CT

    PMID:26746790

    Open questions at the time
    • Molecular target driving ossification defect not identified
    • Non-autonomous palate role unexplained
  10. 2016 Medium

    Detailed the ERα-c-Src axis and uncovered transcriptional control of MEMO1 itself by HER2 via AhR/ARNT.

    Evidence Co-IP, ERα Y537 phosphorylation Western, fractionation; ChIP and luciferase reporter on MEMO1 promoter with migration/invasion assays

    PMID:27472465 PMID:27941874

    Open questions at the time
    • Direct MEMO1-c-Src binding interface unknown
    • Single-lab transcriptional and signaling mechanisms
  11. 2017 High

    Demonstrated an evolutionarily conserved redox-signaling function: the C. elegans orthologue inhibits NADPH oxidase via RhoA, controlling ROS, p38-SKN-1 stress signaling, and longevity.

    Evidence C. elegans genetic epistasis, RHO-1/BLI-3 Co-IP, ROS measurement, pathway reporters, lifespan assays

    PMID:28085666

    Open questions at the time
    • Whether mammalian MEMO1 inhibits or sustains NOX is context-dependent and unreconciled
    • Direct biochemical mechanism of NOX regulation unknown
  12. 2018 Medium

    Linked MEMO1's redox function to mineral homeostasis and skeletal biology, showing it regulates renal calcium transporters, magnesium channels, and redox-dependent alkaline phosphatase dimerization in bone.

    Evidence Kidney-specific and whole-body conditional KO mice, serum biochemistry, transporter qPCR/Western, ALP activity and dimerization assays, redox measurements

    PMID:30038585 PMID:30038965 PMID:32706793

    Open questions at the time
    • Direct molecular substrate of MEMO1's redox effect on transporters/ALP not defined
    • Single-lab in vivo models
  13. 2019 High

    Provided the clearest in vivo cytoskeletal mechanism, showing MEMO1 stabilizes microtubules to govern radial glial tiling via CAMSAP2 minus-end organization and polarized trafficking.

    Evidence Conditional KO and in utero knockdown, live imaging, CAMSAP2/GPR56 immunofluorescence, microtubule dynamics assays

    PMID:31277925

    Open questions at the time
    • How MEMO1 biochemically controls CAMSAP2 distribution unknown
    • Link to the metal/redox functions not addressed
  14. 2022 High

    Defined MEMO1 as a Cu(I) coordinator that shields copper from ROS and exchanges it with Atox1, and identified its proteasomal regulation by HPV16 E7.

    Evidence ITC/ICP-MS/EPR/UV-Vis Cu binding, in vitro Cu(I) exchange with Atox1, proximity ligation; E7 pulldown, Co-IP, Cullin2-dependent degradation assays

    PMID:36067318 PMID:36197110 PMID:36434320

    Open questions at the time
    • Whether copper shuttling explains the migration/redox phenotypes not shown
    • Physiological copper cargo destination beyond Atox1 unclear
  15. 2024 High

    Established MEMO1 as an iron-binding protein with a dioxygenase-like coordination mode, connecting it to ferroptosis, mitochondrial iron supply, and iron-dependent TCA cycle flux.

    Evidence Crystal structures of MEMO1-iron and MEMO1-copper, in vitro iron binding, genetic interactions with TFR2/SLC25A28/IRP1, ferroptosis and metabolomics assays

    PMID:38640016 PMID:40278406

    Open questions at the time
    • Whether iron binding is catalytic or carrier-like unresolved
    • Mechanism linking iron handling to TCA flux not defined
  16. 2025 Medium

    Identified MEMO1 as a negative regulator of VEGF-driven pathological angiogenesis, dampening VEGFR2/STAT3 signaling in retinal endothelium.

