Affinage

TPI1

Triosephosphate isomerase · UniProt P60174

Length
249 aa
Mass
26.7 kDa
Annotated
2026-06-10
40 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/8 claims corpus-supported (88%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TPI1 is the glycolytic isomerase that interconverts DHAP and GAP, a reaction central to controlling carbon partitioning between glycolytic completion and glycerolipid synthesis (PMID:19047824, PMID:36715544). Its catalytic output is tuned by site-specific post-translational modifications: dopaminylation at Gln65 directionally enhances DHAP-to-GAP conversion to redirect ether phospholipid synthesis, attenuate lipid peroxidation, and block ferroptosis (PMID:39111287), while phosphorylation at Ser21 by LKB1-dependent salt-inducible kinases (SIKs) modulates flux between glycolysis and glycerol lipids in human lung adenocarcinoma (PMID:36715544). Enzyme integrity depends on structural elements whose disruption causes loss of function through protein destabilization rather than direct catalytic impairment, as shown for the dimer-interface Arg189 and the R5G allele, in which purified mutant protein retains wild-type activity yet is depleted at steady state (PMID:31075491, PMID:41153421). TPI1 abundance is set by competing protein-stability inputs—SQSTM1/P62-mediated ubiquitin-dependent degradation versus USP5-dependent deubiquitination—and by mRNA-level control through m5C methylation (NSUN2/YBX1 and NOP2) and EIF4A3-mediated transcript stabilization (PMID:35509067, PMID:40956511, PMID:41498196, PMID:42251361, PMID:41857621). Beyond cytoplasmic glycolysis, TPI1 translocates to the nucleus under chemotherapy and peroxide stress, where its nuclear localization, independent of catalytic activity, drives oncogenic transcriptional programs and chemoresistance, including STAT3/P300-dependent SOX9 activation in glioblastoma (PMID:35246510, PMID:39342418). In bladder cancer it acts non-glycolytically by binding the Beclin-1 BH3 domain to disrupt the Bcl-2/Beclin-1 interaction and promote autophagy (PMID:41429797), and by forming an AKT–MDM2 complex that enhances MDM2 Ser166 phosphorylation to drive p53 ubiquitination and degradation (PMID:40097123). The TPI1 product DHAP itself functions as an epigenetic signal, with nuclear DHAP levels modulating H3K27 acetylation at target promoters (PMID:41407053). Compound heterozygous TPI1 mutations cause a human enzymopathy presenting with reduced enzyme protein and neuromuscular dysfunction (PMID:31075491, PMID:41153421).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2008 Medium

    Establishing TPI1's canonical metabolic role: deleting the gene demonstrated it governs the DHAP/GAP equilibrium and thereby controls carbon flux toward glycerol and downstream metabolites.

    Evidence Genetic deletion of tpi1 in S. cerevisiae with heterologous metabolic engineering and metabolite quantification

    PMID:19047824

    Open questions at the time
    • Yeast ortholog; does not address regulation of human TPI1
    • No structural or PTM-level mechanism for flux control
  2. 2019 High

    Defined how point mutations cause disease by showing that an interface salt-bridge residue (Arg189) is required for protein stability and substrate-site coordination, linking structural destabilization to loss of function and motor deficits.

    Evidence Homologous genomic mutagenesis in Drosophila, patient fibroblast analysis, and structural rationale

    PMID:31075491

    Open questions at the time
    • Does not resolve whether instability or catalytic loss dominates for all pathogenic alleles
    • No human in vivo validation
  3. 2022 Medium

    Revealed a moonlighting function: stress-induced nuclear translocation, not glycolytic catalysis, drives TPI1's oncogenic and chemoresistance activity.

    Evidence Subcellular fractionation, immunofluorescence, catalytic mutant vs. localization experiments, and xenografts in lung adenocarcinoma

    PMID:35246510

    Open questions at the time
    • Nuclear import mechanism and transcriptional targets not defined here
    • Single tumor type
  4. 2022 Medium

    Identified protein-turnover and signaling partners: SQSTM1/P62 drives ubiquitin-dependent degradation while CDCA5 stabilization links TPI1 to PI3K/AKT/mTOR-driven EMT and glycolysis.

