Affinage

MTFP1

Mitochondrial fission process protein 1 · UniProt Q9UDX5

Length
166 aa
Mass
18.0 kDa
Annotated
2026-06-10
32 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MTFP1 (MTP18) is a nuclear-encoded inner mitochondrial membrane protein that promotes mitochondrial fission and governs mitochondrial morphology, quality control, and cell fate (PMID:15155745, PMID:15985469, PMID:38851188). Functionally it acts upstream of DRP1, driving pro-fission phosphorylation (p-DRP1 S616) and mitochondrial recruitment of DRP1; overexpression fragments the network while knockdown produces a hyperfused reticulum, and its fission activity is genetically dependent on DRP1 and antagonized by Mfn1 (PMID:15985469, PMID:28918902). MTFP1 also enforces inner-membrane quality control: it negatively regulates IMM fusion to isolate damaged subdomains, which are segregated by peripheral fission into small MTFP1-enriched mitochondria (SMEM) and degraded by autophagy, a process required for nucleoid recycling and maintenance of mtDNA copy number (PMID:38851188). MTFP1 doubles as a mitophagy receptor through an LC3-interacting region (LIR) that binds MAP1LC3 family members to deliver dysfunctional mitochondria to autophagosomes in a PINK1/Parkin-dependent manner (PMID:37313742). MTFP1 abundance is set by multiple inputs: translationally by the mTORC1/4E-BP/eIF4E axis (PMID:28918902) and transcriptionally by HIF-1α (PMID:38689964) and the conserved factor ZBTB48 (PMID:39987415). Through these activities MTFP1 modulates OXPHOS and apoptosis: loss de-represses respiration, blocks mPTP opening, and protects against steatosis and apoptotic damage (PMID:38123539), and it is required for glucose-stimulated insulin secretion in β-cells (PMID:41648185). MTFP1 interacts with ATP synthase subunits and with PPA2, links to fission-driven metabolic reprogramming in cancer, and is recruited to nascent SMEM by MISO [PMID:40873007, PMID:41663153, PMID:bio_10.1101_2025.01.05.631328].

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2004 Medium

    Established MTP18 as a PI3K-dependent mitochondrial protein controlling network morphology and viability, framing it as a signaling-responsive regulator rather than a structural curiosity.

    Evidence Antisense knockdown, overexpression, fractionation, and cytochrome c release in PC-3/HaCaT/COS-7 cells

    PMID:15155745

    Open questions at the time
    • Did not define molecular activity or partners
    • Mechanism linking PI3K to morphology unresolved
    • Single-lab phenotype
  2. 2005 High

    Placed MTP18 in the fission machinery by showing its activity requires DRP1 and is antagonized by Mfn1/fusion, answering whether it acts in division versus fusion.

    Evidence RNAi, overexpression, and genetic epistasis with Mfn1, dominant-negative Drp1(K38A), and hFis1 by confocal imaging

    PMID:15985469

    Open questions at the time
    • Did not establish direct biochemical interaction with DRP1
    • Exact ordering relative to hFis1 ambiguous
  3. 2017 High

    Defined how MTFP1 levels are set and translated that control into fission, showing mTORC1/4E-BP-driven translation couples MTFP1 abundance to DRP1 recruitment and cell fate.

    Evidence Polysome profiling, mTOR inhibition, 4E-BP manipulation, DRP1 phosphorylation/recruitment, and apoptosis assays

    PMID:28643438 PMID:28915614 PMID:28918902

    Open questions at the time
    • Whether MTFP1 directly modifies DRP1 not shown
    • Tissue-specific relevance of translational control untested
  4. 2018 High

    Identified transcriptional/post-transcriptional repression of MTP18 by HIF-1/miR-668, showing MTFP1 is a tunable effector of ischemic mitochondrial dynamics.

    Evidence RISC-IP/RNA-seq, luciferase reporter, and in vivo knockdown/mimic in a mouse AKI model

    PMID:30325740

    Open questions at the time
    • Does not address direct fission machinery interactions
    • Generalizability beyond renal ischemia unknown
  5. 2019 Medium

    Showed MTP18 maintains mitochondrial size and is set by KLF transcription factors, linking its dosage to neuronal axon growth.