    Evidence Reciprocal knockdown/overexpression in RMVECs, phospho-Western, wound closure, endothelial-specific knockdown in rat ROP model

    PMID:40936746

    Open questions at the time
    • Direct molecular target on the VEGFR2 pathway unknown
    • Reconciliation with pro-migratory roles in cancer unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MEMO1's single dioxygenase-like fold integrates its phosphotyrosine-binding, copper/iron coordination, and redox-signaling activities into one mechanism across such diverse tissues remains unresolved.
  • No unifying biochemical model connecting metal binding to signaling output
  • No co-crystal structure of MEMO1 with a full-length partner
  • Tissue-specific substrate/effector selection mechanism unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 3 GO:0042393 histone binding 3 GO:0060089 molecular transducer activity 2 GO:0140104 molecular carrier activity 2 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 4 R-HSA-1430728 Metabolism 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-5357801 Programmed Cell Death 1
Partners
ATOX1C-SRCCOFILINERBB2ESR1IGF1RIRS1RHOA
Complex memberships
FGFR signalosome

Evidence

Reading pass · 28 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 MEMO1 (Memo) was identified as a novel protein that interacts with a phospho-Tyr1227-containing peptide of ErbB2/Neu, most probably through the Shc adaptor protein. In Memo-defective cells, ErbB2-driven lamellipodia form normally but microtubule extension toward the cell cortex fails, establishing Memo as a relay between ErbB2 chemotactic signals and the microtubule cytoskeleton. Co-precipitation with ErbB2 phosphopeptide, dominant-negative/knockdown cell migration assays, live imaging of lamellipodia and microtubule dynamics Nature cell biology High 15156151
2007 Crystal structure of human MEMO1 at 2.1 Å resolution revealed it is homologous to class III nonheme iron-dependent dioxygenases. No metal binding or classical enzymatic (dioxygenase) activity was detected, but MEMO1 directly binds an ErbB2-derived phosphopeptide encompassing Tyr-1227 via its vestigial enzymatic active site, defining it as a new class of phosphotyrosine-binding protein. X-ray crystallography (2.1 Å), in vitro phosphopeptide binding assay, active-site structural comparison The Journal of biological chemistry High 18045866
2008 Memo controls ErbB2-regulated microtubule dynamics by altering the transition frequency between MT growth and shortening phases. Memo is required for proper localization of RhoA GTPase and its effector mDia1 to the plasma membrane; Memo-RhoA-mDia1 signaling coordinates lamellipodial actin network organization, adhesion site formation, and microtubule outgrowth at the leading edge during cell migration. Memo siRNA knockdown, live MT dynamics imaging, immunofluorescence of RhoA/mDia1 localization, adhesion site quantification The Journal of cell biology High 18955552
2009 Memo interacts directly with cofilin (identified by yeast two-hybrid and confirmed by in vitro pulldown with recombinant proteins and co-immunoprecipitation). Memo enhances cofilin F-actin depolymerizing and severing activity in vitro. In Memo-knockdown cells, HRG-induced PLCγ1 phosphorylation is reduced and GFP-cofilin recruitment to lamellipodia is impaired, placing Memo upstream of both PLCγ1 and cofilin in ErbB2-driven chemotaxis. Yeast two-hybrid, recombinant protein pulldown, co-immunoprecipitation, in vitro F-actin binding and depolymerization assay, Memo/PLCγ1 knockdown with live cell migration directionality tracking Journal of cell science High 19223396
2011 Structural and functional analysis defined the minimum ErbB2 phosphopeptide sequence required for MEMO1 recognition. The interaction is pH-dependent and requires phosphorylation of Tyr-1227; a docking-based structural model of the MEMO1/phosphopeptide complex was generated and compared to SH2 and PTB phosphotyrosine motifs, identifying a novel phosphotyrosine recognition motif. NMR/docking structural modeling, peptide binding assays, mutagenesis of phosphopeptide variants FEBS letters Medium 21840311
2012 MEMO1 binds to insulin receptor substrate 1 (IRS1), activates the downstream PI3K/Akt signaling pathway, upregulates Snail1, and thereby triggers the epithelial-mesenchymal transition (EMT) program in mammary epithelial cells downstream of IGF-IR signaling. Co-immunoprecipitation (MEMO1-IRS1 interaction), Western blot for PI3K/Akt activation and Snail1, EMT marker analysis, overexpression/knockdown functional assays Oncogene Medium 22824790