    Evidence Reciprocal Co-IP, ubiquitination assays, and functional knockdown/overexpression in breast cancer cells

    PMID:35509067

    Open questions at the time
    • E3 ligase mediating P62-dependent degradation not identified
    • Direct vs. indirect CDCA5 stabilization unresolved
  5. 2023 High

    Connected TPI1 to a kinase signaling axis: LKB1-dependent SIK phosphorylation at Ser21 modulates the glycolysis/glycerolipid branch point, explaining a human-specific metabolic liability not present in mouse (which has an oxidizable Cys).

    Evidence Phosphoproteomics, metabolomics, and orthogonal human cell line plus GEMM models

    PMID:36715544

    Open questions at the time
    • Structural basis of how Ser21 phosphorylation alters activity not fully resolved
    • Cross-species divergence complicates mouse modeling
  6. 2024 High

    Demonstrated a direct PTM that tunes catalytic directionality: dopaminylation at Q65 enhances DHAP-to-GAP conversion to suppress ferroptosis through redirected ether phospholipid synthesis.

    Evidence Chemoproteomic site identification, in vitro activity assays, Q65 mutagenesis, and rescue in endothelial cells and mouse lung injury

    PMID:39111287

    Open questions at the time
    • Enzyme(s) installing/removing dopaminylation not defined
    • Generality beyond endothelial regeneration unknown
  7. 2024 Medium

    Linked TPI1 transcription to metabolic-epigenetic feedback, showing LDHA-driven H3K18 lactylation at the TPI1 promoter upregulates its expression to amplify glycolysis.

    Evidence LDHA knockdown/knockout, H3K18la ChIP at the TPI1 promoter, K69 mutation, and OA mouse model

    PMID:39086231

    Open questions at the time
    • Direct lactylation writer at TPI1 locus not isolated
    • Limited to OA chondrocyte context
  8. 2024 Low

    Extended the nuclear-moonlighting model mechanistically, showing TPI1 partners with PKM2 and Linc00942 to undergo nuclear translocation and activate a STAT3/P300–SOX9 transcriptional program driving therapy resistance.

    Evidence ChIRP-MS/WB, Co-IP, and functional assays in glioblastoma

    PMID:39342418

    Open questions at the time
    • ChIRP-MS interaction with partial mechanistic follow-up; single lab
    • Direct vs. scaffold role of TPI1 in the complex unclear
  9. 2025 Medium

    Established a non-glycolytic autophagy mechanism: TPI1 binds the Beclin-1 BH3 domain to displace Bcl-2 and promote PIK3C3-C1/ULK1 assembly, driving autophagy and gemcitabine resistance.

    Evidence MS, Co-IP with domain specificity, ChIP-qPCR for c-Myc regulation, and xenografts in bladder cancer

    PMID:41429797

    Open questions at the time
    • Whether catalytic activity is dispensable for Beclin-1 binding not stated
    • Single cancer context
  10. 2025 Medium

    Defined a tumor-suppressor-antagonizing complex: TPI1 scaffolds AKT and MDM2 to enhance MDM2 Ser166 phosphorylation and p53 degradation.

    Evidence Co-IP, MDM2 truncation mapping (residues 181–360), AKT knockdown rescue, and xenografts in bladder cancer

    PMID:40097123

    Open questions at the time
    • Direct vs. AKT-bridged TPI1–MDM2 contact not fully separated
    • Single lab
  11. 2025 Medium

    Showed TPI1 product DHAP acts as an epigenetic signal: GRK4-driven nuclear TPI1 phosphorylation lowers nuclear DHAP, raising H3K27ac at the Hao2 promoter to promote oxidative stress and salt-sensitive hypertension.

    Evidence IP-MS, GRK4 R65L mouse model, DHAP supplementation and C646 rescue, nuclear fractionation

    PMID:41407053

    Open questions at the time
    • Mechanism by which DHAP modulates acetyltransferase activity not defined
    • Phosphosite on nuclear TPI1 not mapped here
  12. 2025 Low

    Identified deubiquitination as a stabilization input: USP5 stabilizes TPI1 protein, and propofol inhibits lung cancer glycolysis by increasing TPI1 ubiquitination through this axis.