    Evidence siRNA, overexpression, mitochondrial imaging, and axon growth assays in retinal ganglion cells

    PMID:31337818

    Open questions at the time
    • Mechanism connecting size control to axon growth unresolved
    • Single-lab observation
  6. 2020 Medium

    Demonstrated direct thyroid-hormone-receptor transcriptional activation of Mtfp1 via an intronic TRE, adding hormonal control to its regulatory repertoire.

    Evidence ChIP for TR binding and H3K79 methylation, RNA Pol recruitment, and reconstituted frog oocyte assay with TRE mutation

    PMID:32827515

    Open questions at the time
    • Xenopus ortholog; human conservation not tested here
    • Downstream physiological output not measured
  7. 2022 Medium

    Used pharmacological inhibition to show MTP18-mediated fission gates a stress axis spanning hyperfusion, lysosomal permeabilization, and apoptosis.

    Evidence Small-molecule (S28) inhibition plus overexpression with membrane potential, superoxide, LMP, and apoptosis readouts in oral cancer cells

    PMID:35985563

    Open questions at the time
    • Inhibitor specificity for MTP18 not fully validated
    • Direct molecular target engagement unclear
  8. 2023 High

    Revealed a second function for MTFP1 as a mitophagy receptor, showing an LIR motif directly engages LC3 to deliver mitochondria to autophagosomes downstream of PINK1/Parkin.

    Evidence LIR mutagenesis, co-IP with LC3 family members, PINK1/Parkin knockdown, CCCP mitophagy and OMM degradation assays

    PMID:37313742

    Open questions at the time
    • Structural basis of LIR engagement not solved
    • Coordination of fission vs receptor roles unresolved
  9. 2023 High

    Defined the in vivo metabolic consequence of MTFP1 loss, showing it restrains OXPHOS and mPTP opening, linking fission control to steatosis and apoptotic protection.

    Evidence Liver-specific knockout mice with respirometry, proteomics, high-fat diet phenotyping, and mPTP assays

    PMID:38123539

    Open questions at the time
    • Mechanism by which MTFP1 suppresses OXPHOS not defined
    • Direct mPTP component interaction unknown
  10. 2024 High

    Established MTFP1 as an inner-membrane quality-control factor that segregates damaged subdomains into SMEM for autophagic mtDNA recycling, unifying its fission and degradation roles.

    Evidence Overexpression/knockout, fusion assays, super-resolution/live imaging, mtDNA copy-number quantification, and autophagy inhibition

    PMID:38689964 PMID:38851188

    Open questions at the time
    • How MTFP1 selectively recognizes damaged IMM unresolved
    • Link between SMEM and mtDNA recycling mechanistically incomplete
  11. 2025 Medium

    Identified direct protein partners (PPA2, ATP synthase subunits) and conserved regulators (ZBTB48), connecting MTFP1 to fission-site selection, OXPHOS modulation, and cancer/longevity phenotypes.

    Evidence Co-IP and GST pull-downs, siRNA epistasis, metabolic flux, in vivo cancer models, and ortholog knockouts in zebrafish and C. elegans

    PMID:39987415 PMID:40873007 PMID:41663153 PMID:41832346

    Open questions at the time
    • Direct binding interfaces not mapped
    • Whether ATP synthase modulation is direct or fission-dependent unclear
    • Ortholog phenotypes' human relevance untested
  12. 2026 Medium

    Extended MTFP1's physiological role to β-cell insulin secretion and to MISO-dependent SMEM assembly, defining recruitment hierarchy and a metabolic-endocrine function (preprints).

    Evidence β-cell conditional knockout, respirometry, EM cristae/ER-mito contacts, miR-125b epistasis; MISO knockout with live imaging and FIS1/DRP1 epistasis (preprints)

    PMID:41648185 PMID:bio_10.1101_2025.01.05.631328

    Open questions at the time
    • Preprints not peer-reviewed
    • Molecular nature of MISO–MTFP1 recruitment undefined
    • How cristae/ER-mito defects arise from MTFP1 loss unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single IMM protein mechanistically toggles between promoting fission, restraining fusion, and acting as a mitophagy receptor, and the structural basis of its DRP1/LC3/PPA2/ATP-synthase interactions, remain open.
  • No structure of MTFP1 or its complexes
  • Direct enzymatic/biochemical activity undefined
  • Regulatory switch between fission and receptor modes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 2 GO:0140097 catalytic activity, acting on DNA 1
Localization
GO:0005739 mitochondrion 2
Pathway
R-HSA-1430728 Metabolism 2 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-9612973 Autophagy 2
Partners
DNM1LMAP1LC3MISOPPA2