2013 MEMO1 physically interacts with estrogen receptor α (ERα) and, through its interactions with growth factor receptors IGF1R and ERBB2, mediates extranuclear ER functions including activation of MAPK and AKT. This leads to ERα phosphorylation and regulation of estrogen-responsive gene expression; MEMO1 is required for estrogen-induced breast tumor growth in vivo. Co-immunoprecipitation (MEMO-ERα, MEMO-IGF1R, MEMO-ERBB2), Western blot for MAPK/AKT activation and ERα phosphorylation, ERα reporter assay, xenograft tumor growth The Journal of biological chemistry Medium 23861392
2013 Memo associates with the FGFR signalosome and is necessary for optimal activation of downstream FGF signaling. Loss of Memo in mouse embryonic fibroblasts reduces FGF-induced signaling responses. Memo conditional-knockout mice show reduced lifespan, premature aging phenotypes, elevated serum 1,25(OH)2D and calcium, identifying Memo as a novel regulator of FGFR signaling that controls vitamin D and calcium homeostasis. Co-immunoprecipitation (Memo-FGFR complex), Memo KO MEFs signaling assays, conditional knockout mouse model with phenotypic analysis FASEB journal Medium 24056085
2014 Memo is a copper-dependent redox enzyme: biochemical assays showed Memo promotes a more oxidized intracellular milieu and stimulates ROS production in cellular structures involved in migration. Memo is required for sustained production of superoxide (O2−) by NADPH oxidase 1 (NOX1) in breast cancer cells. Memo is required for migration/invasion in vitro and spontaneous lung metastasis in vivo. Biochemical redox assays, ROS measurement (intracellular oxidation probes), NOX1 activity assays, Memo knockdown/overexpression, in vivo xenograft metastasis Science signaling High 24917593
2014 Memo null MEFs are impaired in PDGF-induced migration due to a defect in sphingosine-1-phosphate (S1P) cell-autonomous signaling. In endothelial cells (HUVECs), Memo knockdown reduces junctional VE-cadherin and increases sprouting; these phenotypes are rescued by exogenous S1P, placing Memo in the cell-autonomous S1PR signaling pathway. Endothelial-specific Memo KO embryos show vascular defects from E13.5, mimicking S1PR-deficient phenotypes. Memo KO MEF migration assays with S1P rescue, HUVEC knockdown with VE-cadherin immunofluorescence and sprouting assays, conventional and endothelial-specific conditional Memo KO mice PloS one Medium 24714781
2015 Neural crest cell-specific deletion of Memo1 causes failure of anterior cranial base ossification (cell-autonomous role), while palate formation is largely normal in these conditional mutants (suggesting a non-autonomous role for MEMO1 in palatal closure). Memo1 mutants show increased hypertrophic chondrocyte zones, reduced vascular invasion and mineralization, and reduced expression of matrix metalloproteinases and osteoblast lineage markers in the cranial base. ENU-induced recessive mutant mouse, non-complementation mapping to Memo1, neural crest-specific conditional Memo1 KO (Cre/lox), histology, gene expression analysis, micro-CT Developmental biology Medium 26746790
2016 Memo interacts with c-Src and facilitates ERα–c-Src interaction, ERα Y537 phosphorylation, and ERα extra-nuclear localization downstream of heregulin and estrogen in breast cancer cells. Co-immunoprecipitation (Memo-c-Src, ERα-c-Src), Western blot for ERα Y537 phosphorylation, sub-cellular fractionation/immunofluorescence of ERα localization, Memo knockdown Oncotarget Medium 27472465
2016 HER2 activation drives MEMO1 expression in colorectal cancer cells through AhR/ARNT transcriptional complex recruitment to the MEMO1 gene promoter (established by reporter assays and chromatin IP). MEMO1 depletion negatively affects the cellular actin network and is required for HER2-mediated migration and invasion. Chromatin immunoprecipitation (AhR/ARNT on MEMO1 promoter), luciferase reporter assay, MEMO1 siRNA knockdown with actin immunofluorescence and migration/invasion assays Oncogene Medium 27941874
