Affinage

MTCH2

Mitochondrial carrier homolog 2 · UniProt Q9Y6C9

Length
303 aa
Mass
33.3 kDa
Annotated
2026-04-28
52 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MTCH2 is an outer mitochondrial membrane protein that integrates membrane protein biogenesis, apoptosis regulation, mitochondrial dynamics, and metabolic control. It functions as an insertase for α-helical membrane proteins—including tail-anchored, signal-anchored, and multipass substrates—using a membrane-embedded hydrophilic groove that also enables phospholipid scramblase activity (PMID:36264797, PMID:38377988). MTCH2 facilitates tBID recruitment to mitochondria (redundantly with cardiolipin) to promote Bax/Bak-dependent apoptosis, cooperates with MARCH5/UBE2K to drive proteasomal degradation of the MCL1:NOXA complex, and regulates mitochondrial fusion downstream of lysophosphatidic acid, thereby governing stem cell fate transitions, neuronal function, and energy homeostasis (PMID:20436477, PMID:26794447, PMID:32094511, PMID:30510213, PMID:34586346, PMID:28276496). MTCH2 also directly modulates CPT1 sensitivity to malonyl-CoA inhibition, controlling mitochondrial fatty acid oxidation and whole-body energy expenditure in adipose tissue (PMID:41044057).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2002 Medium

    Establishing that MTCH2 is a mitochondrially localized protein whose overexpression uncouples mitochondrial membrane potential answered the initial question of where the gene product resides and suggested a direct role in mitochondrial physiology.

    Evidence Subcellular fractionation, GFP-fusion imaging, and membrane potential assays in cells induced by Met-HGF/SF signaling

    PMID:12407445

    Open questions at the time
    • Endogenous protein localization not confirmed at this stage
    • Mechanism of uncoupling activity undefined
    • Physiological relevance of HGF/SF-dependent induction unclear
  2. 2010 High

    Demonstrating that MTCH2 knockout impairs tBID mitochondrial recruitment and downstream Bax/Bak activation established MTCH2 as a critical receptor/facilitator in death-receptor-mediated apoptosis.

    Evidence Conditional KO mice (liver), ES cell and MEF knockouts with tBID recruitment, MOMP, and apoptosis assays

    PMID:20436477

    Open questions at the time
    • Whether MTCH2 is the sole tBID receptor or acts redundantly was unresolved
    • Direct physical interaction sites not mapped
  3. 2012 High

    Mapping two specific binding interfaces between tBID and MTCH2 resolved how the two proteins physically interact, providing a structural framework for the apoptotic receptor function.

    Evidence Peptide array screening with biophysical validation and functional cell death assays

    PMID:22416135

    Open questions at the time
    • No high-resolution structural data for the complex
    • Whether these interfaces are targetable pharmacologically was untested
  4. 2015 High

    Showing that MTCH2 loss in hematopoietic stem cells increases OXPHOS, ATP, and ROS—driving HSC exit from quiescence—revealed MTCH2 as a negative regulator of mitochondrial metabolism that controls stem cell fate.

    Evidence Conditional hematopoietic KO mice with metabolic profiling, cell cycle analysis, and BID mutant epistasis

    PMID:26219591

    Open questions at the time
    • Molecular mechanism by which MTCH2 restrains OXPHOS undefined
    • Whether metabolic and apoptotic functions are separable was unclear
  5. 2016 High

    Establishing that cardiolipin and MTCH2 serve redundant roles as tBID receptors resolved the earlier puzzle of why single MTCH2 depletion incompletely blocked tBID recruitment.

    Evidence Double depletion of cardiolipin synthase (KO) and MTCH2 (siRNA) in HCT116 cells with tBID recruitment assays

    PMID:26794447

    Open questions at the time
    • Relative contributions of cardiolipin vs. MTCH2 in different tissues not determined
  6. 2017 High

    Conditional forebrain KO revealing impaired mitochondrial motility, calcium handling, LTP, and spatial memory extended MTCH2's physiological significance to neuronal function and cognition.

