Affinage

MTCH2

Mitochondrial carrier homolog 2 · UniProt Q9Y6C9

Length
303 aa
Mass
33.3 kDa
Annotated
2026-06-10
53 papers in source corpus 22 papers cited in narrative 22 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

MTCH2 is a modified mitochondrial carrier residing in the outer mitochondrial membrane that couples membrane protein biogenesis, apoptotic commitment, and mitochondrial dynamics to cellular metabolic and fate decisions (PMID:20436477, PMID:36264797). Mechanistically, it functions as a protein insertase: purified MTCH2 is sufficient to insert biophysically diverse tail-anchored, signal-anchored, and multipass α-helical proteins—but not β-barrels—into the outer membrane, using membrane-embedded hydrophilic residues derived from a solute-carrier scaffold to act as a gatekeeper against mislocalization to the ER (PMID:36264797). In apoptosis, MTCH2 facilitates recruitment of tBID to mitochondria, acting redundantly with cardiolipin, to drive Bax/Bak activation, MOMP, and downstream caspase-dependent death; the tBID interaction is mediated by two mapped binding interfaces (PMID:20436477, PMID:22416135, PMID:26794447). It localizes near BAX/BAK assemblies under apoptotic conditions and accelerates their oligomerization in an LPA-dependent manner, linking pore assembly to sublethal permeabilization, mtDNA release, and cGAS-STING activation (PMID:42056306). MTCH2 also regulates mitochondrial fusion and elongation—governing OXPHOS, naïve-to-primed pluripotency transitions, and hematopoietic stem cell quiescence—through an LPA-dependent mechanism downstream of BID (PMID:26219591, PMID:30510213, PMID:34586346). Beyond these core roles, MTCH2 negatively regulates fatty acid oxidation by directly binding CPT1 and tuning its malonyl-CoA sensitivity, suppresses adipose thermogenesis, and scaffolds MARCH5/UBE2K-mediated proteasomal degradation of the MCL1:NOXA complex (PMID:32094511, PMID:41044057, PMID:40051328).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 Medium

    Established MTCH2 as a mitochondrial protein responsive to growth-factor signaling, the first functional handle on an uncharacterized carrier.

    Evidence Differential display cloning downstream of Met-HGF/SF signaling, subcellular fractionation, and membrane potential measurement

    PMID:12407445

    Open questions at the time
    • Mechanism of membrane potential reduction undefined
    • Link to Met signaling correlative at this stage
  2. 2006 Medium

    Showed MTCH2 selectively modulates Met downstream signaling, narrowing its effect to the Shc/Grb2/SRE branch while sparing PI3K.

    Evidence Ectopic expression with signaling readouts, SRE-luciferase reporter, and in vivo tumor growth assay

    PMID:16951184

    Open questions at the time
    • No direct mechanism linking mitochondrial MTCH2 to cytosolic Shc levels
    • Single lab
  3. 2010 High

    Identified MTCH2's first defined molecular role—facilitating tBID recruitment to mitochondria—placing it as a critical node in death-receptor apoptosis.

    Evidence Conditional and cell-type-specific knockouts with tBID recruitment, Bax/Bak activation, MOMP, and apoptosis readouts

    PMID:20436477

    Open questions at the time
    • Whether MTCH2 is a direct tBID receptor or accessory factor unresolved here
    • No structural detail of the interaction
  4. 2012 Medium

    Mapped the physical tBID-MTCH2 interface to two discrete binding-site pairs, providing molecular resolution to the recruitment step.

    Evidence Peptide array screening with biochemical and biophysical binding characterization

    PMID:22416135

    Open questions at the time
    • No crystal or cryo-EM structure
    • Functional consequence of each site not separated
  5. 2016 Medium

    Resolved why single MTCH2 loss can be tolerated for tBID recruitment—cardiolipin acts as a redundant receptor.