    Evidence Ubiquitination analysis, USP5 manipulation, and xenografts

    PMID:40956511

    Open questions at the time
    • No in vitro reconstitution of USP5 deubiquitination of TPI1
    • Direct vs. indirect USP5–TPI1 action not shown
  13. 2025 Low

    Added a lncRNA stabilization input, showing HANR directly binds and stabilizes TPI1 protein to support prostate tumor glycolysis.

    Evidence RIP/pulldown and knockdown functional and xenograft assays

    PMID:40921293

    Open questions at the time
    • Stabilization mechanism not dissected
    • RIP/pulldown without orthogonal validation
  14. 2025 High

    Confirmed the destabilization-disease paradigm and offered a therapeutic strategy: the R5G allele retains catalytic activity but is depleted, and small molecules restore TPI protein and activity in patient cells.

    Evidence Recombinant protein activity/stability assays, patient cell Western blot, and pharmacological rescue

    PMID:41153421

    Open questions at the time
    • Mechanism of compound-mediated stabilization not defined
    • In vivo efficacy untested
  15. 2026 Medium

    Defined mRNA-stability control of TPI1 through m5C methylation and translation-associated factors, linking RNA modification machinery to glycolytic output and immune evasion.

    Evidence MeRIP, RIP, dual-luciferase reporters and rescue across larynx, breast, and TNBC models (NOP2; NSUN2/YBX1; OTUB2/EIF4A3)

    PMID:41498196 PMID:41857621 PMID:42251361

    Open questions at the time
    • Whether these RNA inputs converge on the same regulatory elements unknown
    • Relative contribution versus protein-level control unquantified
  16. 2026 Low

    Identified post-transcriptional translational control under hypoxia via an IRES element in the TPI1 5'UTR.

    Evidence Dicistronic reporter assays with PTB involvement in C6 glioma cells

    PMID:40105374

    Open questions at the time
    • PTB–TPI1 mRNA interaction not directly validated by RIP/pulldown
    • Single context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the diverse regulatory layers—catalytic-tuning PTMs, nuclear moonlighting, and the multiple protein- and mRNA-stability inputs—are integrated to set TPI1 output in a given cell type, and which are dispensable for its enzymatic versus non-enzymatic functions, remains unresolved.
  • No unified model coordinating PTMs, localization, and stability
  • Catalysis-independent functions not systematically separated from glycolytic role
  • Nuclear import mechanism undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016853 isomerase activity 4 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-9612973 Autophagy 1
Partners
AKT1BECN1CDCA5EIF4A3GRK4MDM2PKMSQSTM1

