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
- Ferroptosis caused by metabolic stress is a main contributor to pancreatic β-cell injury in type 2 diabetes. Orphan nuclear receptor NR4A1 can be activated by various stimuli and stressors, but its role remains unclear in pancreatic β-cell ferroptosis. This study focuses on how NR4A1 transcriptionally regulates pancreatic β-cell ferroptosis and reveals its underlying network. - Source: PubMed
Publication date: 2026/08/06
Guo WenfeiSong MingzeWang YuhuiLiu XinruJin MinhanPu Zeqing - Neuromodulation has recently garnered attention as a potent approach to improve sensorimotor function following neural injury. After spinal cord injury, electrical stimulation targets sensorimotor circuitry to enhance volitional movement; however, motor neurons are located in the ventral gray matter. Previously, we developed a versatile wireless stimulation system and surgical approach to selectively activate motor neurons caudal to a cervical spinal cord injury. Here, we empirically tested if ventral epidural stimulation is sufficient to promote lasting recovery of skilled motor function. Ventrally stimulated animals exhibited significantly improved forelimb function associated with electrically stimulated motor pathways. Further, stimulation produced increases in neuronal Nr4a1 expression, a subacute reduction in microglia Nr4a1 expression, and a shift from activated toward ramified microglial morphologies in the stimulated ventral gray matter. This study reports the first successful application of ventral spinal stimulation to improve function in an animal model and the first sustained improvement in skilled forelimb reaching when behavioral testing was decoupled from the stimulation. - Source: PubMed
Publication date: 2026/08/04
Hogan Matthew KFrazier Allison MDelgado DaisyGutierrez Ana GStigliano CinziaMejia Julio ATorres Isis YTran TheresaKakumanu Akosh CZambelas Joseph MBarber Sean MBritz Gavin WHorner Philip J - Acute myeloid leukemia (AML) is an aggressive hematologic malignancy with poor clinical outcomes and limited therapeutic options. Aberrant activation of the IKKβ-NF-κB pathway occurs in approximately 40% of AML cases and contributes to leukemogenesis. However, pharmacological inhibition of IKKβ has been limited by serious toxicities, including neutrophilia. Here we identify IKKβ and NR4A1 as critical drivers of AML progression in certain models and develop a proteolysis-targeting chimera (PROTAC) capable of degrading the proteins. Although NR4A1 has previously been described as a tumor suppressor in AML, our findings demonstrate that NR4A1 exhibits oncogenic functions in some AMLs of the (pro)monocytic lineage. Notably, elevated expression of IKKβ and NR4A1 in AML is associated with poor clinical outcomes, playing non-redundant oncogenic roles in AML. To therapeutically target IKKβ and NR4A1, we designed and synthesized a series of celastrol-based PROTACs that exploit celastrol's ability to bind both IKKβ and NR4A1. Among these compounds, the lead A9 induces potent cytotoxicity in multiple AML cell lines and primary AML samples through cereblon E3 ligase-dependent degradation of IKKβ and/or NR4A1. In vivo, A9 suppresses leukemia progression in a KMT2A::MLLT3 AML mouse model without inducing neutrophilia, supporting PROTAC-mediated degradation of IKKβ and NR4A1 as a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/07/30
Maharjan Chandra KLiu YiXiao YufengPodder Bristy RMontgomery Tyler HWang LeiKim Myung-ChulJin ZengAnvar SeyedehalalehTithi Tanzia IslamShastri Vivek MStevens Alexandra MKolb RyanZhao ChenQian ZhijianLamba Jatinder KZheng GuangrongZhang Weizhou - Patients with chronic kidney disease (CKD) display a reduced survival following myocardial infarction (MI). As the underlying mechanisms remain unclear, we examined the impact of CKD on cardiac remodeling and function post-MI using a mouse model of adenine-induced CKD. - Source: PubMed
Publication date: 2026/07/24
Schulte CorinnaWollenhaupt JuliaHourtz SinaHarlacher EvaMoellmann JuliaCruz Junho Carolina VictoriaKohlhaas MichaelJankowski VeraJin HanReugels MartinMaryam SidrahHausmann FrancaWong Dickson W Lvan der Vorst Emiel P CBerger MartinVondenhoff SonjaKurt BerkanGhesquière BartMueller ConstanzeSchulze-Späte UlrikeSchmitt-Kopplin PhilippeBiessen Erik A LPrates-Roma LeticiaBiener MoritzGiannitsis EvangelosKatus Hugo ASchunk StefanFliser DaniloMarx-Schütt KatharinaLehrke MichaelKramann RafaelKahles FlorianBoor PeterGoettsch ClaudiaHayat SikanderJankowski JoachimMaack ChristophDöring YvonneMarx NikolausNoels Heidi - - Source: PubMed
Publication date: 2026/05/10
Xu GuanfengWu HangZhang JieWang YaxuanShao ChongyuYang JiehongHan JinWan Haitong