Ask about this productRelated genes to: IDO1 antibody
- Gene:
- IDO1 NIH gene
- Name:
- indoleamine 2,3-dioxygenase 1
- Previous symbol:
- IDO, INDO
- Synonyms:
- -
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2016-01-15
Related products to: IDO1 antibody
Related articles to: IDO1 antibody
- The dense extracellular matrix (ECM) and stromal cells in breast cancer constitute a formidable physical and immunosuppressive barrier that facilitates immune evasion and tumor progression. Within this desmoplastic microenvironment, cancer-associated fibroblasts (CAFs) overexpress indoleamine 2,3-dioxygenase-1 (IDO-1), an enzyme that activates the tryptophan-kynurenine metabolic pathway to induce T cell exhaustion and immune tolerance. Consequently, modulating tryptophan metabolism in CAFs represents a promising strategy to potentiate antitumor immunotherapy. Herein, we develop a CAF-targeted nanomedicine system based on dasatinib-loaded NbGeTe (NGT) nanosheets for ultrasound-mediated immunometabolic modulation. Under low-intensity ultrasound, NGT exhibits efficient piezocatalytic charge separation, efficiently separating electron-hole pairs to trigger the generation of superoxide anions (·O). These reactive species rapidly react with intracellular nitric oxide to form peroxynitrite (ONOO), which induces site-specific tyrosine nitration of IDO-1. This process irreversibly inactivates IDO-1, thereby disrupting the tryptophan-kynurenine immunosuppressive axis. Simultaneously, the controlled release of dasatinib inhibits CAF-mediated fibrosis, dismantling the stromal barrier, reducing tumor stiffness and facilitating the infiltration of cytotoxic T lymphocytes. This study establishes a precise piezocatalysis-driven strategy for reprogramming the tumor microenvironment in desmoplastic malignancies, providing a promising avenue for the development of two-dimensional nanomaterials in cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/01
Zhang JinhuiYan JunxinYe KunFu YangDong ZhechenZhang XuwuHe YuchuLiu YingdanYan XiyunXue WeiliTu WenkangGao Dawei - Noncoding RNAs are emerging players in cell signaling and diseases. Recently, we discovered a series of novel lncRNAs that are critical players in inflammation. Here, we demonstrate that hLinfRNA7, a long human noncoding inflammation-associated RNA 7 (also termed as IDO1-AS6.4) located on the antisense-strand of IDO1 (Indoleamine-2,3 -dioxygenase 1, a tryptophan catabolizing enzyme), plays critical roles in the regulation of inflammation and tryptophan (Trp) catabolism. Our studies demonstrated that hLinfRNA7 expression is induced in human THP1-derived macrophages under inflammation (LPS or IFNγ- stimulation) and is localized in the nucleus. hLinfRNA7 knockdown suppressed LPS-induced IL-6, IL-1β, and iNOS expression and reduced nitric oxide production. Interestingly, hLinfRNA7 knockdown also downregulated the inflammation-induced expression of IDO1 as well as the tryptophan catabolite kynurenine level in macrophages, suggesting critical roles of hLinfRNA7 in inflammation, cytokine regulation, and Trp-catabolism. Furthermore, IDO1 also regulate hLinfRNA7 expression, suggesting their interplay in inflammation and Trp-catabolism. hLinfRNA7 also modulates NF-κB signaling and interacts with an RNA-binding protein, YBX1, which also regulates cytokines, IDO1, hLinfRNA7, and Trp-catabolism under inflammation. Our study demonstrates lncRNA hLinfRNA7 is a novel regulator of inflammation and tryptophan catabolism. By delineating an hLinfRNA7-YBX1-IDO1 axis, our study expands lncRNA roles in immune-metabolic control and inflammatory disease. - Source: PubMed
Publication date: 2026/06/05