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 MTFP1 (MTP18) was identified as a nuclear-encoded mitochondrial protein whose mRNA and protein expression is dependent on PI 3-kinase activity. Knockdown via antisense molecules caused cytochrome c release and apoptosis, and reduced MTP18 levels resulted in a highly interconnected mitochondrial reticulum, while overexpression induced punctate mitochondrial morphology, establishing MTP18 as a downstream target of PI3K signaling that controls mitochondrial morphology and cell viability. Antisense knockdown, confocal microscopy, biochemical fractionation, overexpression studies in PC-3, HaCaT, and COS-7 cells The Journal of biological chemistry Medium 15155745
2005 MTP18 functions as an essential intramitochondrial component of the mitochondrial division apparatus: overexpression induced mitochondrial fragmentation that was blocked by co-expression of Mfn1 or dominant-negative Drp1(K38A), RNAi-mediated knockdown produced highly fused mitochondria, and MTP18 knockdown blocked fission induced by hFis1 overexpression, placing MTP18 downstream of or parallel to hFis1 and requiring Drp1 for its fission activity. RNAi knockdown, overexpression, genetic epistasis with Mfn1, dominant-negative Drp1(K38A), and hFis1 co-expression; confocal microscopy of mitochondrial morphology Journal of cell science High 15985469
2017 mTORC1 stimulates translation of MTFP1 via the eIF4E/4E-BP pathway to promote mitochondrial fission. MTFP1 expression is coupled to pro-fission phosphorylation and mitochondrial recruitment of DRP1. Active-site mTOR inhibitors reduce MTFP1 translation (mediated by 4E-BPs), causing mitochondrial hyperfusion; uncoupling MTFP1 levels from mTORC1/4E-BP upon mTOR inhibition blocks hyperfusion and converts mTOR inhibitor action from cytostatic to cytotoxic. Polysome profiling, mTOR inhibitor treatment, 4E-BP overexpression/knockdown, DRP1 phosphorylation and mitochondrial recruitment assays, cell viability and apoptosis readouts Molecular cell High 28918902
2017 MTFP1 knockdown prevents DRP1 (Dnm1l) accumulation at mitochondria and suppresses doxorubicin-induced mitochondrial fission and apoptosis in cardiac myocytes; conversely, MTFP1 overexpression sensitizes cells to doxorubicin-induced fission and apoptosis, establishing MTFP1 as a pro-fission effector acting upstream of DRP1 mitochondrial translocation. siRNA knockdown, overexpression, mitochondrial morphology imaging, apoptosis assays, DRP1 mitochondrial localization by fractionation/immunofluorescence in HL-1 cardiac myocytes Journal of cellular and molecular medicine Medium 28643438
2017 In gastric cancer cells, MTP18 overexpression enriches DRP1 accumulation at mitochondria and mediates doxorubicin-induced mitochondrial fission and apoptosis; MTP18 expression is downregulated during DOX treatment, suggesting its downregulation contributes to chemoresistance. Overexpression, mitochondrial fragmentation assay, DRP1 mitochondrial accumulation analysis, apoptosis assays in gastric cancer cells Oncotarget Medium 28915614
2018 miR-668 is induced in ischemic AKI via HIF-1 (a functional HIF-1 binding site was identified in the miR-668 promoter) and directly represses MTP18, as validated by luciferase reporter assay and RISC immunoprecipitation-RNA sequencing; MTP18 knockdown suppressed mitochondrial fragmentation and apoptosis in renal tubular cells, positioning MTP18 as a downstream effector of HIF-1/miR-668 in mitochondrial dynamics during ischemia. Anti-miR/mimic transfection, luciferase microRNA target reporter assay, RISC immunoprecipitation + RNA-seq, MTP18 knockdown, mitochondrial morphology and apoptosis assays, in vivo mouse AKI model The Journal of clinical investigation High 30325740
