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identification of NR4A transcription factors as having an important role in the cell-intrinsic program of T cell hyporesponsiveness and point to NR4A inhibition as a promising strategy for cancer immunotherapy
Results from this study revealed a novel anticancer mechanism of RARbeta via miR-22 induction to epigenetically regulate itself and NUR77, providing a promising cancer treatment modality using miR-22 and its inducers
our data show a yet unexplored role for Nur77 in modifying the activation status of murine and human DCs.
Mechanistically, NR4A1 and NR4A2 synergistically activate the CTNNB1 gene promoter . Knocking down CTNNB1 or NR4A1 in AML-MSC-co-cultured-CD34(+) cells increased leukaemia-reactive T-effector cells production and rescued anti-leukaemia immunity.
TR3/Nur77 regulated the expression of DLL4 and Jagged1 in culture endothelial cells. DLL4 and Jagged1 play important roles in the angiogenic responses induced by TR3/Nur77.
TR3/Nur77 differentially regulated the expression of integrins in endothelial cells that played various roles in the angiogenic responses induced by TR3/Nur77.
Inhibition of Nur77 improved nerve cell injury by regulation of Bcl-2 and downstream pathways in vitro and in vivo.
Study demonstrates a novel regulatory function of Nur77 with linkage of the FAO-NADPH-ROS pathway during metabolic stress, suggesting Nur77 as a potential therapeutic target in melanoma.
This study reveals a unique mechanism to suppress hepatocellular carcinoma by switching from glycolysis to gluconeogenesis through Nur77 antagonism of PEPCK1 degradation.
we show here that the BCR/BTK target gene NR4A1 is a potential oncogene in mantle cell lymphoma
this study confirmed that NR4A1 sensitizes gastric cancer cells to TNFalpha-induced apoptosis through the inhibition of JNK/Parkin-dependent mitophagy.
Inhibition of NR4A1 in stromal cells increased the TGF-beta1-dependent elevated expression of fibrotic markers, and loss of NR4A1 stimulated fibrogenesis in mice with endometriosis.
NR4A1 knockdown partly decreased surface NR2B by promoting NR2B internalization.
Data show that SUMOylation is critical in controlling NR4A1 function in inflammatory cytokine signaling and controlling macrophage cell death.
our findings suggest that hypoxia-induced down-regulation of TR3 might play an important role for hypoxia-induced apoptosis resistance in NSCLC.
Nur77 suppresses CD4(+) T cell proliferation and uncover a suppressive role for Irf4 in TH2 polarization; halving Irf4 gene-dosage leads to increases in GATA3(+) and IL-4(+) cells.
our data demonstrated that NR4A1 protein physically associates with the WT1 promoter, and enhanced WT1 promoter transactivation and knockdown of WT1 in MIN6 cells induced apoptosis. These findings suggest that NR4A1 protects pancreatic beta-cells against H2O2 mediated apoptosis by up-regulating WT1 expression.
NR4A modulates the decidualization of hESCs by upregulating prolactin (PRL) and insulin-like growth factor binding protein-1 (IGFBP-1) expression and transformation in vitro.
DNMT1 causes NR4A1 DNA hypermethylation and blocks insulin signaling in an Chinese patients with type 2 diabetes
Data show that nuclear receptor 4A1 (NR4A1) knockdown and the C-DIM/NR4A1 antagonists were comparable as inhibitors of NR4A1-dependent genes/pathways.
Identify the orphan nuclear receptor NR4A1 as a potential early response gene in FGF2 signaling and regulation of sprouty in bovine ovarian granulosa cells.
study thus identifies NR4A1 as a key general regulator in the induction of T cell dysfunction, and a potential target for tumour immunotherapy
This study identifies NR4A1 as a crucial player in the regulation of osteoclast biology and bone remodeling.
these data identify NR4A1 as a previously unrecognized constitutive regulator of AP quiescence and suggest that augmentation of adipose tissue plasticity may attenuate negative metabolic sequelae of obesity.
These results support a model wherein high fat diet increases retinal protein O-GlcNAcylation by promoting NR4A1-dependent GFAT2 expression.
antagonism of NR4A1 is a promising avenue for preventing the regressive synaptic reorganization in cortical systems in the context of chronic stress
NR4A1/Nur77 and NR4A2/Nurr1 dynamically regulated inflammatory gene expression in glia by modulating the transcriptional activity of NF-kappaB.
These results establish crucial residues in Bcl-2 required for Nur77/Nor-1-mediated apoptosis and point to potential new strategies for manipulating Bcl-2 function.
results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPalpha and suppression of activation of NF-kappaB-driven proliferative inflammatory responses.
Results demonstrate that Nr4a1 not only induces Type 2 macrophages/microglia phenotype, but is also a critical inhibitory molecule for Th1/Th17 cell differentiation.
our study provides evidence that a transgenic mouse model commonly used to study the biological function of Nur77 has several major drawbacks, while simultaneously identifying the importance of nongenomic Nur77 activity in the regulation of bone marrow homeostasis.
These results demonstrate that thyroid hormone down-regulated basal NR4A1 mRNA levels in the pituitary, and the direct binding of thyroid hormone receptor was not required.
NR4A1 regulated Parkin activation via post-transcriptional modification by Ca2(+)/calmodulin-dependent protein kinase II (CaMKII).
that Nuclear receptor subfamily 4 group A member 1 modulated Mfn2 expression via the MAPK-ERK-CREB signaling pathway
By facilitating Mff-mediated mitochondrial fission and FUNDC1-required mitophagy, NR4A1 disturbed mitochondrial homeostasis, enhanced endothelial apoptosis and provoked microvascular dysfunction in myocardial ischemia reperfusion injury.
Cd36 deficiency led to reduced expression of phagocytosis receptor Mertk and nuclear receptor Nr4a1 in cardiac macrophages, the latter previously shown to be required for phagocyte survival.
identify Nur77 as a transcriptional regulator of T cell metabolism, which elevates the threshold for T cell activation and confers protection in different T cell-mediated inflammatory diseases.
The data show that NR4A1 expression by multipotent progenitors of the spleen limits erythropoiesis and megakaryopoeisis, permitting development to other myeloid lineages. This effect is specific to the spleen, revealing a unique molecular pathway that regulates myeloid bias in an extramedullary niche.
NR4A1 knockdown interrupted the Mff-related mitochondrial fission and recused Parkin-mediated mitophagy, reducing the hyperglycemia-mediated mitochondrial damage and thus improving renal function.
This gene encodes a member of the steroid-thyroid hormone-retinoid receptor superfamily. Expression is induced by phytohemagglutinin in human lymphocytes and by serum stimulation of arrested fibroblasts. The encoded protein acts as a nuclear transcription factor. Translocation of the protein from the nucleus to mitochondria induces apoptosis. Multiple transcript variants encoding different isoforms have been found for this gene.
, TR3 orphan receptor
, early response protein NAK1
, growth factor-inducible nuclear protein N10
, hormone receptor
, nerve growth factor IB nuclear receptor variant 1
, nuclear hormone receptor NUR/77
, nuclear receptor subfamily 4 group A member 1
, orphan nuclear receptor HMR
, orphan nuclear receptor TR3
, steroid receptor TR3
, testicular receptor 3
, orphan nuclear receptor NGFI-B
, nuclear protein N10
, Orphan nuclear receptor HMR
, immediate early gene transcription factor NGFI-B
, nerve growth factor induced protein I-B
, nerve growth factor-induced protein I-B