Rishi AshcharyaGuha PrarthanaBhat NagashreeChini AvisankarGondrala Pavan KMandal Subhrangsu S - Bovine viral diarrhea virus (BVDV) causes persistent infection and immunosuppression, yet whether it hijacks host immunometabolism to facilitate replication remains unclear. Using untargeted metabolomics in bovine turbinate (BT) cells, we found that BVDV infection significantly elevated xanthurenic acid within the tryptophan-kynurenine (Trp-Kyn) pathway. BVDV persistently upregulated indoleamine 2,3-dioxygenase 1 (IDO1), resulting in decreased extracellular tryptophan and increased kynurenine levels. Supplementation with L-tryptophan or IDO1 inhibition suppressed viral replication, whereas L-kynurenine promoted it. Rescue of viral replication by L-kynurenine in IDO1-silenced cells confirmed that IDO1 promotes BVDV proliferation through downstream kynurenine generation. Mechanistically, IDO1 inhibition enhanced STAT1 phosphorylation and upregulated ISG15, MX1, and OAS1 expression. A negative feedback loop was identified between IFN-γ/STAT1 signaling and the IDO1-kynurenine axis. Furthermore, L-kynurenine activated the aryl hydrocarbon receptor (AhR) target gene CYP1A1, and the AhR antagonist CH-223191 partially reversed its pro-viral effects. In conclusion, BVDV hijacks the IDO1-dependent Trp-Kyn metabolic axis to limit interferon-STAT1 antiviral signaling, while AhR-related signaling may act as a possible partial downstream branch contributing to a pro-viral intracellular environment. - Source: PubMed
Publication date: 2026/05/30
Liu Tian-YiLiu Shan-ShanLi Pei-LongZhou YongSong Yu-XinYao Wei-JiaZhang Ze-ChenZhao ChongLi JiaoTian Lan-BoLi NanLiu YuZhang Ze-CaiZhou Yu-LongWang XueZhu Zhan-Bo - Tryptophan metabolism is known to affect tumor immunity. However, the value of tryptophan metabolism-related genes (TMRGs) in predicting prognosis and reflecting immune status in skin cutaneous melanoma (SKCM) is not yet clear. - Source: PubMed
Publication date: 2026/05/19
Zhao LeiLi Zhi-CaiTang Zhou-YouYuan Yu-TongZhu Shan - High-fat diet (HFD)-induced gut dysbiosis precipitates hippocampal mitochondrial oxidative stress, a pivotal driver of synaptic failure and cognitive decline. However, the molecular conduits linking intestinal microbial shifts to cerebral redox imbalance remain poorly defined, limiting therapeutic strategies. Here, we show that luteolin attenuates HFD-induced cognitive impairment in association with modulation of the gut microbiota-kynurenine (Kyn)-aryl hydrocarbon receptor (AhR) axis and improved mitochondrial redox homeostasis. Luteolin treatment ameliorated HFD-induced memory deficits and metabolic abnormalities in mice, effects that were markedly reduced after gut microbiota depletion and were transmissible via fecal microbiota transplantation. Consistent with this pathway, luteolin suppressed HFD-induced expansion of Proteobacteria (e.g., Escherichia coli), diminished intestinal lipopolysaccharide (LPS) leakage, and normalized colonic indoleamine 2,3-dioxygenase 1 (IDO1) expression. Consequently, luteolin reduced peripheral and hippocampal Kyn accumulation, thereby restricting AhR nuclear translocation and preventing the aberrant transcription of AhR-target genes implicated in mitochondrial respiratory chain disruption. Functionally, luteolin restored hippocampal mitochondrial bioenergetics, attenuated pathological reactive oxygen species (ROS) overload, and preserved synaptic long-term potentiation (LTP). The protective efficacy of luteolin against mitochondrial oxidative insult and cognitive decline was phenocopied by AhR inhibition and abrogated by exogenous Kyn supplementation. Collectively, our findings identify the gut Proteobacteria-Kyn-AhR signaling axis as an important contributor to hippocampal mitochondrial oxidative stress in HFD-challenged brains. Luteolin emerges as a promising microbiota-targeted antioxidant intervention that safeguards cognitive function by rectifying this gut-brain redox relay. - Source: PubMed
Publication date: 2026/06/01
An XiaobinLi ChenhongChai YaniWang HanxiangYang LongkaiQin LongSoprun Lidiya AGavrilova Natalia YuWen ZhengchaoXu JinchengLi QingsuiYang DanLi WeiGuo JunnanLi YuexinWang NingYu Hang