    Evidence Forebrain-specific MTCH2 KO mice with live imaging, electrophysiology, and behavioral testing

    PMID:28276496

    Open questions at the time
    • Which MTCH2-dependent substrates or pathways mediate the neuronal phenotype was unresolved
    • Whether apoptotic or metabolic roles drive the synaptic deficits was unclear
  7. 2018 High

    Demonstrating that MTCH2 is required for mitochondrial elongation during naïve-to-primed pluripotency transition—rescued by MFN2 overexpression—established MTCH2 as a regulator of mitochondrial fusion that governs developmental state changes.

    Evidence MTCH2 KO ESCs with mitochondrial morphology, metabolic, and pluripotency marker assays; genetic rescue with MFN2/DN-DRP1

    PMID:30510213

    Open questions at the time
    • Direct mechanism by which MTCH2 promotes fusion (e.g., lipid remodeling, MFN2 activation) unknown
  8. 2020 High

    Identifying MTCH2 as a cooperating factor with MARCH5/UBE2K for proteasomal degradation of MCL1 when bound to NOXA revealed a new apoptosis-regulatory axis distinct from the tBID recruitment function.

    Evidence Genome-wide CRISPR screen, genetic epistasis, Co-IP, and domain mapping in leukemia cells

    PMID:32094511

    Open questions at the time
    • Whether MTCH2 serves as a scaffold, insertase, or topology modifier for MCL1:NOXA was unclear
    • Structural basis of MARCH5-MTCH2 cooperation not defined
  9. 2021 High

    Showing that MTCH2-dependent mitochondrial fusion during starvation requires lysophosphatidic acid linked MTCH2's fusion activity to lipogenesis flux, providing a metabolic signal mechanism.

    Evidence MTCH2 loss-of-function with starvation-induced hyperfusion assays and LPA rescue

    PMID:34586346

    Open questions at the time
    • Whether MTCH2 directly senses or transports LPA was not established
    • Relationship between insertase function and fusion activity not clarified
  10. 2022 High

    Reconstitution of purified MTCH2 into proteoliposomes demonstrated it is sufficient for insertion of α-helical membrane proteins, establishing MTCH2 as a bona fide outer mitochondrial membrane insertase—a fundamentally new molecular function evolved from a solute carrier fold.

    Evidence Genome-wide CRISPR screen, in vitro reconstitution with purified protein, hydrophilic-groove mutagenesis, subcellular localization assays

    PMID:36264797

    Open questions at the time
    • How insertase activity relates to tBID receptor and fusion functions mechanistically
    • Client specificity determinants not fully defined
    • No high-resolution structure of MTCH2 with a substrate in transit
  11. 2024 Medium

    Molecular dynamics simulations showed that MTCH2's hydrophilic groove reduces the free energy barrier for bidirectional phospholipid movement, providing a mechanistic basis for scramblase activity.

    Evidence Coarse-grained and atomistic MD simulations with free energy calculations

    PMID:38377988

    Open questions at the time
    • No experimental scramblase activity assay performed
    • Relative physiological importance of scramblase vs. insertase function unclear
  12. 2025 High

    Demonstrating that MTCH2 directly interacts with CPT1 and modulates its malonyl-CoA sensitivity established a new mechanism by which MTCH2 controls fatty acid oxidation and whole-body energy expenditure.

    Evidence Co-IP, adipocyte-specific KO mice, CPT1 enzyme activity assays with malonyl-CoA titration

    PMID:41044057

    Open questions at the time
    • Structural basis of MTCH2-CPT1 interaction unknown
    • Whether this involves MTCH2's insertase or lipid-handling activity is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structure of MTCH2 engaged with a substrate protein (insertase mode) or lipid (scramblase mode) is needed to unify its insertase, scramblase, fusion-regulatory, and metabolic functions into a single mechanistic framework.
  • No substrate-engaged structural snapshot exists
  • How insertase, scramblase, tBID receptor, and CPT1-regulatory activities are coordinated or mutually exclusive is unknown
  • Tissue-specific relative importance of each function is poorly defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2 GO:0005198 structural molecule activity 1
Localization
GO:0005739 mitochondrion 5
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-5357801 Programmed Cell Death 4 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-392499 Metabolism of proteins 2 R-HSA-9609507 Protein localization 1
Partners
BIDCPT1AMARCH5MCL1MFN2SELHUBE2K