    Evidence Combined CRISPR cardiolipin synthase knockout and MTCH2 knockdown with tBID recruitment and TRAIL apoptosis assays in HCT116

    PMID:26794447

    Open questions at the time
    • Relative contribution of each receptor in different cell types unknown
    • Single lab epistasis
  6. 2015 High

    Extended MTCH2 beyond apoptosis to metabolic control, showing it negatively regulates OXPHOS downstream of BID to maintain HSC quiescence.

    Evidence Hematopoietic conditional knockout with OXPHOS, ATP, ROS, mitochondrial size, and cell cycle readouts; BID epistasis

    PMID:26219591

    Open questions at the time
    • Molecular mechanism connecting MTCH2 to OXPHOS not defined
    • Whether effect is via fusion or direct ETC modulation unclear
  7. 2018 High

    Defined MTCH2 as a regulator of mitochondrial fusion required for pluripotency state transitions, linking morphology to cell fate.

    Evidence ESC knockout with mitochondrial imaging, metabolic profiling, and MFN2/DN-DRP1 epistasis rescue

    PMID:30510213

    Open questions at the time
    • Direct molecular driver of fusion by MTCH2 not identified here
    • Connection to insertase/apoptotic roles unresolved
  8. 2021 Medium

    Identified the bioactive lipid LPA as the mediator of MTCH2-driven starvation-induced hyperfusion, mechanistically connecting lipogenesis flux to mitochondrial elongation.

    Evidence Loss/gain-of-function with LPA supplementation/depletion and mitochondrial morphology and energetics readouts

    PMID:34586346

    Open questions at the time
    • How MTCH2 senses or routes LPA undefined
    • Single lab
  9. 2020 High

    Revealed a scaffolding role in protein quality control: MTCH2 cooperates with MARCH5/UBE2K to degrade the NOXA-engaged MCL1 complex.

    Evidence Genome-wide CRISPR screen, Co-IP, proteasomal degradation assays, and MCL1 domain/lysine mutant analysis

    PMID:32094511

    Open questions at the time
    • Structural basis of complex assembly unknown
    • Whether this depends on insertase activity untested
  10. 2022 High

    Established the unifying biochemical activity—MTCH2 is a bona fide outer membrane protein insertase for α-helical proteins, recasting earlier phenotypes as consequences of impaired membrane protein biogenesis.

    Evidence Genome-wide CRISPR screens plus reconstitution of purified MTCH2 in proteoliposomes with mutational and localization analysis

    PMID:36264797

    Open questions at the time
    • Full client repertoire not enumerated
    • How insertase activity intersects apoptotic and fusion roles not directly tested
  11. 2026 High

    Connected MTCH2 directly to BAX/BAK pore assembly and innate immune signaling, showing it accelerates oligomerization via LPA and gates mtDNA-driven cGAS-STING activation.

    Evidence In situ proximity labeling, single-particle BAX/BAK oligomerization imaging, knockout cells, LPA rescue, and bacterial infection/cGAS-STING readouts

    PMID:42056306

    Open questions at the time
    • How LPA mechanistically promotes oligomerization unresolved
    • Whether insertase residues mediate this effect untested
  12. 2025 Medium

    Defined MTCH2 as a direct CPT1 partner and brake on fatty acid oxidation and thermogenesis, expanding its metabolic regulatory portfolio in adipose tissue.

    Evidence Adipocyte-specific knockouts with CPT1 co-IP, malonyl-CoA sensitivity assays, metabolic cage, and omics; separate adipose KO linking thermogenesis suppression to Bcl-2-dependent autophagy

    PMID:40051328 PMID:41044057

    Open questions at the time
    • Whether CPT1 binding and thermogenesis pathways are mechanistically linked unclear
    • Bcl-2-autophagy link relies on integrated analysis, not direct reconstitution
  13. 2025 Medium

    Implicated MTCH2 in additional partner interactions (SelH, copper binding) and disease contexts (ferroptosis in colorectal cancer, tumor immunogenicity), broadening its mitochondrial regulatory network.

