Ask about this productRelated genes to: TDO2 Blocking Peptide
- Gene:
- TDO2 NIH gene
- Name:
- tryptophan 2,3-dioxygenase
- Previous symbol:
- -
- Synonyms:
- TDO, TPH2
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-29
- Date modifiied:
- 2016-10-25
Related products to: TDO2 Blocking Peptide
Related articles to: TDO2 Blocking Peptide
- Transarterial chemoembolization (TACE) is a standard treatment for intermediate-stage hepatocellular carcinoma (HCC), but response is highly variable. The systemic metabolic impact of TACE and its connection to tumor-intrinsic factors governing efficacy remain poorly understood. We hypothesized that by comparing host fecal metabolomics with tumor transcriptomics, we could identify convergent pathways suggestive of a gut-liver axis signature of TACE response. - Source: PubMed
Publication date: 2026/06/17
Ren XiaojingLiu ZhenyuWang YifanGuo PengCheng ShuyaoZhang Ruiping - Mitochondrial metabolic dysregulation is associated with periodontitis (PD); however, related biomarkers remain unclear. In this study, we identified key mitochondrial metabolism-related biomarkers in PD through integrated bioinformatics technology. - Source: PubMed
Publication date: 2026/06/13
Wu JiahuaWu JuanHong YubingRao LijiaChen Mu - Fetal growth restriction (FGR), a major perinatal complication, is causally linked to lifelong cognitive deficits in offspring; however, its underlying mechanisms remain poorly defined. Here, the SIRT6-TDO2/KYNA-mTOR axis is identified as a critical mediator of synaptic dysfunction and cognitive deficits in FGR offspring. Hippocampal excitatory neurons in FGR mice exhibit markedly reduced SIRT6 expression, and SIRT6 conditional knockout in CaMKIIα⁺ neurons (Sirt6 cKO) recapitulates FGR-induced synaptic and cognitive impairments. Mechanistically, SIRT6 governs synaptic plasticity and cognition via its histone deacetylase activity, independent of its ADP-ribosyltransferase function. SIRT6 deficiency increases histone H3K9 acetylation at the Tdo2 promoter, enhancing kynurenine pathway flux and leading to pathological accumulation of hippocampal kynurenic acid (KYNA). Elevated KYNA suppresses AKT/mTOR/p70S6K1 signaling, disrupting synaptic protein synthesis. Strikingly, pharmacological TDO2 blockade, neuronal TDO2 knockdown or mTOR activation reverses synaptic and cognitive deficits in Sirt6 cKO mice. Crucially, hippocampal SIRT6 overexpression in FGR mice normalizes KYNA levels, reactivates mTOR signaling, and restores synaptic plasticity and cognitive performance. These findings uncover a neurodevelopmental axis wherein neuronal SIRT6 deficiency dysregulates tryptophan metabolism to impair synaptic plasticity, identifying actionable targets for treating FGR-induced cognitive disorders. - Source: PubMed
Publication date: 2026/06/11
Chang ShujuanChen WenZhu WeiLiu NanaWang YuhangLi JianguoKang Jiuhong - Lung cancer is a leading cause of cancer-related mortality, necessitating accurate prognostic assessment and optimized treatment. Telomerase-related genes are pivotal in tumor development, yet their prognostic value and mechanisms within the lung cancer tumor microenvironment (TME) remain unclear. - Source: PubMed
Publication date: 2026/06/10
Wei WeiWang YuhengAbudukeremu DiliyaerLuo JinhuaDu Mingjun - Joint effect of cancer-associated fibroblasts (CAFs) and regulatory T cells (Tregs) can drive immunosuppression in high-grade serous ovarian cancer (HGSOC), thereby promoting tumor metastasis and limiting the clinical benefit of PD-1/PD-L1 blockade. However, the mechanistic crosstalk between CAFs and Tregs remains unclear. By integrating bulk RNA-seq, single-cell RNA-seq datasets, and spatial transcriptomics datasets with functional assays, we identified a population of TGF-β1-driven Gremlin1 (GREM1) myofibroblastic CAFs (myCAFs) enriched in HGSOC metastatic lesions. These GREM1 myCAFs activated the FGFR1-MAPKs-NFκB-TDO2-kynurenine axis via autocrine signaling, promoting tumor growth, metastasis, and immune evasion characterized by the infiltration of CD4 Tregs and dysfunctional CD8 T cells. GREM1 knockdown suppressed tumor metastasis, restored antitumor T cells response, remodeled CAF subtype composition and potentiated anti-PD-1 therapy efficacy. This study highlights the pro-metastatic role of GREM1 myCAFs across multiple tumors and provides a rationale for combining anti-PD-1 therapy for metastatic HGSOC. - Source: PubMed
Publication date: 2026/06/10
Li RunrongHuang XizhanChen YueChen XiaowenYang YueLiu YuruiBai BinyiMeng FanliangLi YanNing Yunshan