2017 In C. elegans, MEMO-1 (the orthologue of mammalian MEMO1) inhibits BLI-3/NADPH oxidase. Loss of memo-1 results in enhanced interaction of RHO-1/RhoA with BLI-3/NADPH oxidase, stimulating ROS production that signals via p38 MAP kinase to the transcription factor SKN-1/NRF1,2,3, promoting stress resistance and longevity. Either loss of memo-1 or overexpression of BLI-3 is sufficient to increase lifespan. C. elegans genetic epistasis (memo-1 loss-of-function, bli-3 overexpression), co-immunoprecipitation (RHO-1 with BLI-3), ROS measurement, p38/SKN-1 pathway reporter assays, lifespan assays eLife High 28085666
2018 MEMO1 binding specificity for the ErbB2 phosphopeptide (pTyr1227) was quantitatively mapped using a fluorescence polarization assay and molecular dynamics simulations: the interaction requires phosphorylation of the tyrosine residue and is pH-dependent; mutagenesis identified residues contributing to favorable interactions at the MEMO1-peptide interface. Fluorescence polarization assay, molecular dynamics simulations, site-directed mutagenesis of MEMO1 Biochemistry Medium 30067338
2018 Renal Memo1 deletion in mice leads to elevated serum FGF23 and increased expression/protein abundance of distal renal calcium transporters TRPV5, NCX1, and calbindin-D28k. TRPV5 membrane abundance was vitamin D-dependent while NCX1 abundance was vitamin D-independent, revealing distinct Memo1-dependent and Memo1-independent regulatory mechanisms for renal calcium handling. Inducible kidney-specific Memo1 KO mouse model (Cre/lox), serum biochemistry, qPCR and Western blot for transporter expression, vitamin D-deficient diet challenge Frontiers in physiology Medium 30038585
2018 Memo1 deletion in mice results in severely altered trabecular bone with lower mineralization. Alkaline phosphatase (ALP) activity is decreased in serum and bone without change in ALPL expression; the bone intracellular redox state is altered and ALP dimerization is reduced in Memo cKO bone, linking Memo's redox function to ALP post-translational regulation (dimerization-dependent activity). Whole-body Cre/lox Memo cKO mice, micro-CT, ALP activity assays, detergent sensitivity assay for ALP dimerization, redox state measurements in bone JBMR plus Medium 30038965
2019 Memo1 is a critical determinant of radial glial cell (RGC) tiling during neocortical development. Memo1 deletion or knockdown causes hyperbranching of RGC basal processes, disrupted tiling, and aberrant neuronal layering. Mechanistically, Memo1 regulates microtubule stability required for RGC tiling: Memo1 deficiency disrupts MT minus-end CAMSAP2 distribution, initiates aberrant MT branching, and alters polarized trafficking of basal domain proteins such as GPR56. Conditional Memo1 KO and in utero knockdown in developing mouse cortex, live imaging, immunofluorescence for CAMSAP2 and GPR56, MT dynamics assays Neuron High 31277925
2020 Memo1 KO mice show higher serum magnesium and decreased calcification propensity compared to Klotho/Fgf23-deficient models. Both inducible whole-body and kidney-specific Memo1 KO mice display increased expression of intestinal and renal magnesium channels and the regulator EGF, identifying MEMO1 as a regulator of magnesium homeostasis through control of magnesium channel expression. Inducible whole-body and kidney-specific Memo1 KO mouse models, serum magnesium biochemistry, qPCR for magnesium channel genes, calcification propensity assay PloS one Medium 32706793
2022 Purified MEMO1 coordinates two reduced Cu(I) ions per protein under reducing conditions in vitro, shielding them from ROS generation. The cytoplasmic copper chaperone Atox1 can interact with and exchange Cu(I) with MEMO1 in vitro, and the two proteins show spatial proximity in breast cancer cells, suggesting MEMO1 acts as a Cu(I) chelator/shuttle toward Atox1 and the secretory pathway. Multiple biophysical methods (ITC, ICP-MS, EPR, UV-Vis spectroscopy) for Cu-binding characterization, in vitro Cu(I) exchange assay between MEMO1 and Atox1, proximity ligation assay in breast cancer cells Proceedings of the National Academy of Sciences of the United States of America High 36067318
2022 HPV16 E7 interacts with MEMO1 through its C-terminal E80/D81 residues and targets MEMO1 for proteasomal degradation via a Cullin2-dependent mechanism. MEMO1 overexpression decreases cell transformation and proliferation; knockdown of MEMO1 correlates with Akt activation in HPV-positive cervical cancer cells. Pulldown assay (HPV16 E7 peptide), co-immunoprecipitation, proteasome inhibitor rescue, Cullin2 knockdown, MEMO1 overexpression and knockdown with Akt Western blot Journal of virology Medium 36197110