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2024 Dopamine directly modifies TPI1 by dopaminylating the glutamine 65 (Q65) residue in endothelial cells. This post-translational modification directionally enhances TPI1's catalytic activity to convert DHAP to GAP, shifting ether phospholipid synthesis toward glucose metabolism, thereby attenuating lipid peroxidation and blocking ferroptosis in regenerating lung endothelial cells. Chemoproteomic approach identifying dopaminylation site; in vitro TPI1 activity assays; metabolic flux measurements; mutagenesis of Q65; loss-of-function and rescue experiments in endothelial cells and mouse lung injury models Cell metabolism High 39111287
2023 In human lung adenocarcinoma (hLUAD), TPI1 activity is regulated by phosphorylation at Ser21 by salt-inducible kinases (SIKs) in an LKB1-dependent manner. This phosphorylation modulates metabolic flux between the completion of glycolysis and production of glycerol lipids. Mouse TPI1 has a Cys at the equivalent position that can be oxidized to alter activity, representing an evolutionary divergence that explains why LKB1 loss creates a metabolic liability specifically in human tumors with KRAS/TP53 mutations. Phosphoproteomics; metabolomics; genetically engineered human cell lines with LKB1/SIK manipulation; genetically engineered mouse models (GEMM) comparison Cancer discovery High 36715544
2022 TPI1 undergoes nuclear translocation in lung adenocarcinoma tumor tissues (compared to cytoplasmic localization in adjacent normal tissues), and this nuclear localization—rather than its glycolytic catalytic activity—is required for its oncogenic function and for promoting chemoresistance. Nuclear translocation is induced by extracellular stresses including chemotherapy agents and peroxide. Subcellular fractionation; immunofluorescence; knockdown of TPI1; catalytic mutant experiments; xenograft tumor growth assays; TCGA data analysis Cell death & disease Medium 35246510
2022 TPI1 interacts with SQSTM1/P62, which promotes ubiquitin-dependent proteasomal degradation of TPI1, decreasing TPI1 protein levels in breast cancer cells. TPI1 also interacts with and stabilizes CDCA5, activating the PI3K/AKT/mTOR pathway to regulate EMT and aerobic glycolysis. Co-immunoprecipitation; mass spectrometric analysis; ubiquitination assay; immunofluorescence; overexpression and knockdown functional experiments; Western blotting; in vivo mouse models Journal of translational medicine Medium 35509067
2019 The Arg189 residue in TPI1 participates in two salt bridges on the backside of the TPI enzyme dimer; mutation of this residue (Arg189Gln) alters the coordination of the substrate-binding site and important catalytic residues, causing reduced protein stability and loss of function. This was demonstrated by homologous mutagenesis in Drosophila using genomic engineering, showing motor behavioral deficits and markedly reduced protein levels. Genomic engineering in Drosophila (homologous mutagenesis); compound heterozygote animal generation; patient fibroblast analysis; structural analysis of salt bridge coordination Biochimica et biophysica acta. Molecular basis of disease High 31075491
2025 TPI1 interacts with AKT and MDM2 to form a protein complex that enhances AKT-driven phosphorylation of MDM2 at serine 166, thereby promoting p53 ubiquitination and degradation in bladder cancer cells. The MDM2-F2 truncation mutant (spanning residues 181–360) with amino acid 317 was identified as critical for TPI1 binding. Reducing AKT expression counteracted p53 ubiquitination triggered by elevated TPI1. Co-immunoprecipitation; truncation mutagenesis of MDM2; AKT knockdown rescue experiments; functional cell assays; in vivo xenograft models Pharmacological research Medium 40097123
2021 TPI1 is incorporated into extracellular vesicles (EVs) in a manner positively regulated by Rab20 expression in the releasing hepatocellular carcinoma cells. EVs with reduced TPI1 (from Rab20-knockdown cells) enhance aerobic glycolysis in recipient cells, promoting HCC cell growth and motility; this promoting effect is blocked by a glycolytic inhibitor. Rab20 restoration and knockdown in HCC cells; proteomic profiling of EVs; TPI1 targeted expression in EVs; glycolytic inhibitor rescue experiments; cell proliferation and motility assays Journal of extracellular vesicles Medium 34401050
2025 TPI1 directly binds to the BH3 domain of Beclin-1, competitively disrupting the Bcl-2/Beclin-1 interaction and relieving Bcl-2-mediated inhibition of Beclin-1. This interaction promotes PIK3C3-C1 complex formation and enhances its interaction with the ULK1 complex, increasing Beclin-1 phosphorylation at Ser15 and promoting autophagy, which contributes to gemcitabine resistance in bladder cancer cells. c-Myc was identified as a transcription factor that binds the TPI1 promoter to regulate its expression. Mass spectrometry; co-immunoprecipitation; transcriptome sequencing; transmission electron microscopy; dual luciferase assay; ChIP-qPCR; in vivo xenograft models Cell death & disease Medium 41429797
2024 In LPS-induced OA chondrocytes, LDHA mediates H3K18 lactylation (H3K18la) at the TPI1 promoter, enhancing TPI1 transcriptional activity and glycolysis. Mutation of the K69 site ameliorated LPS-induced glycolysis, and LDHA knockout recovered cartilage injury in OA mice. LDHA knockdown and knockout (loss-of-function); H3K18la ChIP at TPI1 promoter; K69 mutation in TPI1; glycolysis functional assays (glucose consumption, lactate production); in vivo OA mouse model Autoimmunity Medium 39086231