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 MTCH2/MIMP is a surface-exposed outer mitochondrial membrane protein that acts as a receptor facilitating recruitment of tBID to mitochondria; knockout in embryonic stem cells, mouse embryonic fibroblasts, and conditional knockout in liver hinders tBID recruitment, Bax/Bak activation, MOMP, and apoptosis, establishing MTCH2 as a critical facilitator of the death-receptor apoptotic pathway Conditional knockout mice (liver-specific), ES cell and MEF knockouts, in vitro and in vivo tBID recruitment assays, MOMP assay, apoptosis assays Nature cell biology High 20436477
2012 The molecular interaction between tBID and MTCH2 involves two specific binding sites: tBID residues 59–73 bind MTCH2 residues 140–161, and tBID residues 111–125 bind MTCH2 residues 240–290, as determined by peptide array screening combined with biochemical and biophysical characterization Peptide array screening, biochemical and biophysical binding assays, cell death assays with derived peptides The Journal of biological chemistry High 22416135
2015 MTCH2 is a negative regulator of mitochondrial oxidative phosphorylation (OXPHOS) downstream of BID; loss of MTCH2 in haematopoietic stem cells increases mitochondrial OXPHOS, mitochondrial size, ATP and ROS levels, and triggers HSC and progenitor entry into cell cycle, demonstrating MTCH2's indispensable role in maintaining HSC homeostasis Conditional knockout mice (haematopoietic), metabolic assays (OXPHOS, ATP, ROS), flow cytometry for cell cycle, irradiation-induced apoptosis assays, phosphorylation-deficient BID mutant analysis Nature communications High 26219591
2016 Cardiolipin (CL) and MTCH2 have redundant functions as tBID receptors at the mitochondrial outer membrane; depletion of either alone does not prevent tBID recruitment, but combined depletion of both CL and MTCH2 significantly reduces tBID recruitment to mitochondria in HCT116 cells Homologous recombination knockout of cardiolipin synthase, siRNA knockdown of MTCH2, tBID recruitment assays, apoptosis assays in response to TRAIL Cell death and differentiation High 26794447
2018 MTCH2 is a regulator of mitochondrial fusion essential for naïve-to-primed pluripotency interconversion in murine ESCs; MTCH2-/- ESCs fail to elongate mitochondria and fail to exit naïve pluripotency, and enforced mitochondrial elongation via MFN2 overexpression or dominant-negative DRP1 rescues this defect MTCH2 knockout ESCs, mitochondrial morphology imaging, metabolic assays, histone acetylation analysis, pluripotency marker expression, genetic rescue with MFN2/DN-DRP1 Nature communications High 30510213
2021 MTCH2 is a selective effector of starvation-induced mitochondrial hyperfusion; MTCH2 stimulates mitochondrial fusion in a manner dependent on the bioactive lipogenesis intermediate lysophosphatidic acid (LPA), linking lipogenesis flux to mitochondrial dynamics and energy production under nutrient deprivation MTCH2 loss-of-function in mammalian cells, mitochondrial morphology assays under starvation, LPA supplementation rescue experiments, lipid metabolic assays The Journal of cell biology High 34586346
2022 MTCH2 is a mitochondrial outer membrane protein insertase required for insertion of biophysically diverse tail-anchored (TA), signal-anchored, and multipass α-helical proteins but not β-barrel proteins; purified MTCH2 is sufficient to mediate insertion into reconstituted proteoliposomes; membrane-embedded hydrophilic residues are functionally critical; MTCH2 acts as a gatekeeper preventing mislocalization of TAs to the ER and modulates leukemia cell apoptosis sensitivity; MTCH2 appears to have evolved from a solute carrier transporter Genome-wide CRISPR screens, in vitro reconstitution with purified MTCH2 into proteoliposomes, mutational analysis of hydrophilic residues, subcellular localization assays, apoptosis assays in leukemia cells Science (New York, N.Y.) High 36264797