2019 In retinal ganglion cells (RGCs), MTP18/MTFP1 is critical for maintaining mitochondrial size and volume; MTP18 expression is regulated by KLF7 and KLF9 transcription factors, and MTP18 knockdown promotes axon growth, placing MTP18 as a downstream component of KLF-mediated axon regenerative signaling. siRNA knockdown, overexpression, mitochondrial morphology imaging, axon growth assays, transcription factor regulation analysis in RGCs Scientific reports Medium 31337818
2020 In Xenopus tropicalis, the Mtfp1 gene is directly transcriptionally activated by thyroid hormone (T3) via thyroid hormone receptors (TRs) binding to a T3-response element (TRE) within the first intron, mediating local histone H3K79 methylation and RNA polymerase recruitment; Mtfp1 promoter activation by T3 was confirmed in a reconstituted frog oocyte system and found to require the intronic TRE. ChIP assay for TR binding and H3K79 methylation, RNA polymerase recruitment assay, reconstituted frog oocyte transcription assay, TRE deletion/mutation analysis General and comparative endocrinology Medium 32827515
2022 A small-molecule inhibitor (S28) of MTP18 induces stress-induced mitochondrial hyperfusion (SIMH) by inhibiting MTP18-mediated fission (decreased p-DRP1, increased Mfn1), leading to loss of mitochondrial membrane potential, mitochondrial superoxide generation, lysosomal membrane permeabilization (LMP), impaired autophagosome-lysosome fusion, and intrinsic apoptosis; MTP18 overexpression restored mitochondrial fission, induced mitophagy, and suppressed LMP and apoptosis. Small-molecule inhibition, overexpression, mitochondrial morphology imaging, p-DRP1 western blot, membrane potential assay, superoxide detection, lysosomal pH and LMP assays, apoptosis assays in oral cancer cells Free radical biology & medicine Medium 35985563
2023 MTP18/MTFP1 functions as a mitophagy receptor: it contains an LC3-interacting region (LIR) that directly interacts with MAP1LC3 family members to target dysfunctional mitochondria to autophagosomes; LIR mutation (mLIR) abolishes this interaction and suppresses mitophagy; PINK1/Parkin deficiency abrogates MTP18-dependent mitophagy, and Parkin-mediated proteasomal degradation of the outer mitochondrial membrane is required for effective mitophagy downstream of MTP18. LIR motif mutation, co-immunoprecipitation of MTP18 with LC3 family members, PINK1/Parkin knockdown, CCCP-induced mitophagy assays, TOM20/COX IV degradation analysis, apoptosis assays in FaDu oral cancer cells Journal of cell science High 37313742
2023 Hepatocyte-specific deletion of Mtfp1 in mice is physiologically benign but leads to upregulation of oxidative phosphorylation (OXPHOS) activity and mitochondrial respiration independently of mitochondrial biogenesis, and protects against high-fat diet-induced steatosis. Additionally, Mtfp1 deletion inhibits mitochondrial permeability transition pore (mPTP) opening, conferring protection against apoptotic liver damage. Liver-specific Mtfp1 knockout mice, respirometry (Seahorse), proteomics, high-fat diet metabolic phenotyping, mPTP opening assay, ex vivo apoptosis assays Nature communications High 38123539
2024 MTFP1 is an inner mitochondrial membrane (IMM) protein that negatively regulates IMM fusion. Manipulation of MTFP1 levels modulates mtDNA copy number (CN). Mechanistically, MTFP1 inhibits mitochondrial fusion to isolate and exclude damaged IMM subdomains, which are then segregated by peripheral fission into small MTFP1-enriched mitochondria (SMEM) that are targeted for autophagic degradation; this MTFP1-dependent IMM quality control is essential for basal nucleoid recycling and maintaining adequate mtDNA levels. MTFP1 overexpression/knockout, mitochondrial fusion assays, super-resolution and live-cell imaging, mtDNA CN measurement, autophagy inhibition experiments, SMEM isolation and characterization Cell High 38851188
2024 HIF1A directly binds the MTFP1 promoter (validated by ChIP assay) and upregulates MTFP1 expression; MTFP1 overexpression promotes lung squamous cell carcinoma cell proliferation and metastasis by activating the glycolytic pathway. ChIP assay, western blot, cell proliferation/colony formation/migration assays, glycolysis pathway analysis in LUSC cells Heliyon Medium 38689964
