INDO_1, AM ESTER
- Known as:
- INDO_1, ESTER
- Catalog number:
- 50044
- Product Quantity:
- 1 MG
- Category:
- -
- Supplier:
- Biotium
- Gene target:
- INDO_1 ESTER
Related products to: INDO_1, AM ESTER
Related articles to: INDO_1, AM ESTER
- Major depressive disorder (MDD) is a complex disorder caused by genetic and environmental factors. Previous evidence implicates a potential depression subtype from interaction between childhood maltreatment (CM) and kynurenine pathway (KP) gene. Here, we investigated the top-down multi-omics KP alterations for this subtype. - Source: PubMed
Publication date: 2026/09/28
Sun YaoyaoSu MenghanKang ZheweiZhao GuoruiBai XueyingGuo JingWang YueqiLu ZheZhang YuyananFeng XiaoyangSun JunyuanYue Weihua - The tryptophan (TRP)-serotonin pathway is disrupted and redirected towards kynurenine by the action of indoleamine 2,3-dioxygenase 2 (IDO2) and kynureninase (KYNU). In ovarian cancer, concurrent kynurenine activation encourages tumor growth and immune evasion. The investigation of phytochemicals has focused on identifying therapeutic targets in ovarian cancer. - Source: PubMed
Publication date: 2026/07/20
Velmurugan PavithraParsanathan RajeshShankari GopalakrishnanGanapathi HaemaMoovarkumudalvan BalasubramanianSingh Abhimanyu KSaravanan Suresh KumarRajamanikandan SundararajSubramanyam Veni - Indoleamine 2,3-dioxygenase 2 (IDO2) and tryptophan 2,3-dioxygenase (TDO2) are rate-limiting enzymes of the kynurenine pathway, well-characterized in mammals. Unlike all other vertebrates, chickens lack the IDO1 gene and exclusively rely on IDO2/TDO2 for tryptophan (Trp) catabolism; however, their biochemical features and physiological regulatory functions remain poorly defined. Here, we integrated dietary Trp intervention, multi-omics profiling, recombinant enzyme kinetics, and in vitro/inflammatory animal models to characterize chicken IDO2 and TDO2. Supplementary dietary Trp maintained circulating Trp homeostasis while activating hepatic kynurenine metabolism being associated with reduced PPAR signaling and altered lipid and energy balance. Hepatic combined IDO2/TDO2 catalytic activity increased markedly with Trp supplementation; this increase was accompanied by only modest transcriptional upregulation of kynurenine pathway genes (including IDO2, TDO2, and KYNU) and no major changes in their protein abundance, indicating post-translational functional modulation. Recombinant enzyme assays demonstrated optimal activity at chicken physiological pH of 7.2 and temperature of 42 °C; chicken IDO2 displayed measurable catalytic efficiency, which was lower than that of chicken TDO2, whereas its human ortholog showed no detectable activity under the same conditions. Furthermore, LPS and APEC infection significantly suppressed the combined total IDO2/TDO2 activity during inflammatory stress, revealing an avian-specific metabolic-immune regulatory pattern. This work defines the unique biochemical and physiological functions of avian IDO2 and TDO2, offering mechanistic references for poultry nutritional regulation and disease control. - Source: PubMed
Publication date: 2026/09/12
Li WanliZhang ChenWu PinhuiFeng KangfeiZhang GuozhiYuan LinJin WeiWang BingxunLi ShengliLiu WeiLi Wenqing - RNA virus infections are shaped by the interplay among viral replication, innate immune sensing, and host metabolism, which together determine the magnitude, duration, and quality of antiviral responses. The tryptophan-kynurenine (Trp-Kyn) pathway has emerged as an important immunometabolic axis linking interferon-driven inflammation, amino acid availability, immune-cell function, tissue homeostasis, and viral persistence. This review examines the roles of indoleamine 2,3-dioxygenase 1 (IDO1), IDO2, tryptophan 2,3-dioxygenase (TDO), Trp depletion, general control nonderepressible 2 (GCN2) signaling, mechanistic target of rapamycin complex 1 (mTORC1), Kyn-derived metabolites, and