2025 TPI1 nuclear phosphorylation is increased by GRK4 R65L in high-salt conditions; this reduces nuclear DHAP levels, increases H3K27ac at the Hao2 promoter, and upregulates Hao2 expression, leading to increased renal oxidative stress and salt-sensitive hypertension. DHAP (downstream metabolite of TPI1) directly reduced H3K27ac and Hao2 levels in cells. Immunoprecipitation-mass spectrometry (identifying TPI1-GRK4 interaction and TPI1 phosphorylation); GRK4 depletion via AAV9; DHAP supplementation rescue; H3K27ac inhibitor C646 treatment; in vivo GRK4 R65L mouse model; nuclear fractionation Free radical biology & medicine Medium 41407053
2025 USP5 deubiquitinates TPI1, stabilizing its protein levels. Propofol increases TPI1 ubiquitination and reduces TPI1 protein stability, and the inhibitory effects of propofol on lung cancer glycolysis and progression are mediated through this USP5/TPI1 axis. Ubiquitination analysis; Western blot for TPI1 protein levels upon USP5 manipulation; qRT-PCR; xenograft mouse models; IHC Biochemical genetics Low 40956511
2026 NOP2 promotes m5C methylation of TPI1 mRNA, enhancing its stability. Knockdown of NOP2 reduced m5C modification on TPI1 mRNA and decreased TPI1 expression; overexpression of TPI1 rescued glycolysis impaired by NOP2 knockdown in larynx cancer cells. MeRIP (methylated RNA immunoprecipitation) for m5C on TPI1 mRNA; RIP; dual-luciferase reporter assay; NOP2 knockdown and TPI1 overexpression rescue; xenograft tumor models; IHC Molecular carcinogenesis Medium 41498196
2026 NSUN2 promotes m5C methylation of TPI1 mRNA in a manner recognized by YBX1, enhancing TPI1 mRNA stability. TPI1 overexpression reversed the inhibition of breast cancer glycolysis, immune evasion, and tumor growth caused by NSUN2 silencing. RNA immunoprecipitation; methylated RNA immunoprecipitation (MeRIP); dual-luciferase reporter assay; NSUN2 knockdown/TPI1 overexpression rescue; tumor-bearing mouse model Journal of translational medicine Medium 42251361
2026 EIF4A3 interacts with TPI1 mRNA to stabilize it. OTUB2 deubiquitinates and stabilizes EIF4A3 protein, which in turn promotes TPI1 expression and glycolysis in triple-negative breast cancer. Co-immunoprecipitation; RNA immunoprecipitation; Western blot for protein stability; OTUB2/EIF4A3/TPI1 knockdown and overexpression rescue; xenograft mouse model Breast cancer research : BCR Medium 41857621
2025 lncRNA HANR directly interacts with TPI1 protein to stabilize it, promoting aerobic glycolysis and tumor growth in prostate cancer. Silencing HANR or TPI1 reduced prostate tumor growth in vitro and in vivo. RNA immunoprecipitation/pulldown (HANR-TPI1 interaction); HANR and TPI1 knockdown functional assays; in vivo xenograft model Experimental cell research Low 40921293
2024 In GBM cells, TPI1 interacts with PKM2 and the lncRNA Linc00942 (ChIRP-MS and ChIRP-WB assays). This interaction promotes phosphorylation, dimerization, and nuclear translocation of TPI1 and PKM2, leading to increased H3K4 acetylation and STAT3/P300 axis activation, which transcriptionally activates SOX9 to drive TMZ resistance and self-renewal. ChIRP-MS (chromatin isolation by RNA purification followed by mass spectrometry); ChIRP-WB; Co-immunoprecipitation; in vitro and in vivo functional assays Advanced science (Weinheim, Baden-Wurttemberg, Germany) Low 39342418
2025 Hypoxia upregulates HK2 and TPI1 protein levels in non-neuronal C6 glioma cells without increasing their mRNA levels, implicating post-transcriptional regulation. Using dicistronic and promoter-less dicistronic reporter assays, IRES (internal ribosome entry site) elements were identified in the 5'UTR of TPI1 mRNA that are more active in C6 glioma cells, with PTB (polypyrimidine tract binding) protein involved. Dicistronic reporter assays; promoter-less dicistronic assays; MTT assay; LDH leakage assay; Western blot; qRT-PCR Artificial cells, nanomedicine, and biotechnology Low 40105374
2008 Deletion of the tpi1 (triosephosphate isomerase) gene in Saccharomyces cerevisiae increases carbon flux to DHAP in glycolysis, resulting in increased glycerol production. Introduction of bacterial mgs and gldA genes (converting DHAP to 1,2-propanediol) into the tpi1-deleted strain confirmed that DHAP accumulation from TPI1 loss drives metabolic flux to methylglyoxal and then 1,2-propanediol. Genetic deletion of tpi1 in yeast; metabolic engineering with heterologous gene expression; metabolite measurement in flask culture Journal of microbiology and biotechnology Medium 19047824
2025 A compound heterozygous TPI1 allele carrying an R5G missense mutation results in markedly reduced steady-state TPI protein levels despite the purified TPIR5G protein retaining wild-type catalytic activity and modestly increased dimer stability, indicating protein instability (not catalytic defect) as the pathogenic mechanism. Three newly identified compounds significantly increased TPI protein levels in patient cells, also increasing TPI enzymatic activity. Recombinant protein expression and purification; in vitro TPI activity assay; dimer stability assay; patient cell (TPIpatient) Western blot; treatment with pharmacological compounds and TPI activity measurement Genes High 41153421