2022 Memo1 is required for renal FGF23-Klotho signaling: Memo cKO mice show impaired FGF23-driven renal ERK phosphorylation and transcriptional responses. FGF23 actions involve activation of oxidation-sensitive protein phosphotyrosyl phosphatases; redox proteomics revealed excessive reduced thiols of Rho-GDI1 in Memo cKO, and Memo's redox function interacts with oxidation at Rho-GDI1 Cys79, with disturbed small Rho-GTPase abundance in cKO kidney. Postnatally induced whole-body Memo cKO mice, FGF23 injection + ERK phosphorylation Western blot, phosphotyrosyl phosphatase activity assay, redox proteomics (thiol trapping), Rho-GDI1 Cys79 oxidation assay, Rho-GTPase activity assays Journal of cell communication and signaling Medium 36434320
2023 Copper additions to MDA-MB-231 breast cancer cells increase intracellular ROS, and this effect is further elevated when MEMO1 is silenced. MEMO1 knockdown exaggerates copper-induced cell death, supporting that MEMO1 protects cancer cells from copper-mediated redox toxicity in a cellular context. MEMO1 siRNA knockdown, copper addition to breast cancer cells, multiple commercial ROS probes, cell viability assay Journal of inorganic biochemistry Medium 37487298
2024 Purified MEMO1 binds iron with high affinity under redox conditions mimicking the intracellular environment, and crystal structures of MEMO1 in complex with iron and copper were solved. The iron coordination mode in MEMO1 closely resembles that of iron-containing extradiol dioxygenases (sharing a similar structural fold). MEMO1 exhibits genetic interactions with iron-related proteins TFR2, mitoferrin-2 (SLC25A28), and IRP1/ACO1 in cancer cells and is involved in ferroptosis and iron supply to mitochondria. X-ray crystallography (MEMO1-iron and MEMO1-copper complexes), in vitro iron binding assays, genetic interaction analysis (cancer cell line essentiality data), co-immunoprecipitation/proximity assays for TFR2/SLC25A28/IRP1 interactions, ferroptosis assays eLife High 38640016
2021 Phenazine-based small-molecule inhibitors of MEMO1 were identified that competitively disrupt MEMO1's interaction with its ErbB2 phosphopeptide partner (KI ~2.7 µM in fluorescence polarization assay) and slow breast cancer cell migration in a scratch assay, confirming that the MEMO1 phosphopeptide-binding interface is functionally important for cell motility. Virtual screening, competitive fluorescence polarization assay, molecular dynamics simulations, scratch/wound-healing migration assay ChemMedChem Medium 33332774
2023 Conditional deletion of MEMO1 from ameloblasts results in enamel mineralization defects (reduced mineral density and tooth integrity) associated with disruption of ameloblast morphology, reduction in late-stage ameloblast markers, and disruption of cytoskeletal-associated gene expression, establishing a cell-autonomous role for MEMO1 in ameloblast maturation and enamel formation. Ameloblast-specific conditional Memo1 KO (Cre/lox), micro-CT for mineral density, histology, single-cell/molecular profiling of ameloblasts Journal of dental research Medium 37475472
2025 MEMO1 knockdown in retinal microvascular endothelial cells (RMVECs) enhances VEGF-induced VEGFR2 and STAT3 phosphorylation and increases wound closure; conversely, MEMO1 overexpression suppresses VEGF-induced VEGFR2/STAT3 phosphorylation and dampens VEGF-induced wound closure. In the absence of VEGF, MEMO1 overexpression promotes proliferation via AKT phosphorylation. In vivo, endothelial-specific MEMO1 knockdown increases intravitreal neovascularization (IVNV) in a rat ROP model, identifying MEMO1 as a negative regulator of VEGF-driven pathological angiogenesis. MEMO1 siRNA knockdown and overexpression in cultured RMVECs, Western blot for VEGFR2/STAT3/AKT phosphorylation, wound closure assay, endothelial-specific in vivo MEMO1 knockdown in rat ROP model with IVNV quantification FASEB bioAdvances Medium 40936746
2025 MEMO1 KO in MDA-MB-231 breast cancer cells causes increased α-ketoglutarate and citrate levels regardless of iron availability, and elevated fumarate, malate, and glutamate specifically under low iron conditions, indicating MEMO1 regulates TCA cycle metabolite flux in an iron-dependent manner. ACO2 and OGDH knockdowns inhibit MDA-MB-231 proliferation, confirming TCA cycle essentiality. ShRNA MEMO1 knockdown and KO, LC-MS/MS quantification of TCA cycle metabolites under varying iron conditions, ACO2/OGDH knockdown proliferation assays Metabolites Medium 40278406

