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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.
mRNAs expression and methylation pattern of RARB, NR4A1 and HSD3B2 genes in human adrenal tissues (HAT) and in pediatric virilizing adrenocortical tumors (VAT) were analyzed.
NR4A sub-family of nuclear orphan receptors (Nor-1, Nurr-1 and Nur-77) may have a role in trophoblastic cell differentiation.
beta1-integrin expression is regulated in pancreatic and colon cancer cells by the pro-oncogenic orphan nuclear receptor 4A1
Inhibition of NR4A1-mediated transcriptional activity was involved in the anticancer effects of fangchinoline; fangchinoline represents a novel class of mechanism-based anticancer agents targeting NR4A1 that is overexpressed in pancreatic cancer.
Transcript analysis of four different aggressive lymphoma cell lines overexpressing either NR4A3 or NR4A1 revealed that apoptosis was driven similarly by induction of BAK, Puma, BIK, BIM, BID, and Trail. Overall, our results showed that NR4A3 possesses robust tumor suppressor functions of similar impact to NR4A1 in aggressive lymphomas
NR4A1 expression is specific to a quiescent subset of T-cells.
we demonstrate that endogenous Nur77 protein expression can serve as a reporter of T-cell receptor and B-cell receptor specific signaling in human peripheral blood mononuclear cells.
we report overexpression of the nuclear receptor NR4A1 in rhabdomyosarcomas that is sufficient to drive high expression of PAX3-FOXO1A
Identify the orphan nuclear receptor NR4A1 as a potential early response gene in FGF2 signaling and regulation of sprouty in bovine ovarian granulosa cells.
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.
we found that either knockdown of Nr4a1 or 3, 3'- Diindolylmethane (DIM), an Nr4a1 antagonist, were able to rescue the effects of SNRPN knockdown on neurite outgrowth of embryonic cortical neurons, providing the potential therapeutic methods for SNRPN deletion disorders. We thus concluded that maintaining the proper level of SNRPN is critical in cortical neurodevelopment.
new insights into the understanding the mechanisms of the effects of Nur77 on LPS-activated microglia
These results suggest that berberine-induced activation of AMPK may contribute to hepatic FGF21 expression via NUR77.
we found that KLF6 transcriptionally cooperates with NUR77 and SF1
Ca(2+) signaling pathway increases Nr4a1 expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1, and CREB transcription factors thus demonstrating an important interplay between the Ca(2+) and cAMP pathways in regulating Nr4a1 expression.
additional loss of Nur77 in the absence of Bim led to diabetes induction, suggesting that Nur77 promotes tolerance in this context. Together, these data reveal novel nondeletional roles for Nur77 that differ between T cell subsets and have implications for self-tolerance.
current data identify Nr4a1 as regulator of microglia activation and potentially new target for the treatment of inflammatory CNS diseases such as multiple sclerosis.
Celastrol promotes Nur77 migration from the nucleus to mitochondria, where it is ubiquitinated by TRAF2. Ubiquitinated Nur77 then interacts with p62/SQSTM1, leading to autophagy of dysfunctional mitochondria and alleviation of inflammation.
New transcript variants encode for NUR77 protein isoforms which are significantly smaller in size due to lack of transactivation domain and a part of DNA binding domain. Western blot analysis using NUR77 specific antibody confirmed the existence of these smaller variants in mouse.
Nur77 deficiency compromises myofiber growth, but not the regenerative capacity of myogenic progenitor cells.
Using Nr4a1 transgenic mice, electrically evoked dopamine release was shown to differ between the striosome and matrix compartments of the corpus striatum in a regionally-distinct manner.
Nur77 was found to be an important modulator in microglia function and attenuated pro-inflammatory mediator production.
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