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2022 TPI1 activates the PI3K/AKT/mTOR signaling pathway to induce breast cancer progression by stabilizing CDCA5. Journal of translational medicine 54 35509067
2022 Elevated nuclear localization of glycolytic enzyme TPI1 promotes lung adenocarcinoma and enhances chemoresistance. Cell death & disease 45 35246510
2021 TPI1-reduced extracellular vesicles mediated by Rab20 downregulation promotes aerobic glycolysis to drive hepatocarcinogenesis. Journal of extracellular vesicles 44 34401050
2024 LDHA-induced histone lactylation mediates the development of osteoarthritis through regulating the transcription activity of TPI1 gene. Autoimmunity 38 39086231
1979 Regional assignment of human genes TPI1, GAPDH, LDHB, SHMT, and PEPB on chromosome 12. Cytogenetics and cell genetics 38 477403
2024 Dopaminylation of endothelial TPI1 suppresses ferroptotic angiocrine signals to promote lung regeneration over fibrosis. Cell metabolism 31 39111287
2023 LKB1-Dependent Regulation of TPI1 Creates a Divergent Metabolic Liability between Human and Mouse Lung Adenocarcinoma. Cancer discovery 29 36715544
2022 Daidzin inhibits hepatocellular carcinoma survival by interfering with the glycolytic/gluconeogenic pathway through downregulation of TPI1. BioFactors (Oxford, England) 25 35118741
2020 Proteomics analysis identified TPI1 as a novel biomarker for predicting recurrence of intrahepatic cholangiocarcinoma. Journal of gastroenterology 23 33089343
2008 Enhanced production of 1,2-propanediol by tpi1 deletion in Saccharomyces cerevisiae. Journal of microbiology and biotechnology 21 19047824
2022 Atractylenolide-1 affects glycolysis/gluconeogenesis by downregulating the expression of TPI1 and GPI to inhibit the proliferation and invasion of human triple-negative breast cancer cells. Phytotherapy research : PTR 20 36420870
2024 LncRNA-Mediated TPI1 and PKM2 Promote Self-Renewal and Chemoresistance in GBM. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 18 39342418
2023 TPI1 promotes MAPK/ERK-induced EMT, cell migration and invasion in lung adenocarcinoma. Thoracic cancer 15 38130074
2019 Missense variant in TPI1 (Arg189Gln) causes neurologic deficits through structural changes in the triosephosphate isomerase catalytic site and reduced enzyme levels in vivo. Biochimica et biophysica acta. Molecular basis of disease 15 31075491
1993 Mapping of MYF5, C1R, MYHL, TPI1, IAPP, A2MR and RNR onto sheep chromosome 3q. Animal genetics 14 8273915
2008 Sequencing and genotypic analysis of the triosephosphate isomerase (TPI1) locus in a large sample of long-lived Germans. BMC genetics 13 18510744
2024 Identification of TPI1 As a potential therapeutic target in pancreatic cancer with dependency of TP53 mutation using multi-omics analysis. Cancer science 10 39259678
2022 miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells. PloS one 10 36137140
2025 TPI1 promotes p53 ubiquitination in bladder cancer by recruiting AKT to enhance MDM2 phosphorylation. Pharmacological research 7 40097123
2022 Systemic Analyses of the Expression of TPI1 and Its Associations with Tumor Microenvironment in Lung Adenocarcinoma and Squamous Cell Carcinoma. Disease markers 7 35126788
2025 Inhibition of TPI1 Sensitizes Cisplatin-Resistant Oral Cancer to Ferroptosis. Biomedicines 6 40427052