2020 MTCH2 cooperates with the ubiquitin E3 ligase MARCH5 and E2 conjugating enzyme UBE2K to mark MCL1 for proteasomal degradation specifically when MCL1 is engaged by NOXA; this requires the MCL1 transmembrane domain and specific MCL1 lysine residues, suggesting the complex acts on MCL1:NOXA within the mitochondrial outer membrane Genome-wide CRISPR-Cas9 screen, genetic epistasis, co-immunoprecipitation, proteasome inhibitor assays, domain mapping by mutagenesis Cell death and differentiation High 32094511
2024 Molecular dynamics simulations demonstrate that MTCH2's membrane-spanning hydrophilic groove significantly reduces the free energy barrier for bidirectional lipid movement (scramblase activity), at a rate similar to VDAC scramblase activity in the outer mitochondrial membrane Coarse-grained and atomistic molecular dynamics simulations, free energy barrier calculations Structure (London, England : 1993) Medium 38377988
2017 Loss of forebrain MTCH2 in mice decreases mitochondria motility and calcium handling in hippocampal neurons, impairs long-term potentiation, reduces spontaneous excitatory synaptic currents, and results in deficits in hippocampus-dependent spatial memory, identifying MTCH2 as a regulator of mitochondrial function critical for neuronal biology Conditional forebrain-specific MTCH2 knockout mice, live mitochondria motility imaging, calcium imaging, electrophysiology (LTP, mEPSCs), behavioral tests (spatial memory) Scientific reports High 28276496
2002 MTCH2/MIMP is induced by Met-HGF/SF signaling, localizes to mitochondria (confirmed by immunostaining of HA-tagged protein, GFP fusion, and subcellular fractionation), and ectopic expression reduces mitochondrial membrane potential (uncoupling activity) in a dose-dependent manner Differential display PCR cloning, Northern/Western blot, immunostaining with HA-tag and GFP fusion, subcellular fractionation, mitochondrial membrane potential assay Neoplasia (New York, N.Y.) Medium 12407445
2006 MTCH2/MIMP induction leads to G1/S arrest in response to HGF/SF, increases Met protein levels and phosphorylation, but prevents HGF/SF-induced tyrosine phosphorylation of Grb2 and Shc, while leaving PI3K phosphorylation unaffected; MTCH2 attenuates HGF/SF-induced scattering in vitro and tumor growth in vivo by altering downstream Met signaling Inducible MTCH2 expression, cell cycle analysis (FACS), Western blot for signaling components (Shc, Grb2, PI3K), SRE-luciferase reporter, in vivo tumor growth assay Cancer research Medium 16951184
2020 Stop codon read-through of MTCH2 mRNA generates two additional isoforms (MTCH2x and MTCH2xx); MTCH2 and MTCH2x localize to mitochondria with long half-life (>36 h), but MTCH2xx mislocalizes to the cytoplasm with rapid degradation (t1/2 <1 h); MTCH2 read-through-deficient cells generated by CRISPR-Cas9 show increased MTCH2 expression and decreased mitochondrial membrane potential, indicating that double-SCR regulates MTCH2 expression levels and mitochondrial membrane potential Luminescence- and fluorescence-based read-through assays, ribosome profiling and mass spectrometry data analysis, CRISPR-Cas9 read-through-deficient cell generation, subcellular fractionation, protein stability assays, mitochondrial membrane potential measurement The Journal of biological chemistry High 33028634
2025 MTCH2 directly interacts with and modulates the sensitivity of carnitine palmitoyltransferase 1 (CPT1) to malonyl-CoA inhibition, regulating mitochondrial influx of free fatty acids; adipocyte-specific ablation of MTCH2 improves mitochondrial function and whole-body energy expenditure independent of UCP1 Co-immunoprecipitation (direct physical interaction), adipocyte-specific knockout mice, metabolic phenotyping, CPT1 activity assays with malonyl-CoA, fatty acid oxidation assays Nature communications High 41044057
