Ask about this productRelated genes to: KYNU Blocking Peptide
- Gene:
- KYNU NIH gene
- Name:
- kynureninase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-20
- Date modifiied:
- 2018-03-26
Related products to: KYNU Blocking Peptide
Related articles to: KYNU Blocking Peptide
- L-tryptophan (Trp) metabolism through the L-kynurenine (Kyn) pathway contributes to immune escape in neoplasms, including bladder cancer (BC). Indoleamine 2,3-dioxygenase-1 (IDO1) is a key enzyme, and its catabolites-Kyn, 3-hydroxykynurenine (3HK), and 3-hydroxyanthranilate (3HAA)-depend on other enzymes and play a crucial role in immunomodulation. - Source: PubMed
Lemes Douglas EdgardSantos Aline Áurea de Souzade Oliveira Jéssica LopesRoman-Ramos HenriqueMoreno Ana Carolina RamosCamacho Cleber PintoPontes-Junior JoséDellê Humberto - Eleutherococcus senticosus fruit (ESF) originates from the mature fruit of Eleutherococcus senticosus (Rupr. & Maxim.) Maxim, which is effective in treating essential hypertension (EH). However, the incomplete comprehension of how ESF antihypertensives impedes its further development. - Source: PubMed
Publication date: 2026/04/13
Li ZhinengYang LeKong LingSun HuiSun YeYin FengtingYan GuangliWang Xijun - The poor prognosis of lung adenocarcinoma (LUAD) remains unimproved. This study aimed to identify lymph node metastasis (LNM)-related and cellular immunity-related prognostic genes in LUAD and propose novel strategies to improve its prognosis. LUAD-related datasets were obtained from public databases. Prognostic genes and a prognostic model were obtained through various bioinformatics analyzes, and the immunotherapy response in risk groups was assessed. Subsequently, the expression levels of prognostic genes and the intercellular communication relationships were explored at the single-cell level. Moreover, malignant cells were identified, and their differentiation mechanisms were explored via inferCNV analysis. Additionally, FURIN was silenced and overexpressed to investigate its effects on the invasion, metastasis, and lymphangiogenesis of LUAD cells in vitro. RGS20, KYNU, RAET1E, FGF12, GJB2, CACNA2D2, FURIN, and GDF10 were identified as prognostic genes with LNM. In 4 datasets, LUAD patients with the high LNM and immune cell-related risk scores exhibited higher mortality rates compared to those in the low-risk group. Furthermore, individuals in the low-risk group demonstrated a greater propensity to derive advantages from immunotherapeutic interventions. Epithelial cells were identified as key cells, with CACNA2D2 being significantly up-regulated during their late-stage differentiation. Basal cells, the malignant subset within epithelial cells, showed elevated FURIN expression in the pre-differentiation phase, which declined in the middle and late phases. Functionally, FURIN was found to enhance the migratory and proliferative capacities of LUAD cells. Moreover, we demonstrated that FURIN accelerated lymphatic metastasis and lymphangiogenesis in vitro. In this paper, we identified LUAD prognostic genes with LNM and immune cell signatures, emphasized treating LUAD patients according to LNM- and immune cell-related risk scores, and provided novel ideas on how to improve poor prognosis and develop targeted therapy for LUAD. - Source: PubMed
Lin ChuanChen XuanSun YongTang XiaomeiJiang Yi - Neurofibromatosis type 1 (NF1) is characterized by the development of benign plexiform neurofibromas (PNFs). In 10%-15% of patients, these tumors undergo malignant transformation into aggressive malignant peripheral nerve sheath tumors (MPNSTs). The underlying mechanisms driving this malignant progression remain poorly understood, hindering the development of effective therapies. To address this gap, we performed single-cell RNA sequencing on nine PNF and five MPNST samples. Our analysis revealed tumor microenvironment remodeling during malignant progression, marked by a significant increase in immune cells. Within the macrophage compartment, we identified three distinct SPP1 subpopulations. Among these, the SPP1KYNU subset exhibited pronounced upregulation of genes related to tryptophan metabolism. This metabolically active macrophage population exhibited strong interaction with POSTN fibroblasts enriched in MPNSTs. Functional experiments found that this crosstalk promotes fibroblast activation and enhances migratory capacity. Furthermore, the metabolic reprogramming of SPP1KYNU macrophages was associated with the establishment of an immunosuppressive microenvironment characterized by T cell dysfunction. Collectively, our findings define a central role for SPP1KYNU macrophages in coordinating both stromal remodeling and immune suppression during MPNST progression. These results not only advance our understanding of NF1-associated tumorigenesis but also identify tryptophan metabolism as a promising therapeutic target and potential diagnostic biomarker for MPNSTs. - Source: PubMed
Publication date: 2026/03/30
Ge Ling-LingLi Yue-HuaYu XuanXing Ming-YanGu Yi-HuiWang WeiHuang Jing-XuanLiu JunZhang Hai-BingWei Cheng-JiangWang Zhi-ChaoLi Qing-Feng - The persistent HIV reservoir constitutes the main obstacle to curing HIV/AIDS disease. Our understanding of how non-productive HIV infections are established in primary human CD4 T cells during the first round of infection remains, however, incomplete. In this study, we leveraged the HIV reporter virus pMorpheus-V5 to delineate cellular expression patterns that are upregulated in non-productively infected primary CD4 T memory stem cells (T). We found that CD4 T harboring non-productive proviruses displayed a distinct transcriptomic signature comprising 118 upregulated genes. This non-productive expression profile was distinct from that of productively infected cells as well as from negative-exposed and mock-infected cells. Among the cellular genes most upregulated in CD4 T cells harboring non-productive proviruses were CCR4-binding migratory chemokines (), tryptophan catabolic enzymes (), and genes encoding cytoskeletal rearrangement proteins (). Intracellular flow cytometry-based analyses confirmed that non-productively infected CD4 T cells were enriched for CCL22 and IDO1 co-expression compared to the other CD4 memory subsets, underscoring a clear CD4 T cell subset specificity for the upregulation of these two immune gene sets associated with non-productive infections. These findings suggest that primary human CD4 T harboring non-productive proviruses display a distinct immunoregulatory phenotype which may facilitate immune evasion and contribute to the persistence of the HIV reservoir. - Source: PubMed
Publication date: 2026/03/21
Butta Giacomo MAlburquerque BremyKearns CharlotteHadas YoavVanDyck Max WScaglioni SusannaPeña NoahWong Hoi TongLevendosky ElizabethGleason CharlesLin XiaoManganaro LaraPinto DalilaMulder Lubbertus C FSimon Viviana