    Evidence Co-IP/MS with SelH, copper-binding characterization, E2F4 ubiquitination and TFRC ChIP, and covalent CuB targeting with cGAS-STING readouts

    PMID:40582210 PMID:40600459 PMID:41314281

    Open questions at the time
    • These roles are individually single-lab
    • Copper-binding role is from a preprint
    • Mechanistic integration with core insertase/apoptotic functions undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single insertase scaffold integrates protein biogenesis, apoptotic pore assembly, LPA-dependent fusion, and lipid/metabolic regulation into one coherent mechanism remains unresolved.
  • No structure of MTCH2 with a client or with tBID/BAX
  • Whether scramblase activity is real (computational only)
  • Causal hierarchy among insertase, fusion, and apoptotic roles untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008289 lipid binding 2 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005739 mitochondrion 2
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-168256 Immune System 2 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-5357801 Programmed Cell Death 2
Partners
BAKBAXBIDCPT1MARCH5SELENOHSENP1UBE2K
Complex memberships
MARCH5/UBE2K/MTCH2 MCL1-degradation complex

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 facilitates recruitment of tBID to mitochondria; knockout in embryonic stem cells, mouse embryonic fibroblasts, and conditional knockout in liver hindered tBID recruitment, Bax/Bak activation, MOMP, and apoptosis, establishing MTCH2 as a critical facilitator of the Fas/death-receptor apoptotic pathway. Conditional knockout mice (liver-specific), embryonic stem cell and MEF knockout, in vivo and in vitro tBID recruitment assays, MOMP measurement, apoptosis assays Nature cell biology High 20436477
2012 The molecular interaction between tBID and MTCH2 was mapped to two specific binding sites: tBID residues 59–73 binding MTCH2 residues 140–161, and tBID residues 111–125 binding MTCH2 residues 240–290, as determined by peptide array screening combined with biochemical and biophysical characterization. Peptide array screening, biochemical binding assays, biophysical techniques (characterizing tBID–MTCH2 interaction at structural/molecular level) The Journal of biological chemistry Medium 22416135
2015 MTCH2 acts as a negative regulator of mitochondrial OXPHOS downstream of BID in haematopoietic stem cells (HSCs); loss of MTCH2 increases mitochondrial OXPHOS, mitochondrial size, ATP and ROS levels, and triggers HSC and progenitor entry into cell cycle, demonstrating MTCH2 is indispensable for HSC homeostasis. Conditional knockout mice (MTCH2 deletion in haematopoietic system), measurement of OXPHOS, ATP, ROS, mitochondrial size, cell cycle analysis, irradiation-induced apoptosis assays Nature communications High 26219591
2016 Both cardiolipin (CL) and MTCH2 can serve as redundant receptors for tBID at the mitochondrial outer membrane; depletion of either alone did not block tBID recruitment in HCT116 cells, but combined depletion of both CL and MTCH2 significantly reduced tBID recruitment, indicating functional redundancy. CRISPR/homologous recombination knockout of cardiolipin synthase in HCT116 cells, siRNA knockdown of MTCH2, tBID recruitment assay, TRAIL-induced apoptosis assay Cell death and differentiation Medium 26794447
2018 MTCH2 is a regulator of mitochondrial fusion required for naïve-to-primed pluripotency interconversion in murine ESCs; MTCH2-/- ESCs fail to elongate mitochondria and alter metabolism, and enforced mitochondrial elongation via MFN2 overexpression or dominant-negative DRP1 rescues exit from naïve pluripotency in MTCH2-/- ESCs. MTCH2 knockout ESCs, live mitochondrial imaging, metabolic profiling (glutamine utilization), histone acetylation measurement, epistasis rescue with MFN2 overexpression and DN-DRP1 Nature communications High 30510213
2020 MTCH2 cooperates with the E3 ubiquitin ligase MARCH5 and E2 conjugating enzyme UBE2K to mediate proteasomal degradation of MCL1 specifically when MCL1 is engaged by NOXA; this requires the MCL1 transmembrane domain and specific MCL1 lysine residues, placing MTCH2 as an essential component of a complex that marks the MCL1:NOXA complex for degradation. Genome-wide CRISPR-Cas9 screen, genetic validation, co-immunoprecipitation, proteasomal degradation assays, domain/mutant analysis Cell death and differentiation High 32094511
