Recombinant Human Tryptophan 2,3-Dioxygenase TDO2
- Known as:
- Recombinant Human Tryptophan 2,3-Dioxygenase TDO2
- Catalog number:
- enz-081
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Tryptophan 2 3-Dioxygenase TDO2
Related genes to: Recombinant Human Tryptophan 2,3-Dioxygenase TDO2
- 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: Recombinant Human Tryptophan 2,3-Dioxygenase TDO2
Related articles to: Recombinant Human Tryptophan 2,3-Dioxygenase TDO2
- Inflammation is a central mediator linking metabolic dysfunction to severe human disease. Imbalance or loss of ovarian hormone (such as in post-menopausal women) contributes to increased risk of cardiovascular diseases, obesity and others. Here, using ovariectomized (OVX) Long-Evans rats as model for estrogen deprivation, we demonstrate that estrogen deprivation induces hepatic inflammation, activates tryptophan catabolism, systemic inflammation and disrupted cholesterol homeostasis. OVX animals gained more weight and developed an atherogenic plasma profile with increased LDL and total cholesterol and reduced HDL levels compared to intact female animals, which was reversed by estradiol (E2) administration. Ovariectomy results in elevation of hepatic pro-inflammation cytokine (e.g. TNFα, IL6), tryptophan catabolic enzymes (e.g. IDO1, and TDO2) and reduced reverse cholesterol associated gene SR-BI expression and E2- administration also suppressed the ovariectomy-induced hepatic inflammation resulting in reduction of TNFα, IL6, IDO1 and TDO2 while elevation of SR-BI expression. Plasma kynurenine, nitric oxide and lactate were elevated upon ovariectomy suggesting increased system Trp-catabolism, inflammation, each was reversed by estrogen. Targeted LC-MS metabolomics analysis revealed enhanced Trp-to-kynurenine flux, elevated lactate, accumulation of citrate/isocitrate/aconitate, and a reduced α-ketoglutarate/aconitate ratio (~ 0.6) restored by estradiol (~ 3.6). Together, our studies suggest a a link between estrogen signaling and hepatic immune-metabolism via regulation of Trp-catabolism, this open up potential novel signaling pathways for treating cardiometabolic disease and hormonal disorders. - Source: PubMed
Publication date: 2026/04/24
Guha PrarthanaRishi AshcharyaChini AvisankarBhat NagashreeGondrala Pavan KBrady BlakeBaniasadi Hamid RPerrotti Linda IMandal Subhrangsu S - Cholangiocarcinoma (CCA) is a prevalent hepatobiliary disease in northeast Thailand, where late diagnosis and limited treatment options contribute to poor prognosis. The kynurenine pathway (KP) of tryptophan metabolism, is controlled by two key enzymes indoleamine-2,3-dioxygenase (IDO1) and tryptophan-2,3-dioxygenase (TDO2) linking with downstream effector aryl-hydrocarbon receptor (AhR) signaling, which has been tied to immune escape and tumor growth but its clinical relevance in CCA remains unclear. - Source: PubMed
Publication date: 2026/04/10
Naeklang MallikaDokduang HasayaPrajumwongs PiyaKlanrit PoramateWangwiwatsin ArpornNamwat NisanaTitapun AttapolSa-Ngiamwibool PrakasitLoilome Watcharin - Glioblastoma (GBM) is a universally fatal cancer for which the standard of care has remained largely unchanged for the last 20 years. Recent work has demonstrated that most therapeutic trials for GBM fail due to complex mechanisms of immunosuppression mediated by both the innate and adaptive immune systems. Various metabolic alterations in the tumor microenvironment help maintain this local and systemic immunosuppression, of which the axis of hypoxia-driven tryptophan degradation has garnered substantial attention over the last decade. This paper synthesizes a much-needed elucidation of the immunometabolic reshaping of glioma, myeloid, endothelial, and lymphoid cell lineages induced by hypoxia. The current paper critically evaluates the role of IDO1/TDO2-mediated breakdown of tryptophan and the consequent accumulation of kynurenine, a metabolite that triggers GCN2- and AHR-mediated CD8+ T-cell exhaustion and supports regulatory T-cell differentiation and expansion. Furthermore, we propose a synthesis of mechanistic evidence that establishes a role for the Trp-GCN2-ATF4-VEGFA axis in hypoxia-induced immunosuppression, supporting that pro-tumoral metabolic dysregulation is directly linked to angiogenesis. In GBM, hypoxia and tryptophan-kynurenine pathway dysregulation operate as an integrated metabolic circuit that drives widespread immunosuppression. These mechanisms can be captured by a metabolic signature shared across nearly every cell type in the GBM microenvironment. Drawing on recent spatial transcriptomic, metabolomic, and pharmacologic studies, we outline how this metabolic axis shapes disease biology and how it can be targeted to restore effective antitumor immunity. - Source: PubMed
Publication date: 2026/03/10
Abikenari MatthewNageeb GeorgeHa Joseph HSjoholm Matthew AdamLiu JustinBergsneider BrandonValenzuela JocelynPoe JamesBog Cho KwangVerma RohitWu CarenSanker VivekMedikonda RaviKim Lily HChoi JohnBanu Matei ALim Michael - Chronic fatigue is a prolonged and persistent state of mental and physical exhaustion that is not readily relieved by rest. Dendrobium officinale Kimura & Migo (D. officinale), a traditional tonic medicinal and edible herb, which have been reported to possess diverse pharmacological activities, including anti-fatigue, immunomodulatory, and gut microbiota-modulating effects. Nevertheless, the effects and underlying mechanisms on chronic fatigue remain largely unexplored. - Source: PubMed
Publication date: 2026/03/18
Yan MeiqiuShi MenglinLi ChunwanYu BingqingZhou HengpuSu JieYu JingjingLv GuiyuanChen Suhong - Tertiary lymphoid structures (TLSs) promote antitumor immunity and predict favorable immunotherapy outcomes in breast cancer. The study aimed to investigate how Tryptophan 2,3-dioxygenase (TDO2)-associated tryptophan metabolism influences TLS maturation and B cell class switching in breast cancer. - Source: PubMed
Publication date: 2026/02/24
Yang WeipingXiao WeiXu WenhaoRen LijunLi XianYu JunhuaWang Ronghua