Source papers

Stage 0 corpus · 64 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Memo is a copper-dependent redox protein with an essential role in migration and metastasis. Science signaling 122 24917593
2004 Memo mediates ErbB2-driven cell motility. Nature cell biology 109 15156151
2002 Iron metabolism and the risk of restless legs syndrome in an elderly general population--the MEMO-Study. Journal of neurology 106 12242538
2006 MeMo: a web tool for prediction of protein methylation modifications. Nucleic acids research 105 16845004
2008 Memo-RhoA-mDia1 signaling controls microtubules, the actin network, and adhesion site formation in migrating cells. The Journal of cell biology 97 18955552
2017 NADPH oxidase-mediated redox signaling promotes oxidative stress resistance and longevity through memo-1 in C. elegans. eLife 68 28085666
2012 MEMO1, a new IRS1-interacting protein, induces epithelial-mesenchymal transition in mammary epithelial cells. Oncogene 66 22824790
2020 Exosomal Circ-MEMO1 Promotes the Progression and Aerobic Glycolysis of Non-small Cell Lung Cancer Through Targeting MiR-101-3p/KRAS Axis. Frontiers in genetics 63 33005174
2019 Memo1-Mediated Tiling of Radial Glial Cells Facilitates Cerebral Cortical Development. Neuron 51 31277925
2022 Memo1 binds reduced copper ions, interacts with copper chaperone Atox1, and protects against copper-mediated redox activity in vitro. Proceedings of the National Academy of Sciences of the United States of America 50 36067318
2011 Brain-derived neurotrophic factor (BDNF) gene: a gender-specific role in cognitive function during normal cognitive aging of the MEMO-Study? Age (Dordrecht, Netherlands) 40 21695421
1998 Which drugs benefit diabetic patients for secondary prevention of myocardial infarction? DARTS/MEMO Collaboration. Diabetic medicine : a journal of the British Diabetic Association 33 9585392
2009 Memo is a cofilin-interacting protein that influences PLCgamma1 and cofilin activities, and is essential for maintaining directionality during ErbB2-induced tumor-cell migration. Journal of cell science 32 19223396
2007 CRP gene haplotypes, serum CRP, and cerebral small-vessel disease: the Rotterdam Scan Study and the MEMO Study. Stroke 31 17600233
2006 MeMo: a hybrid SQL/XML approach to metabolomic data management for functional genomics. BMC bioinformatics 29 16753052
2013 Mediator of ERBB2-driven cell motility (MEMO) promotes extranuclear estrogen receptor signaling involving the growth factor receptors IGF1R and ERBB2. The Journal of biological chemistry 28 23861392
1996 A human modifier of methylation for class I HLA genes (MEMO-1) maps to chromosomal bands 1p35-36.1. Human molecular genetics 28 8852654
2022 Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease. Molecular neurodegeneration 27 36397124
1996 Lack of class I HLA expression in neuroblastoma is associated with high N-myc expression and hypomethylation due to loss of the MEMO-1 locus. Oncogene 27 8895520
2016 HRG/HER2/HER3 signaling promotes AhR-mediated Memo-1 expression and migration in colorectal cancer. Oncogene 26 27941874
2011 Review of stem-cell transplantation for myelodysplastic syndromes in older patients in the context of the Decision Memo for Allogeneic Hematopoietic Stem Cell Transplantation for Myelodysplastic Syndrome emanating from the Centers for Medicare and Medicaid Services. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 25 21220586