2025 PPA2 (inorganic pyrophosphatase, matrix-localized) directly interacts with MTFP1 and activates mitochondrial fission signaling by upregulating phosphorylated DNM1L S616 and its mitochondrial translocation; MTFP1 knockdown in PPA2-overexpressing cells abolishes DNM1L activation and fission. PPA2 utilizes the C-terminal LIR of MTFP1 for mitophagy-mediated clearance of damaged mitochondria, and PPA2 directs midzone fission (via MFF-DNM1L) for mitochondrial proliferation or peripheral fission (via FIS1-DNM1L) for mitophagy under stress. Co-immunoprecipitation of PPA2 with MTFP1, MTFP1 siRNA knockdown epistasis, overexpression studies, mitochondrial morphology imaging, DNM1L phosphorylation assays, CCCP-induced mitophagy assays, LIR mutation analysis Autophagy Medium 40873007
2025 In zebrafish, the transcription factor Zbtb48 positively regulates Mtfp1 expression; zbtb48 knockout resulted in downregulation of mtfp1 at both mRNA and protein levels, particularly in ovary and testis, suggesting mtfp1 is an evolutionarily conserved transcriptional target of Zbtb48. CRISPR-Cas9 zbtb48 knockout zebrafish, RT-qPCR, western blot for Mtfp1 protein levels in gonads Communications biology Medium 39987415
2025 In C. elegans, loss of mtp-18 increases longevity and stress resistance; mtp-18-mediated longevity requires the Forkhead transcription factor DAF-16 but is not mediated through the canonical IIS (insulin/IGF-1 signaling) cascade; MTP-18 shows unique genetic interactions with components of the mitochondrial electron transport chain, specifically coenzyme Q and cytochrome c mobile electron carrier system. mtp-18 loss-of-function mutants, lifespan assays, epistasis with daf-16 and IIS pathway mutants, genetic interaction with ETC component genes in C. elegans Biogerontology Medium 41832346
2025 MTFP1 acts as a novel ATP synthase modulator through its interaction with multiple ATP synthase subunits (identified by GST pull-down), thereby enhancing oxidative phosphorylation; increased mitochondrial fission and ROS production downstream of MTFP1 upregulates SLC1A5 expression via the PI3K/AKT/c-MYC pathway, promoting glutamine uptake and impairing CD8+ T cell antitumor responses in pancreatic cancer liver metastasis. CRISPR loss-of-function screen, GST pull-down assay for ATP synthase subunit interaction, metabolic flux analysis, single-cell RNA-seq, spatial metabolomics, in vivo mouse models, PDAC organoids Gut Medium 41663153
2025 MISO (Mitochondrial Inner membrane Subdomain Organizer) is required for SMEM formation; SMEM functionality requires MISO-dependent recruitment of MTFP1 and subsequent engagement of the FIS1-DRP1 fission machinery; MISO knockout completely abolishes SMEM generation, establishing MTFP1 as a downstream effector recruited by MISO to form SMEM and mediate peripheral fission and lysosomal mtDNA degradation. MISO knockout (Drosophila and mammalian cells), live-cell imaging of SMEM, MTFP1 localization assays, FIS1/DRP1 epistasis, lysosomal mtDNA degradation assays bioRxivpreprint Medium bio_10.1101_2025.01.05.631328
2026 MTFP1 is essential for normal glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells; β-cell-specific MTFP1 knockout mice develop glucose intolerance, with sharply reduced oxidative phosphorylation and ATP production, disrupted mitochondrial cristae structure, and reduced ER-mitochondria contact surface. MTFP1 overexpression in mouse and human islets improved mitochondrial respiration and GSIS. MTFP1 was identified as a downstream effector of miR-125b: MTFP1 downregulation blocked the positive effects of miR-125b elimination on GSIS and mitochondrial respiration. β-cell-specific conditional knockout mice, glucose tolerance tests, respirometry, cristae ultrastructure (EM), ER-mitochondria contact quantification, MTFP1 overexpression in human islets, miR-125b epistasis experiments bioRxivpreprint Medium 41648185