aryl hydrocarbon receptor (AhR) activation in host responses to RNA virus infection. We integrate genetic, pharmacological, cellular, animal, and clinical evidence across positive-sense and negative-sense single-stranded RNA viruses, double-stranded RNA viruses, and reverse-transcribing RNA viruses, including SARS-CoV-2, dengue virus, Zika virus, hepatitis C virus, influenza A virus, respiratory syncytial virus, rotavirus, reovirus, HIV-1, and SIV. Across these systems, the Trp-Kyn-AhR axis can influence interferon responses, viral replication, immune-cell function, tissue injury, and disease outcome. EMCV myocarditis provides causal proof of principle, whereas other RNA-virus models provide complementary functional and clinical evidence. Importantly, pathway activation does not confer a uniform antiviral or pathogenic phenotype; its biological consequences depend on viral class, tissue tropism, viral burden, inflammatory intensity, cell type, and disease stage. On this basis, we propose a time-phase model in which early or excessive IDO1-Kyn-AhR signaling may impair type I interferon responses, NK-cell function, CD8+ T-cell expansion, and viral clearance, whereas appropriately regulated activation during later inflammatory or resolution phases may limit immunopathology, support epithelial repair, and preserve tissue homeostasis. Persistent or dysregulated activation may instead contribute to exhaustion-like immune states, chronic inflammation, neuroimmune dysfunction, and post-acute viral sequelae. Finally, we discuss phase-adapted therapeutic strategies, including IDO1 inhibition, AhR agonism or antagonism, KMO-directed modulation, Trp-based entry inhibitors, and biomarker-guided combination approaches. Together, these findings position the Trp-Kyn-AhR axis as a dynamic, context-dependent target for precision host-directed antiviral immunometabolism. - Source: PubMed
Publication date: 2026/09/07
Calderón-Sandate Daniela NahomiHuerta-Garza Manuel JosafatMárquez-Reyna Blanca AzucenaCañedo-Figueroa David MauricioHernández-Rodríguez XimenaLira-Hernández Flor ItzelOsuna-Ramos Juan FidelCardoso-Ortiz JaimeDel Ángel Rosa MaríaSantos-Mena Alan OrlandoDe Jesús-González Luis Adrián - Dysregulation of the kynurenine pathway (KYNP) is increasingly recognized as a hallmark of cancer-associated metabolic reprogramming, contributing to immune evasion, oxidative stress, and tumor progression through the activity of enzymes such as indoleamine 2,3-dioxygenase 1 (IDO1), indoleamine 2,3-dioxygenase 2 (IDO2), and tryptophan 2,3-dioxygenase (TDO2). This systematic review aimed to evaluate the current evidence on the ability of phytochemicals to modulate the KYNP and their potential implications for cancer prevention and therapy. The review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and included English-language articles and book chapters published between 2016 and 2026 that were retrieved from the Scopus and PubMed databases. A keyword co-occurrence network was generated using VOSviewer (v1.6.20) based on the complete Scopus and PubMed exports of the included studies to identify major research themes. The available evidence indicates that phytochemicals restore anticancer immunity by targeting multiple components of the KYNP, including inhibition of IDO1-mediated kynurenine production and suppression of downstream aryl hydrocarbon receptor signalling, thereby enhancing cytotoxic T-cell responses, reducing immunosuppressive cell populations, and improving antitumor immune activity. Collectively, these findings support the KYNP as a promising immunometabolic target and highlight phytochemicals as potential complementary agents for cancer immunotherapy while emphasizing the need for further investigation of the biological and immunological roles of IDO2. - Source: PubMed
Publication date: 2026/08/22
Tsantila Evgenia MariaChristodoulou Marios CEsslinger NilsNeophytou Christiana M