2025 MTCH2 negatively regulates thermogenesis in adipose tissue through a Bcl-2-dependent autophagy mechanism; adipose-specific MTCH2 depletion stimulates thermogenesis in brown and subcutaneous white adipose tissue, upregulates UCP1, enhances mitochondrial biogenesis and lipolysis, and protects against HFD-induced obesity Adipose-specific MTCH2 knockout mice, RNA sequencing, proteomics, thermogenesis assays, UCP1/mitochondrial biogenesis measurements, lipolysis assays, Bcl-2 interaction analysis Advanced science Medium 40051328
2025 Selenoprotein H (SelH) physically interacts with MTCH2 (identified by Co-IP combined with mass spectrometry); SelH targets MTCH2 to regulate MFN2-dependent mitochondrial fusion and mitochondrial quality control, with MTCH2/MFN2 axis mediating protection against oxidative stress and apoptosis in acute kidney injury Co-IP combined with mass spectrometry, molecular docking, laser confocal microscopy, SelH/MTCH2 knockdown and overexpression in HEK293t cells, mitochondrial dynamics and oxidative stress assays Journal of advanced research Medium 41314281
2025 MTCH2 deficiency promotes proteasome-dependent ubiquitination of E2F4, relieving transcriptional inhibition of transferrin receptor (TFRC) and facilitating TFRC-mediated ferroptosis in colorectal cancer cells; MTCH2 loss combined with sorafenib synergistically triggers ferroptosis and suppresses liver metastasis MTCH2 conditional knockout mice (AOM/DSS model), in vitro/in vivo ferroptosis assays, ubiquitination assays for E2F4, ChIP/reporter assays for TFRC transcription, xenograft and liver metastasis models Advanced science Medium 40600459
2025 CuB (Cucurbitacin B) covalently targets MTCH2 on the mitochondrial outer membrane, disrupting mitochondrial integrity and causing mtDNA release into the cytosol, which activates the cGAS-STING innate immune pathway leading to type I interferon production and anti-tumor immunity Quantitative Thiol Reactivity Profiling (QTRP), microscale thermophoresis, CETSA, activity-based protein profiling, cell lines, tumor organoids, in vivo breast cancer models Phytomedicine Medium 40582210
2025 MTCH2 co-immunoprecipitates with SENP1 (Sentrin-specific protease 1) in macrophages; Momordin Ic reduces SENP1 levels via NFκB pathway and upregulates MTCH2, restoring mitochondrial function and reducing M1 macrophage polarization Co-IP, proteomic analysis, NFκB pathway inhibition, macrophage polarization assays, mitochondrial function assays (MitoTracker, JC-1, DCFH-DA) Phytotherapy research Low 42007543
2025 USP34 maintains stability of eIF3m protein through deubiquitination; eIF3m binds to the 5'UTR of MTCH2 mRNA to promote MTCH2 expression, thereby maintaining mitochondrial function in triple-negative breast cancer cells (USP34/eIF3m/MTCH2 axis) Co-immunoprecipitation, GST-pulldown, RNA immunoprecipitation, RNA-pulldown, deubiquitination assays, MTCH2 knockdown/overexpression, mitochondrial function assays Journal of histotechnology Low 42023842
2025 MTCH2 identified as a copper-binding protein and regulator of mitochondrial copper distribution; in skeletal muscle-specific Ctr1 knockout mice with copper deficiency, MTCH2 is required for proper mitochondrial morphology and copper distribution, and copper restoration rescues mitochondrial hyperfusion Skeletal muscle-specific Ctr1 knockout mice, AAV-mediated Ctr1 re-expression rescue, copper ionophore treatment, mitochondrial morphology and function assays, identification of MTCH2 as copper-binding protein bioRxivpreprint Low 41332672
2017 MTCH2 knockdown reduces lipid accumulation in adipocyte-like cells in vitro and in C. elegans and mice in vivo, while MTCH2 overexpression increases fat accumulation; MTCH2 influences lipid homeostasis at least in part through effects on estrogen receptor 1 (ESR1) activity, establishing MTCH2 as a conserved regulator of lipid homeostasis RNAi and genetic mutant in C. elegans, shRNA knockdown and overexpression in cells and mice, high-fat diet model, ESR1 activity assay Obesity (Silver Spring, Md.) Medium 28127879