2016 Memo interacts with c-Src to control Estrogen Receptor alpha sub-cellular localization. Oncotarget 23 27472465
2013 Using MEMo to discover mutual exclusivity modules in cancer. Current protocols in bioinformatics 23 23504936
2013 Loss of Memo, a novel FGFR regulator, results in reduced lifespan. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 23 24056085
2007 Memo is homologous to nonheme iron dioxygenases and binds an ErbB2-derived phosphopeptide in its vestigial active site. The Journal of biological chemistry 23 18045866
2022 Knockdown of circRNA-Memo1 Reduces Hypoxia/Reoxygenation Injury in Human Brain Endothelial Cells Through miRNA-17-5p/SOS1 Axis. Molecular neurobiology 22 35041140
2020 Finding MEMO-Emerging Evidence for MEMO1's Function in Development and Disease. Genes 17 33172038
2015 MEMO1 drives cranial endochondral ossification and palatogenesis. Developmental biology 15 26746790
2024 MEMO1 binds iron and modulates iron homeostasis in cancer cells. eLife 14 38640016
2020 miR-219a-1 inhibits colon cancer cells proliferation and invasion by targeting MEMO1. Cancer biology & therapy 14 33218285
2018 γ-, Diastereo-, and Enantioselective Addition of MEMO-Substituted Allylboron Compounds to Aldimines Catalyzed by Organoboron-Ammonium Complexes. Angewandte Chemie (International ed. in English) 14 29969173
2014 Memo has a novel role in S1P signaling and is [corrected] crucial for vascular development. PloS one 14 24714781
2015 Non-invasive prenatal diagnosis of monogenic disorders: an optimized protocol using MEMO qPCR with miniSTR as internal control. Clinical chemistry and laboratory medicine 13 25274949
2006 MemO: a consensus approach to the annotation of a protein's membrane organization. In silico biology 13 17274768
2018 Renal Memo1 Differentially Regulates the Expression of Vitamin D-Dependent Distal Renal Tubular Calcium Transporters. Frontiers in physiology 12 30038585
2016 Non-invasive prenatal diagnosis (NIPD) of cystic fibrosis: an optimized protocol using MEMO fluorescent PCR to detect the p.Phe508del mutation. Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society 12 28040480
2018 Redox-Dependent Bone Alkaline Phosphatase Dysfunction Drives Part of the Complex Bone Phenotype in Mice Deficient for Memo1. JBMR plus 11 30038965
2013 Establishment and characterization of an oral mucosal melanoma cell line (MEMO) derived from a longstanding primary oral melanoma. The American Journal of dermatopathology 11 23249835
2020 Elevated serum magnesium lowers calcification propensity in Memo1-deficient mice. PloS one 8 32706793
2007 Memo to the FDA and ICH: appeal for in vivo drug target identification and target pharmacokinetics Recommendations for improved procedures and requirements. Drug discovery today 8 17706540
2002 Frequency and genetic basis of MHC, beta-2-microglobulin and MEMO-1 loss of heterozygosity in sporadic breast cancer. Tissue antigens 8 12445306
2023 Memo1 reduces copper-mediated reactive oxygen species in breast cancer cells. Journal of inorganic biochemistry 7 37487298