1991 Tpi-1 and Gapd are linked very closely on mouse chromosome 6. Genetical research 6 2040452
2024 Single-Cell RNA Sequencing Revealed That the Enrichment of TPI1+ Malignant Hepatocytes Was Linked to HCC Metastasis and Immunosuppressive Microenvironment. Journal of hepatocellular carcinoma 5 38410699
2025 LncRNA HANR promotes the aerobic glycolysis in prostate cancer by stabilizing TPI1. Experimental cell research 2 40921293
2024 circular RNA circ-231 promotes protein biogenesis of TPI1 and PRDX6 through mediating the interaction of eIF4A3 with STAU1 to facilitate unwinding of secondary structure in 5' UTR, enhancing progression of human esophageal squamous cell carcinoma (ESCC). Journal of Cancer 2 38577609
1995 The gene for the peroxisomal targeting signal import receptor (PXR1) is located on human chromosome 12p13, flanked by TPI1 and D12S1089. Genomics 2 8586442
2025 IRES activation: HK2 and TPI1 glycolytic enzymes play a pivotal role in non-neuronal cell survival under hypoxia. Artificial cells, nanomedicine, and biotechnology 1 40105374
2025 TPI1 enhances gemcitabine resistance in bladder cancer by promoting autophagy through activating Beclin-1. Cell death & disease 1 41429797
2024 Ebselen and TPI-1, as RecG helicase inhibitors, potently enhance the susceptibility of Pseudomonas aeruginosa to DNA damage agents. Biochemical pharmacology 1 38354956
2026 NOP2 Promotes Glycolysis and Tumor Development in Larynx Cancer by Stabilizing TPI1 mRNA Through N5-Methylcytosine Modification. Molecular carcinogenesis 0 41498196
2026 TPI1 and TPM4 are strong candidate RNA biomarkers for systemic sclerosis. Arthritis research & therapy 0 41634796
2026 Familial Dystonia Due to Homozygous TPI1 c.718G>A (p.Glu240Lys): A Three-Sibling Case Series Including Two Treated with Deep Brain Stimulation of the Globus Pallidus Internus. Annals of Indian Academy of Neurology 0 41692693
2026 Deubiquitination and stabilization of EIF4A3 by OTUB2 contributes to TPI1-mediated glycolysis and TNBC progression. Breast cancer research : BCR 0 41857621
2026 5-O-Methylembelin disrupts the ACO1-TPI1 interaction to promote ferroptosis in clear cell renal cell carcinoma. Phytomedicine : international journal of phytotherapy and phytopharmacology 0 42166976
2026 NSUN2/m5C/TPI1 axis promotes glycolysis and immune evasion in breast cancer. Journal of translational medicine 0 42251361
2025 Propofol Inhibits Lung Cancer Glycolysis by Influencing the Deubiquitination Modification of TPI1 Regulated by USP5. Biochemical genetics 0 40956511
2025 Newly Identified TPI Deficiency Treatments Function for Novel Disease-Causing Allele, TPI1. Genes 0 41153421
2025 Increased Serum Levels of LDHA and TPI1 in Patients With Polycystic Ovary Syndrome. Proteomics. Clinical applications 0 41273239
2025 GRK4 R65L causes salt-sensitive hypertension by augmenting renal Hao2-mediated oxidative stress via increasing the phosphorylation of TPI1 and promoting H3K27ac expression. Free radical biology & medicine 0 41407053
2025 TPI1 promotes tumor progression and M2 macrophage polarization: Integrated pan-cancer and lung adenocarcinoma insights. Biochemical and biophysical research communications 0 41447883

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