Source papers

Stage 0 corpus · 52 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 An MTCH2 pathway repressing mitochondria metabolism regulates haematopoietic stem cell fate. Nature communications 201 26219591
2010 MTCH2/MIMP is a major facilitator of tBID recruitment to mitochondria. Nature cell biology 181 20436477
2022 MTCH2 is a mitochondrial outer membrane protein insertase. Science (New York, N.Y.) 120 36264797
2018 MTCH2 promotes adipogenesis in intramuscular preadipocytes via an m6A-YTHDF1-dependent mechanism. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 74 30339471
2018 MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells. Nature communications 71 30510213
2013 miR-135b coordinates progression of ErbB2-driven mammary carcinomas through suppression of MID1 and MTCH2. The American journal of pathology 56 23623609
2021 The modified mitochondrial outer membrane carrier MTCH2 links mitochondrial fusion to lipogenesis. The Journal of cell biology 55 34586346
2015 MIMP: predicting the impact of mutations on kinase-substrate phosphorylation. Nature methods 55 25938373
2018 Micro Integral Membrane Protein (MIMP), a Newly Discovered Anti-Inflammatory Protein of Lactobacillus Plantarum, Enhances the Gut Barrier and Modulates Microbiota and Inflammatory Cytokines. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 46 29402771
2016 Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis. Cell death and differentiation 45 26794447
2017 Loss of forebrain MTCH2 decreases mitochondria motility and calcium handling and impairs hippocampal-dependent cognitive functions. Scientific reports 39 28276496
2012 Mitochondrial carrier homolog 2 (MTCH2): the recruitment and evolution of a mitochondrial carrier protein to a critical player in apoptosis. Experimental cell research 37 22326460
2020 MARCH5 requires MTCH2 to coordinate proteasomal turnover of the MCL1:NOXA complex. Cell death and differentiation 35 32094511
2012 Molecular basis of the interaction between proapoptotic truncated BID (tBID) protein and mitochondrial carrier homologue 2 (MTCH2) protein: key players in mitochondrial death pathway. The Journal of biological chemistry 35 22416135
2024 Insertases scramble lipids: Molecular simulations of MTCH2. Structure (London, England : 1993) 32 38377988
2017 MTCH2 is a conserved regulator of lipid homeostasis. Obesity (Silver Spring, Md.) 32 28127879
2011 MTCH2 in human white adipose tissue and obesity. The Journal of clinical endocrinology and metabolism 26 21795451
2002 Met-HGF/SF signal transduction induces mimp, a novel mitochondrial carrier homologue, which leads to mitochondrial depolarization. Neoplasia (New York, N.Y.) 26 12407445
2021 Inhibition of mitochondrial carrier homolog 2 (MTCH2) suppresses tumor invasion and enhances sensitivity to temozolomide in malignant glioma. Molecular medicine (Cambridge, Mass.) 25 33509092
2006 Mimp, a mitochondrial carrier homologue, inhibits Met-HGF/SF-induced scattering and tumorigenicity by altering Met-HGF/SF signaling pathways. Cancer research 23 16951184
2016 Mimp/Mtch2, an Obesity Susceptibility Gene, Induces Alteration of Fatty Acid Metabolism in Transgenic Mice. PloS one 21 27359329
2008 Genome-wide analysis of the Fusarium oxysporum mimp family of MITEs and mobilization of both native and de novo created mimps. Journal of molecular evolution 20 18982380
2021 Silica nanoparticles inducing the apoptosis via microRNA-450b-3p targeting MTCH2 in mice and spermatocyte cell. Environmental pollution (Barking, Essex : 1987) 16 33652185
2020 Stop codon read-through of mammalian MTCH2 leading to an unstable isoform regulates mitochondrial membrane potential. The Journal of biological chemistry 16 33028634
2013 Structural insights into proapoptotic signaling mediated by MTCH2, VDAC2, TOM40 and TOM22. Cellular signalling 16 24269536
2023 APOC1 promotes the progression of osteosarcoma by binding to MTCH2. Experimental and therapeutic medicine 14 36911382
2019 Identification of mimp-associated effector genes in Fusarium oxysporum f. sp. cubense race 1 and race 4 and virulence confirmation of a candidate effector gene. Microbiological research 13 31783262
