EGR2
- Known as:
- EGR2
- Catalog number:
- Y213661
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- EGR2
Related genes to: EGR2
- Gene:
- EGR2 NIH gene
- Name:
- early growth response 2
- Previous symbol:
- KROX20
- Synonyms:
- -
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2019-04-23
Related products to: EGR2
Related articles to: EGR2
- Current research into the actions of psychedelic drugs is focused on 5-HT2A receptor-coupled signaling pathways, particularly β-arrestin2 signaling. Here, we investigated the involvement of β-arrestin2 in psychedelic drug-induced mouse markers of hallucinogenic effects, molecular plasticity, and structural plasticity; specifically, the head-twitch response, cortical expression of plasticity-related genes (cFos, Egr1, Egr2, and Arc), and dendritogenesis (primary cortical neuron cultures), respectively. Psilocin-induced head-twitches, plasticity gene expression, and dendritogenesis were all blocked by the 5-HT2A receptor antagonist MDL-100,907. The head-twitch response to psilocin was not different between wildtype and β-arrestin2 knockout (KO) mice, and the head-twitch responses to 2,5-dimethoxy-4-iodoamphetamine (DOI) and lysergic acid diethylamide (LSD) were similarly unaffected by β-arrestin2 KO. Psilocin-evoked gene expression showed a trend to be less in β-arrestin2 KO compared to wildtype mice, but the gene expression response to DOI was clearly not altered by β-arrestin2 KO. Finally, psilocin-induced dendritogenesis was attenuated in β-arrestin2 KO versus wild-type cultured neurons, and similar findings were obtained with DOI. In summary, the current study found no convincing evidence to support a role for β-arrestin2 signaling in either the head-twitch or plasticity-related gene responses to the psychedelic drugs tested. However, our data suggest a role for the β-arrestin2 pathway in psychedelic drug-evoked dendritogenesis of cultured neurons. Thus, the β-arrestin2 pathway unlikely mediates the hallucinogenic effects of psychedelic drugs but may contribute to neural plasticity changes in certain models. - Source: PubMed
Ippolito AurelijaTiranti AgneseHurley ShaunGilmour GaryChurchill GrantSharp Trevor - BACKGROUND Allergic rhinitis (AR) is a common inflammatory disorder of the nasal mucosa triggered by allergens and characterized by sneezing, nasal congestion, and itching. This study aimed to identify and validate potential biomarkers associated with immune dysregulation in AR via bioinformatics analyses initiated with chemokine-related genes. MATERIAL AND METHODS AR-related datasets (GSE75011 and GSE50223) and 69 chemokine-related genes were analyzed via differential expression analysis and weighted gene co-expression network analysis to identify candidate genes. Random forest analysis was used to select optimal features. Expression analysis identified potential immunoregulatory biomarkers that were downregulated in AR samples. A nomogram incorporating these biomarkers was constructed as an exploratory tool to estimate individual AR probability and support future diagnostic model development. RESULTS Early growth response protein 2 (EGR2) and transforming growth factor-ß1 (TGFB1) were identified as chemokine-related biomarkers in AR. Immune infiltration analysis showed significant correlations between TGFB1 and M2 macrophages, as well as activated memory CD4+ T cells. Drug prediction identified tretinoin as a potential therapeutic agent targeting both biomarkers; molecular docking confirmed stable binding of the 3 top-ranked predicted drugs with TGFB1. Pilot reverse transcription-quantitative polymerase chain reaction analysis demonstrated downregulation of EGR2 and TGFB1 in AR samples, providing preliminary supportive evidence. Gene set enrichment analysis indicated involvement in the MAPK and p53 signaling pathways, suggesting roles in cell proliferation, apoptosis, cell cycle regulation, and stress responses. CONCLUSIONS EGR2 and TGFB1 offer potential immunoregulatory biomarkers for AR diagnosis and may provide preliminary insights into AR pathogenesis and potential treatment strategies. - Source: PubMed
Publication date: 2026/08/03
Liu YisenGuo ShuoCao FengChen XixiLiu Yehai - Macrophages in breast cancer are highly heterogeneous and targeting both tissue-resident and bone marrow-derived macrophages represents a high-potential strategy in breast cancer immunotherapy. - Source: PubMed
Publication date: 2026/07/21
Ning YonglingWu CaijunPhuyal SaileshHu XiaolingLi HongMitchell Robert AYan JunDing Chuanlin - Arteriovenous fistula (AVF) maturation is characterized by outward remodeling presented mainly as wall thickening and lumen enlargement, probably mediated by increased differentiated vascular smooth muscle cells (VSMCs) and extracellular matrix (ECM) deposits, at least in part. Our previous study revealed that the highly conserved transcription factor early growth response protein 2 (EGR2) promoted renal tubular epithelial cell differentiation and ECM accumulation. Here, we found that EGR2 expression was enhanced in venous outflow tracts from end-stage renal disease (ESRD) patients and mice with AVF surgery accompanied by a thickened venous wall and enlarged lumen. Then, the knockdown of EGR2 could inhibit AVF maturation while EGR2 overexpression further promoted outward remodeling in AVF mice with adeno-associated virus (AAV) administration regulated by differentiated VSMCs and ECM deposition. Mechanistically, gene deletion of EGR2 inhibited c-Myc possibly by binding to the promoter region of the insulin-like growth factor 2 binding protein 2 (IGF2BP2) gene. Moreover, EGR2 was upregulated by histone deacetylase 4 (HDAC4) which probably negatively regulated transcription factor c-Jun, the latter was reported to antagonize the effect of EGR2. Thus, we speculated that EGR2 is upregulated by HDAC4 possibly by negatively regulating c-Jun and promoting outward remodeling through the IGF2BP2/ c-Myc signaling axis during AVF maturation. - Source: PubMed
Publication date: 2026/07/29
Song AnniYan RuiweiHuang MingyuZou XingjianGao PanCai ChuanqiYin XingjieLuo PengliZhu PingZhang Chun - Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease with limited treatment options. Here, we demonstrate that fucoxanthin (FUCO), a natural marine carotenoid, attenuates free fatty acid (FFA)-induced hepatocellular steatosis and inflammatory responses in vitro by targeting the EGR2-CD36 axis (EGR2, early growth response protein 2; CD36, cluster of differentiation 36). In FFA-induced hepatocyte models (HepG2, Hep3B, and AML12), FUCO significantly reduced lipid accumulation and inflammatory markers without cytotoxicity. Mechanistic studies revealed that FUCO specifically inhibited fatty acid uptake and transport by downregulating CD36, while triglyceride (TG) degradation remained unaffected. RNA sequencing identified EGR2 as a master regulator induced by FFA and suppressed by FUCO. Functional validation showed that EGR2 overexpression completely blocked FUCO's lipid-lowering effects and restored CD36 expression, confirming that FUCO acts through EGR2-dependent CD36 inhibition. Bioinformatic analysis further supported EGR2-mediated regulation of CD36 via tumor necrosis factor (TNF) and sterol regulatory element-binding factor (SREBF) pathways. Collectively, our findings establish EGR2 as a critical molecular target for FUCO and provide mechanistic insights that may support its further evaluation in preclinical models for MASH therapy. - Source: PubMed
Publication date: 2026/07/10
Li XiangyuYang ChenChen QionghuiXu XianchuanWang LianZhang PengHu QiangHan DanxiangYu AiqunJiang JingLian Qizhou