2021 MTCH2 is a selective effector of starvation-induced mitochondrial hyperfusion (a cytoprotective response to nutrient deprivation) that stimulates mitochondrial fusion in a manner dependent on the bioactive lipogenesis intermediate lysophosphatidic acid (LPA), linking flux through the lipogenesis pathway to mitochondrial elongation and enhanced energy production. MTCH2 loss-of-function and gain-of-function in cell culture, starvation-induced hyperfusion assays, LPA supplementation/depletion, mitochondrial morphology imaging, energy production measurements The Journal of cell biology Medium 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 into the outer mitochondrial membrane but not β-barrel proteins; purified MTCH2 was sufficient to mediate insertion into reconstituted proteoliposomes; MTCH2 uses membrane-embedded hydrophilic residues (evolved from a solute carrier transporter) to act as a gatekeeper controlling mislocalization of TAs to the ER and modulating apoptosis sensitivity. Genome-wide CRISPR screens, purified protein reconstitution into proteoliposomes, functional and mutational studies, subcellular localization assays Science (New York, N.Y.) High 36264797
2002 MIMP/MTCH2 is induced by Met-HGF/SF signal transduction and localizes to mitochondria; ectopic MTCH2 expression reduces mitochondrial membrane potential (uncoupling activity) in a level-dependent manner, linking Met tyrosine kinase signaling to mitochondrial depolarization. Differential display PCR cloning, Northern and Western blot, immunostaining of HA-tagged and GFP-fusion MTCH2, subcellular fractionation, mitochondrial membrane potential measurement Neoplasia (New York, N.Y.) Medium 12407445
2006 MTCH2/MIMP overexpression attenuates HGF/SF-induced cellular scattering and tumor growth by reducing Shc levels, preventing HGF/SF-induced tyrosine phosphorylation of Grb2 and Shc, and suppressing SRE-dependent transcription, while leaving PI3K signaling unaffected; this defines MTCH2 as a selective modulator of Met downstream signaling. Ectopic MTCH2 expression in cancer cells, HGF/SF stimulation, Western blotting for Met, Shc, Grb2, PI3K phosphorylation, SRE-luciferase reporter assay, in vivo tumor growth assay Cancer research Medium 16951184
2017 Deletion of forebrain MTCH2 impairs mitochondria motility and calcium handling in hippocampal neurons, leading to deficits in spatial memory, long-term potentiation (LTP), and spontaneous excitatory synaptic currents, establishing MTCH2 as a critical regulator of neuronal mitochondria function required for hippocampus-dependent cognition. Forebrain-specific conditional MTCH2 knockout mice, live mitochondria motility imaging, calcium buffering assays, LTP electrophysiology, behavioral memory tests Scientific reports Medium 28276496
2017 MTCH2 is a conserved regulator of lipid homeostasis; its knockdown reduced lipid accumulation in adipocyte-like cells and in C. elegans and mice in vivo, while overexpression increased fat accumulation across species; MTCH2 influences lipid homeostasis partly through modulation of estrogen receptor 1 (ESR1) activity. RNAi knockdown and genetic mutant in C. elegans, shRNA knockdown and overexpression in cells and mice, lipid accumulation assays, ESR1 activity measurement Obesity (Silver Spring, Md.) Medium 28127879
2020 Stop codon read-through of MTCH2 mRNA generates two longer isoforms (MTCH2x and MTCH2xx); MTCH2xx is predominantly cytoplasmic (unlike mitochondrially-localized MTCH2 and MTCH2x) and rapidly degraded (t1/2 <1 h); CRISPR-generated read-through-deficient cells show increased MTCH2 expression and decreased mitochondrial membrane potential, demonstrating that double stop codon read-through regulates MTCH2 protein 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, mitochondrial membrane potential assay The Journal of biological chemistry Medium 33028634
2024 Molecular dynamics simulations (coarse-grained and atomistic) demonstrate that MTCH2's membrane-spanning hydrophilic groove significantly reduces the free energy barrier for lipid movement across the membrane, enabling it to function as a lipid scramblase with a rate comparable to VDAC in the outer mitochondrial membrane. Coarse-grained and atomistic molecular dynamics simulations, free energy barrier calculations for lipid flip-flop Structure (London, England : 1993) Low 38377988