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 mTOR Controls Mitochondrial Dynamics and Cell Survival via MTFP1. Molecular cell 295 28918902
2017 Circular RNA mediates cardiomyocyte death via miRNA-dependent upregulation of MTP18 expression. Cell death and differentiation 287 28498369
2005 The mitochondrial protein MTP18 contributes to mitochondrial fission in mammalian cells. Journal of cell science 195 15985469
2004 Knockdown of MTP18, a novel phosphatidylinositol 3-kinase-dependent protein, affects mitochondrial morphology and induces apoptosis. The Journal of biological chemistry 124 15155745
2018 MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury. The Journal of clinical investigation 114 30325740
2024 MTFP1 controls mitochondrial fusion to regulate inner membrane quality control and maintain mtDNA levels. Cell 86 38851188
2021 Genetically Encoded, pH-Sensitive mTFP1 Biosensor for Probing Lysosomal pH. ACS sensors 64 34102054
2017 Knockdown of Mtfp1 can minimize doxorubicin cardiotoxicity by inhibiting Dnm1l-mediated mitochondrial fission. Journal of cellular and molecular medicine 38 28643438
2023 Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis. Nature communications 27 38123539
2017 Mitochondrial protein 18 (MTP18) plays a pro-apoptotic role in chemotherapy-induced gastric cancer cell apoptosis. Oncotarget 22 28915614
2012 Fluorescence lifetime readouts of Troponin-C-based calcium FRET sensors: a quantitative comparison of CFP and mTFP1 as donor fluorophores. PloS one 21 23152874
2022 MTP18 inhibition triggers mitochondrial hyperfusion to induce apoptosis through ROS-mediated lysosomal membrane permeabilization-dependent pathway in oral cancer. Free radical biology & medicine 20 35985563
2019 MTP18 is a Novel Regulator of Mitochondrial Fission in CNS Neuron Development, Axonal Growth, and Injury Responses. Scientific reports 20 31337818
2023 The inner mitochondrial membrane fission protein MTP18 serves as a mitophagy receptor to prevent apoptosis in oral cancer. Journal of cell science 17 37313742
2019 MTFP1 overexpression promotes the growth of oral squamous cell carcinoma by inducing ROS production. Cell biology international 17 31814213
2022 Transcriptome Profiling of Developing Ovine Fat Tail Tissue Reveals an Important Role for MTFP1 in Regulation of Adipogenesis. Frontiers in cell and developmental biology 12 35350385
2010 Modeling spectral tuning in monomeric teal fluorescent protein mTFP1. Biophysical chemistry 12 20442006
2024 SIRT1-activating butein inhibits arecoline-induced mitochondrial dysfunction through PGC1α and MTP18 in oral cancer. Phytomedicine : international journal of phytotherapy and phytopharmacology 10 38723523
2022 MiR-125b-5p Targets MTFP1 to Inhibit Cell Proliferation, Migration, and Invasion and Facilitate Cell Apoptosis in Endometrial Carcinoma. Molecular biotechnology 9 36380260
2025 Hypoxia induces ferroptotic cell death mediated by activation of the inner mitochondrial membrane fission protein MTP18/Drp1 in invertebrates. The Journal of biological chemistry 8 39971157
2018 DARPins recognizing mTFP1 as novel reagents for in vitro and in vivo protein manipulations. Biology open 7 30237292
2024 HIF1A-dependent overexpression of MTFP1 promotes lung squamous cell carcinoma development by activating the glycolysis pathway. Heliyon 5 38689964
2025 PPA2 activates MTFP1-DNM1L fission signaling to govern mitochondrial proliferation and mitophagy. Autophagy 4 40873007
2020 Thyroid hormone directly activates mitochondrial fission process 1 (Mtfp1) gene transcription during adult intestinal stem cell development and proliferation in Xenopus tropicalis. General and comparative endocrinology 3 32827515
2026 MTFP1 drives pancreatic cancer liver metastatic colonisation by regulating mitochondrial metabolism reprogramming. Gut 1 41663153
2025 Mitochondrial fission genes MTFP1/MTFP2 as predictive biomarkers in prostate cancer: a mendelian randomization study. Discover oncology 1 40824549
2023 MTFP1 is a mitophagy receptor that operates in PINK1/PRKN-dependent mitophagy and promotes oral cancer cell survival. Autophagy reports 1 40395309
2026 MTFP1 preserves β-cell cristae structure and bioenergetics to ensure insulin release and glucose homeostasis. bioRxiv : the preprint server for biology 0 41648185
2026 Noncanonical role of MTP-18 in mitochondrial function and aging via electron transport chain interactions in Caenorhabditis elegans. Biogerontology 0 41832346
2026 Identification and Validation of MTFP1 as a Mitochondrial Target Restoring Dynamics and ECM Remodeling in Acute Myocardial Infarction. Current issues in molecular biology 0 41899445
2026 Expression and purification of the ectodomain of erythropoietin receptor fused to mCitrine or mTFP1 fluorescent protein in Escherichia coli. Protein expression and purification 0 41905612
2025 Zbtb48 is a regulator of Mtfp1 expression in zebrafish. Communications biology 0 39987415

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