Ask about this productRelated genes to: NR4A1 Blocking Peptide
- Gene:
- NR4A1 NIH gene
- Name:
- nuclear receptor subfamily 4 group A member 1
- Previous symbol:
- HMR, GFRP1
- Synonyms:
- TR3, N10, NAK-1, NGFIB, NUR77
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2017-03-28
Related products to: NR4A1 Blocking Peptide
Related articles to: NR4A1 Blocking Peptide
- The formation of foam cells (FCs) is the major contributor to the development of atherosclerosis (AS). Gynostemma pentaphyllum is widely used to treat AS and exhibits biological activity against FCs formation. Narcissoside (Nar) is an important component from G. pentaphyllum flavonoids. This study aimed to reveal the beneficial effect and underlying mechanism of Nar on inhibiting the formation of FCs in AS. - Source: PubMed
Publication date: 2026/05/20
Wang ZiyuanZhou LameiZhang XiaorongYao ZhirenHuang YapingWang LeiPan KeZhang JianZhi HaoYin Zhiqi - Y-box binding protein 1 (YB-1) is a multifunctional RNA- and DNA-binding protein with broad regulatory functions in gene expression, particularly at the posttranscriptional level. Here, we demonstrate that conditional deletion of YB-1 at the double-positive (DP) thymocyte stage causes an ∼80% reduction of invariant natural killer T (iNKT) cells in thymus, spleen, and liver, evident already in day-14 neonates and persisting into adulthood. Our data reveal CD44NK1.1 stage 1 accumulation and a selective loss of CD44NK1.1 stage 3 iNKT cells, indicating a postselection maturation defect. All iNKT cell subsets (iNKT1, iNKT2, iNKT17) were reduced, with thymic iNKT1 and splenic iNKT17 cells most severely affected. PMA/ionomycin-stimulated YB-1-deficient iNKT cells showed preserved IFN-γ/IL-4 frequencies but reduced per-cell cytokine production and a loss of IL-17 production. Interestingly, YB-1 DP thymocytes showed increased CD1d levels, suggesting increased TCR signal strength in the thymus of YB-1-deficient mice. Whereas CD5 levels were elevated, basal Nur77, ICOS, and CD122 (IL-15Rβ) expression were reduced in iNKT cells. Furthermore, apoptosis was increased, particularly at iNKT stages 2-3. Together, these findings identify YB-1 as a central regulator of iNKT cell development that integrates TCR, co-stimulatory, and IL-15 signaling to ensure postselection iNKT cell maturation, effector subset specification, and survival. - Source: PubMed
Schulze SilviaKnop LauraJantz-Naeem NouriaDovhan VladyslavaFricke StephanKahlfuß SaschaSchüler ThomasBommhardt Ursula - Hydrogen sulfide (HS) has been reported to exert both protumor and antitumor functions. It is worthy to clarify the condition under which HS exerts antitumor effects and its underlying mechanism. Our previous study connected the immune checkpoint indoleamine 2,3-dioxygenase 1 (IDO1) and HS by revealing that HS downregulates IDO1 expression, leading to our hypothesis that antitumor effect of HS is associated with IDO1 expression in tumor cells. - Source: PubMed
Publication date: 2026/05/13
He Zhen Ning TonyMeng FangzhouQian XiaoyangLiu YuyingFang XinYang DanYang Qing - Human CD8 T cells undergo significant metabolic and transcriptional shifts during activation and differentiation. The orphan nuclear receptor Nur77 plays a role in modulating these processes and has been linked to T cell dysfunction. However, few studies have addressed its role in the memory potential and functionality of human CD8 T cells. Here, we evaluated the expression of Nur77 in human CD8 T cells, focusing on its relationship with their differentiation profile and functionality. Our findings indicate that Nur77 is associated with an early-differentiated, T cell factor 1 (TCF-1) memory-like phenotype in both total and virus-specific human CD8 T cells across contexts of acute resolved or chronic viral infection and vaccination. Nur77 expression was associated with cytokine polyfunctionality and increased proliferative capacity in long-lived antigen-responsive cells. Moreover, the modulation of Nur77 activity in vitro enhanced the functionality of chronic human immunodeficiency virus (HIV) and hepatitis B virus (HBV)-specific CD8 T cells. These results suggest that Nur77 is associated with polyfunctional properties in virus-specific CD8 T cell responses in humans. In addition, this study provides insights into novel strategies for enhancing CD8 T cell functionality in settings of chronic antigen stimulation. - Source: PubMed
Martel FabiolaRincón DanielPassaes CarolineArévalo LeonardoTorres MarcelaRamirez NataliaNarváez Carlos FToro Jessica FSussmann OttoFranco Manuel AMateus JoséSidney JohnSette AlessandroSáez-Cirión AsierPerdomo-Celis Federico - Nur77, an orphan nuclear receptor, is involved in the development and progression of multiple tumors. In our previous study, we have shown that the protein level of Nur77 is elevated in colon tumors compared to adjacent normal tissues, highlighting its potential as a promising target for colorectal cancer therapy. Significantly, we have identified BI1071 as a Nur77-targeting compound that induces apoptosis in colorectal cancer cells. Based on the scaffold of BI1071, by substituting the indole group of BI1071 with a pyrrolyl group on one side, we rationally designed and synthesized a series of novel BI1071 analogues named SIM-C-PhCFCl targeting Nur77, and the structure-activity relationship of these BI1071 derivatives was summarized. From this series of compounds, A6 exhibited the strongest binding affinity to Nur77 (K = 0.40 ± 0.05 μM) and the most potent anti-proliferative activity against HCT116 and MC38 colorectal tumor cell lines, with IC values of 0.53 ± 0.06 μM and 0.16 ± 0.007 μM, respectively. Interestingly, unlike BI1071, which triggers Nur77-dependent apoptosis, compound A6 suppressed colon cancer cell proliferation predominantly by inducing Nur77-dependent mitotic arrest. Collectively, our findings provide a foundation for further investigation and development of Nur77-targeting antimitotic molecules toward colorectal cancer therapy. - Source: PubMed
Publication date: 2026/05/05
Zhao QiLiang JingmeiZhou JinZeng MeifengZhang WenbiaoCao YuanZhang XiaokunChen XiaohuiXie GuobinSu YingZeng Zhiping