2025 MTCH2 directly interacts with carnitine palmitoyltransferase 1 (CPT1) and modulates CPT1 sensitivity to malonyl-CoA inhibition, thereby regulating mitochondrial influx of free fatty acids and energy expenditure in adipocytes; adipocyte-specific ablation of MTCH2 improves mitochondrial function and whole-body energy expenditure independent of UCP1. Adipocyte-specific MTCH2 knockout mice, direct physical interaction assay (co-immunoprecipitation/pull-down), CPT1 activity and malonyl-CoA sensitivity assay, metabolic cage measurements, proteomic and RNA sequencing analyses Nature communications Medium 41044057
2025 MTCH2 deficiency promotes ubiquitin-proteasome-dependent degradation of E2F4, relieving E2F4-mediated transcriptional repression of transferrin receptor (TFRC) and thereby facilitating TFRC-mediated ferroptosis in colorectal cancer cells. MTCH2 conditional knockout mice, in vitro KO/OE in CRC cell lines, proteasomal ubiquitination assays for E2F4, chromatin immunoprecipitation for TFRC promoter, ferroptosis markers (ferrous ion, lipid ROS) Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 40600459
2025 MTCH2 suppresses thermogenesis in brown and subcutaneous white adipose tissue by negatively regulating autophagy through a Bcl-2-dependent mechanism; adipose-specific MTCH2 depletion stimulates thermogenesis, upregulates UCP1, enhances mitochondrial biogenesis, and increases lipolysis. Adipose-specific MTCH2 knockout mice, high-fat diet model, RNA sequencing + proteomics, Bcl-2 pathway epistasis, UCP1 and mitochondrial biogenesis measurements Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 40051328
2025 Selenoprotein H (SelH) interacts directly with MTCH2 (identified by Co-IP combined with mass spectrometry and molecular docking), and SelH targets MTCH2 to regulate mitofusin 2 (MFN2)-dependent mitochondrial fusion and quality control, thereby alleviating oxidative stress and apoptosis in acute kidney injury. Co-immunoprecipitation with mass spectrometry, laser confocal co-localization, molecular docking, SelH/MTCH2 knockdown and overexpression in HEK293t cells and SelH KO mice, mitochondrial dynamics and MFN2 assays Journal of advanced research Medium 41314281
2025 MTCH2 directly binds copper and functions as a copper-binding regulator that coordinates mitochondrial copper distribution and morphology; skeletal muscle-specific deletion of copper importer Ctr1 causes copper deficiency, mitochondrial hyperfusion, and myopathic features that are mechanistically linked to MTCH2, and copper restoration rescues mitochondrial function. Skeletal muscle-specific Ctr1 knockout mice, MTCH2 copper-binding characterization, AAV-mediated Ctr1 re-expression rescue, copper ionophore treatment, electron transport chain proteomics, mitochondrial morphology imaging bioRxiv : the preprint server for biologypreprint Medium 41332672
2026 MTCH2 localizes near BAX and BAK assemblies specifically under apoptotic conditions (mapped by in situ proximity labeling); cells lacking MTCH2 exhibit delayed BAX and BAK oligomerization at the single-particle level, which is rescued by addition of lysophosphatidic acid (LPA); MTCH2 depletion decreases apoptosis sensitivity, sublethal mitochondrial permeabilization during bacterial infection, mitochondrial DNA release, and cGAS-STING activation. In situ proximity labeling (BioID/APEX), single-particle BAX/BAK oligomerization imaging, MTCH2 knockout cells, LPA rescue experiments, apoptosis assays, bacterial infection model, mtDNA release and cGAS-STING activation measurement Nature structural & molecular biology High 42056306
2025 CuB (Cucurbitacin B) covalently targets MTCH2 at the mitochondrial outer membrane; CuB binding to MTCH2 disrupts mitochondrial integrity, causes mitochondrial DNA release into the cytosol, and activates the cGAS-STING innate immune pathway, establishing MTCH2 as a node linking mitochondrial function to tumor immunogenicity. Quantitative Thiol Reactivity Profiling (QTRP), microscale thermophoresis, cellular thermal shift assay, activity-based protein profiling, in vitro/in vivo tumor models, cGAS-STING pathway activation assays Phytomedicine : international journal of phytotherapy and phytopharmacology Medium 40582210
2026 MTCH2 interacts with SENP1 (Sentrin-specific protease 1) as shown by co-immunoprecipitation; MIc (Momordin Ic) reduces SENP1 levels in M1 macrophages via an NFκB-dependent mechanism, thereby activating MTCH2 and rescuing mitochondrial dysfunction to suppress colitis-associated colorectal cancer. Co-immunoprecipitation (SENP1-MTCH2 interaction), proteomics, MTCH2 knockdown/overexpression, macrophage polarization assays, mitochondrial function assays (Mito-tracker, JC-1, DCFH-DA), NF-κB inhibitor epistasis Phytotherapy research : PTR Low 42007543