2022 Repression of Memo1, a Novel Target of Human Papillomavirus Type 16 E7, Increases Cell Proliferation in Cervical Cancer Cells. Journal of virology 7 36197110
2021 Identification of Phenazine-Based MEMO1 Small-Molecule Inhibitors: Virtual Screening, Fluorescence Polarization Validation, and Inhibition of Breast Cancer Migration. ChemMedChem 7 33332774
2022 Anesthetic propofol suppresses growth and metastasis of lung adenocarcinoma in vitro through downregulating circ-MEMO1-miR-485-3p-NEK4 ceRNA axis. Histology and histopathology 6 35521898
2022 LncRNA cancer susceptibility 20 regulates the metastasis of human gastric cancer cells via the miR-143-5p/MEMO1 molecular axis. World journal of gastroenterology 6 35581960
2018 Analysis of MEMO1 Binding Specificity for ErbB2 Using Fluorescence Polarization and Molecular Dynamics Simulations. Biochemistry 6 30067338
2016 MEMO: multi-experiment mixture model analysis of censored data. Bioinformatics (Oxford, England) 6 27153627
2011 MEMO associated with an ErbB2 receptor phosphopeptide reveals a new phosphotyrosine motif. FEBS letters 6 21840311
2022 Renal FGF23 signaling depends on redox protein Memo1 and promotes orthovanadate-sensitive protein phosphotyrosyl phosphatase activity. Journal of cell communication and signaling 4 36434320
2021 Physiological Dose of EGCG Attenuates the Health Defects of High Dose by Regulating MEMO-1 in Caenorhabditis elegans. Oxidative medicine and cellular longevity 4 34257807
2020 MEMO: A Method for Computing Metabolic Modules for Cell-Free Production Systems. ACS synthetic biology 4 32069395
2019 Finding MEMo: minimum sets of elementary flux modes. Journal of mathematical biology 4 31388689
2017 The Memo Slide: An explorative study into a novel mechanical follow-the-leader mechanism. Proceedings of the Institution of Mechanical Engineers. Part H, Journal of engineering in medicine 4 29125034
2025 MEMO: A micro memo sensor detecting microRNA-RISC using an accurate cell-free expression platform. Biosensors & bioelectronics 2 40513293
2023 FGFR regulator Memo1 is dispensable for FGF23 expression by osteoblasts during folic acid-driven kidney injury. Physiological reports 2 36967231
2023 MEMO1 Is Required for Ameloblast Maturation and Functional Enamel Formation. Journal of dental research 2 37475472
2014 Mutant Enrichment with 3'-Modified Oligonucleotides (MEMO)-Quantitative PCR for Detection of NPM1 Mutations in Acute Myeloid Leukemia. Journal of clinical laboratory analysis 2 25384962
2026 Molecular Landscape of Advanced Endometrial Cancer: Exploratory Analyses at Modena Cancer Center (MEMO). International journal of molecular sciences 1 41596744
2023 MiR-485-3p/MiR-543/MiR-337-3p is Required for the Oncogenic Potential of the Hsa_circ_0007385-MEMO1 Axis in Colorectal Cancer. Biochemical genetics 1 37561333
2025 Metabolic Effects of the Cancer Metastasis Modulator MEMO1. Metabolites 0 40278406
2025 Endothelial MEMO1 Regulates Angiogenic Signaling in a Model of Retinopathy of Prematurity. FASEB bioAdvances 0 40936746
2025 MEMO-Stab2: Multi-View Sequence-Based Deep Learning Framework for Predicting Mutation-Induced Stability Changes in Transmembrane Proteins. Journal of chemical information and modeling 0 41021316
2019 Memo1 Tiles the Radial Glial Cell Grid. Neuron 0 31487522

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