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Promoter-activity assays confirmed that exposure of cells to full-length Nurr1 fusion protein activated not only its cognate human tyrosine hydroxylase promoter but also the corresponding mouse sequence, although at a reduced efficiency.
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.
PARP1 inhibitor also suppressed the aldosterone secretion in response to the angiotensin II. Together, these results suggest PARP1 is a prime coregulator for Nurr1.
Data expand the understanding of the mechanism by which the NR4A2 nuclear receptor can facilitate DNA DSB repair.
An association was identified in a Mexican population between genotype and mRNA expression levels of NR4A2 in patients with Parkinson's disease.
miR-34 was identified as a direct negative regulator of NR4A2. A novel regulatory network linking p53, miR-34, and NR4A2 was revealed, in which p53 can overcome its inhibition by endogenous NR4A2 through upregulating miR-34.
Nurr1 was induced during intestinal regeneration after I/R injury. Nurr1 promoted proliferation of intestinal epithelial cells after H/R injury. Nurr1 inhibited p21 expression in a p53-independent manner. Nurr1 inhibited p21 gene transcription by binding to p21 promoter directly.
Our findings of a de novo deletion of NR4A2 in an individual with mild intellectual disability and prominent speech and language impairment provides further evidence for NR4A2 haploinsufficiency being causative for neurodevelopmental and particularly language phenotypes
Findings support that Notch1/NR4A2 co-regulate HCC cell functions by playing oncogenic roles and regulating the associated downstream signaling pathways.
NR4A sub-family of nuclear orphan receptors (Nor-1, Nurr-1 and Nur-77) may have a role in trophoblastic cell differentiation.
this study shows over-expression of NR4A2 mRNA in peripheral CD4+ T cells of Sjogren's syndrome patients
NR4A2 and NR4A3 are components of a downstream transcriptional response to PKA activation in the neutrophil, and that they positively regulate neutrophil survival and homeostasis.
Study found a marked down-regulated gene expression of the NR4A subfamily (NR4A1, NR4A2, and NR4A3) obtained from Parkinson's disease patients, but only a NR4A1 decrease in Alzheimer's disease patients compared to healthy controls. This study reports that the entire NR4A subfamily and not only NR4A2 could be systemically involved in Parkinson's disease.
show that unsaturated fatty acids also interact with the Nurr1 LBD, and solution NMR spectroscopy reveals the binding epitope of DHA at its putative ligand-binding pocket
NURR1 is an essential transcription factor for the differentiation, maturation, and maintenance of midbrain dopaminergic neurons.
Nurr1 overexpression exerts neuroprotective and anti-inflammatory roles via down-regulating CCL2 in both in vivo and in vitro Parkinson's disease models, contributing to developing mechanism-based and neuroprotective strategies against PD
In the PPI network, genes may be involved in Down syndrome (DS) by interacting with others, including nuclear receptor subfamily 4 group A member 2 (NR4A2)early growth response (EGR)2 and NR4A2EGR3. Therefore, RUNX1, NR4A2, EGR2, EGR3 and ID4 may be key genes associated with the pathogenesis of DS.
Our results suggest that NLK inhibits transcriptional activation of Nurr1 gene by impeding CBP's role as a co-activator of NF-kappaB and CREB in prostate cancer.
decreased expression levels of Nurr1 were associated with chronic inflammation and insulin resistance in patients with T2D.
The immunohistochemical, qRT-PCR and western blot analyses revealed that Nurr1 expression was increased in gastric cancer tissues compared with normal gastric tissue.
the pathogenesis of cerebral ischemia-reperfusion injury is associated with Nurr1 upregulation followed by augmented mitochondrial fission via an abnormal YAP-INF2 pathways
miR-137 enhances the endothelial progenitor cell proliferation and angiogenesis in CIS mice by targeting NR4A2 through the Notch signaling pathway.
NR4A1/Nur77 and NR4A2/Nurr1 dynamically regulated inflammatory gene expression in glia by modulating the transcriptional activity of NF-kappaB.
Nurr1 suppressed the production of TNF-alpha via interaction with NF-kappaB/p65 and inhibiting its nuclear translocation. In addition, both NF-kappaB and Nurr1 appeared to be regulated by the TLR4-mediated signal pathway. Study demonstrated that TLR4 recognized alpha-synuclein and activated downstream signaling mechanisms leading to the release of pro-inflammatory mediators that are contra-balanced by Nurr1 expression.