2011 Expression of the Lactobacillus plantarum surface layer MIMP protein protected NCM460 epithelial cells from enteroinvasive Escherichia coli infection. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 12 21325827
2011 Functional characterization of MIMP for its adhesion to the intestinal epithelium. Frontiers in bioscience (Landmark edition) 12 21622165
2020 Downregulated miR-150 in bone marrow mesenchymal stem cells attenuates the apoptosis of LPS-stimulated RAW264.7 via MTCH2-dependent mitochondria transfer. Biochemical and biophysical research communications 10 32247615
2015 MTCH2 is differentially expressed in rat testis and mainly related to apoptosis of spermatocytes. Cell and tissue research 10 25813787
1991 Methyl inosine monophosphate (MIMP), a new purine immunomodulator for HIV infection. International journal of immunopharmacology 10 1823907
2025 MTCH2 Suppresses Thermogenesis by Regulating Autophagy in Adipose Tissue. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 9 40051328
2014 Knockout of MIMP protein in lactobacillus plantarum lost its regulation of intestinal permeability on NCM460 epithelial cells through the zonulin pathway. BMC gastroenterology 9 25277875
1992 Potentiation of immune responses in mice by a new inosine derivative--methyl inosine monophosphate (MIMP). International journal of immunopharmacology 8 1452410
2024 MTCH2 stimulates cellular proliferation and cycles via PI3K/Akt pathway in breast cancer. Heliyon 6 38560664
2023 Opposing effects of genetic variation in MTCH2 for obesity versus heart failure. Human molecular genetics 6 35904451
2023 Insertases Scramble Lipids: Molecular Simulations of MTCH2. bioRxiv : the preprint server for biology 6 37645813
1995 Methyl inosine monophosphate (MIMP) augments T-lymphocyte mitogen responses and reverses various immunosuppressants. International journal of immunopharmacology 6 8582788
2025 SNHG16 alleviates pulmonary ischemia-reperfusion injury by promoting the Warburg effect through regulating MTCH2 expression: experimental studies. International journal of surgery (London, England) 5 39784903
2025 METTL3/YTDHF1 Stabilizes MTCH2 mRNA to Regulate Ferroptosis in Glioma Cells. Frontiers in bioscience (Landmark edition) 5 40018930
2025 Cucurbitacin B stimulates PD-1 immunotherapy response in malignant breast cancer by covalent targeting MTCH2. Phytomedicine : international journal of phytotherapy and phytopharmacology 5 40582210
2025 MTCH2 Deficiency Promotes E2F4/TFRC-Mediated Ferroptosis and Sensitizes Colorectal Cancer Liver Metastasis to Sorafenib. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2 40600459
2025 MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes. Nature communications 2 41044057
2025 MTCH2 regulates NRF2-mediated RRM1 expression to promote melanoma proliferation and dacarbazine insensitivity. Cell death & disease 1 40204724
2025 Epigenetically modulated MTCH2 and regulated ATP5 in the liver of obese mice subjected to strength training. Life sciences 1 41270824
2025 Selenoprotein H targets MTCH2 to regulate MFN2-dependent mitochondrial quality control to alleviate acute kidney injury. Journal of advanced research 1 41314281
2026 Longitudinal analysis of weight regain after Roux-en-Y gastric bypass ‒ The role of the MTCH2 gene polymorphism and dietary factors. Nutricion hospitalaria 0 41960826
2026 Activation of MTCH2 by Momordin Ic Prevents Colitis and Colitis-Associated Colorectal Cancer Through Rescuing the Mitochondrial Dysfunction of Macrophage. Phytotherapy research : PTR 0 42007543
2026 USP34 modulates mitochondrial function in triple-negative breast cancer cells through the eIf3m/MTCH2 axis. Journal of histotechnology 0 42023842
2025 Copper deficiency disrupts OXPHOS and mitochondrial dynamics through MTCH2-dependent copper trafficking in skeletal muscle. bioRxiv : the preprint server for biology 0 41332672
2024 Benzylurea Protects hPDLFs Against LPS-Induced Mitochondrial Dysfunction Through MTCH2. Oral diseases 0 39491029