Source papers

Stage 0 corpus · 53 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 206 26219591
2010 MTCH2/MIMP is a major facilitator of tBID recruitment to mitochondria. Nature cell biology 183 20436477
2022 MTCH2 is a mitochondrial outer membrane protein insertase. Science (New York, N.Y.) 127 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 76 30339471
2018 MTCH2-mediated mitochondrial fusion drives exit from naïve pluripotency in embryonic stem cells. Nature communications 72 30510213
2021 The modified mitochondrial outer membrane carrier MTCH2 links mitochondrial fusion to lipogenesis. The Journal of cell biology 58 34586346
2013 miR-135b coordinates progression of ErbB2-driven mammary carcinomas through suppression of MID1 and MTCH2. The American journal of pathology 57 23623609
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 46 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 36 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
2017 MTCH2 is a conserved regulator of lipid homeostasis. Obesity (Silver Spring, Md.) 33 28127879
2024 Insertases scramble lipids: Molecular simulations of MTCH2. Structure (London, England : 1993) 32 38377988
2021 Inhibition of mitochondrial carrier homolog 2 (MTCH2) suppresses tumor invasion and enhances sensitivity to temozolomide in malignant glioma. Molecular medicine (Cambridge, Mass.) 27 33509092
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
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 22 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
2013 Structural insights into proapoptotic signaling mediated by MTCH2, VDAC2, TOM40 and TOM22. Cellular signalling 17 24269536
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
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 Functional characterization of MIMP for its adhesion to the intestinal epithelium. Frontiers in bioscience (Landmark edition) 13 21622165
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
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 11 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 7 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 modulates CPT1 activity to regulate lipid metabolism of adipocytes. Nature communications 5 41044057
2025 MTCH2 Deficiency Promotes E2F4/TFRC-Mediated Ferroptosis and Sensitizes Colorectal Cancer Liver Metastasis to Sorafenib. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 3 40600459
2025 MTCH2 regulates NRF2-mediated RRM1 expression to promote melanoma proliferation and dacarbazine insensitivity. Cell death & disease 2 40204724
2025 Epigenetically modulated MTCH2 and regulated ATP5 in the liver of obese mice subjected to strength training. Life sciences 2 41270824
2026 MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth. Nature structural & molecular biology 1 42056306
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

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