The study comprehensively evaluated the association of NR4A2 variation with PD, and the results failed to demonstrate that the NR4A2 polymorphisms significantly associated with PD except for rs35479735, suggesting that more studies are needed to elucidate if NR4A2 is a risk of PD.
The Nurr1 expression may play a significant role in regulating inflammation in the brain.
Knockdown of DJ-1 attenuates Nurr1 activity.
Overexpression of Nurr1 and Pitx3 in iPSCs could efficiently program induced pluripotent stem cells into functional dopaminergic-like neurons. This finding may have an impact on future stem cell therapy of Parkinson's disease.
Overexpression and knockdown of Nr4a2 demonstrated that Nr4a2 orchestrates the expression of immunoregulatory genes, hence inducing a tolerogenic phenotype in bone marrow derived dendritic cells (DC) in mice. The findings suggest a previously unidentified role for Nr4a2 as a regulator of dendritic cell tolerogenicity and demonstrate its potential as therapeutic target in DC-associated pathophysiologies.
Nurr1 defect induces early experimental autoimmune encephalomyelitis (EAE) onset and increases inflammatory infiltrates in spinal cord suggesting a Nurr1 role in the early phase of EAE
Nuclear receptors of the NR4a family are not required for the development and function of follicular T helper cells
Nr4a2 factor plays crucial role regulatory T cells, mediating the two defining characteristics of regulatory T cells: stability of cell lineage and immunosuppressive functions.
Results indicate that Nurr1 overexpression in olfactory bulb stem cells induces the formation of two populations of mature dopaminergic neurons with features of the ventral mesencephalon or of the olfactory bulb
Nurr1 +/- genotype predisposes mice to T. gondii-induced alterations in behaviors that involve dopamine neurotransmission
The authors show herein that Nurr1 and Foxa2 interact to protect midbrain dopaminergic neurons against various toxic insults, but their expression is lost during aging and degenerative processes.
Because the phosphorylation site mutants of NR4A2 cannot rescue the cell death-promoting activity, ASK1-p38 pathway-dependent phosphorylation and subsequent cytoplasmic translocation of NR4A2 may be required for oxidative stress-induced cell death.
Nurr1 protein is prominently expressed in brain areas with Abeta accumulation, that is, the subiculum and the frontal cortex, in the 5XFAD mouse and that Nurr1 is highly co-expressed with Abeta at early stages.
This study showed that nurr1 has a similar mRNA expression pattern and low levels of expression at rest.
Induction of Nurr1 expression is mediated by voltage-dependent calcium channels.
The interplay of Nurr1 and Foxa2 is the crucial determinant for dopamine phenotype acquisition during midbrain dopaminergic neuron development.
data indicate a conserved evolutionary role of Nr4a2 proteins in specification of the neurotransmitter phenotype
Results shed new light on NR4A2 function in the dopamine differentiation pathway, and stress the effect of dopamine dysregulation on the control of locomotor activity.
This gene encodes a member of the steroid-thyroid hormone-retinoid receptor superfamily. The encoded protein may act as a transcription factor. Mutations in this gene have been associated with disorders related to dopaminergic dysfunction, including Parkinson disease, schizophernia, and manic depression. Misregulation of this gene may be associated with rheumatoid arthritis. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.
nuclear receptor subfamily 4, group A, member 2
, nuclear receptor
, nuclear receptor related 1
, nuclear receptor subfamily 4 group A member 2
, Nuclear receptor subfamily 4 group A member 2
, NGFI-B/nur77 beta-type transcription factor homolog
, T-cell nuclear receptor NOT
, immediate-early response protein NOT
, intermediate-early receptor protein
, nur related protein-1, human homolog of
, orphan nuclear receptor NR4A2
, orphan nuclear receptor NURR1
, transcriptionally inducible nuclear receptor related 1
, transcriptionally-inducible nuclear receptor
, NUR-related factor 1
, nuclear orphan receptor HZF-3
, nuclear receptor subfamily 4 group A member 2 variant TINUR
, nuclear receptor subfamily 4 group A member 2 variant NURR1a
, nuclear receptor subfamily 4 group A member 2 variant NURR1b
, nuclear receptor subfamily 4 group A member 2 variant NURR1c
, nuclear receptor subfamily 4 group A member 2 variant NURR2c
, nur related protein 1
, regenerating liver nuclear receptor 1
, nerve growth factor 1b
, neural orphan nuclear receptor