EGR2 EMSA Probe Set
- Known as:
- EGR2 EMSA Probe Set
- Catalog number:
- AY1305P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- EGR2 EMSA Probe Set
Related genes to: EGR2 EMSA Probe Set
- 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 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: EGR2 EMSA Probe Set
- Dominant loss-of-function mutations in cause Charcot-Marie-Tooth neuropathy characterized by sensory and motor deficits associated with myelin and/or axonal abnormalities and muscle atrophy. Increasing DNM2 activity from embryogenesis has been reported to ameliorate neuromuscular phenotypes in the Charcot-Marie-Tooth mouse; however, this model displays predominantly muscle pathology and limited nerve involvement, precluding rigorous evaluation of neuropathic mechanisms and potential therapies. Here, we performed comprehensive behavioural, electrophysiological, histological and molecular analyses to characterize the mouse, which combines systemic heterozygosity for the common K562E mutation together with Schwann cell-specific deletion of wild-type . This model faithfully reproduces key clinical and pathological features of -Charcot-Marie-Tooth, including motor deficits, reduced general force and coordination, and severe sensory and motor conduction deficits associated with axonal loss, demyelination and inflammation. Mechanistically, we delineate a coherent pathological sequence that explains the profound functional deficits. In particular, a downregulation of the transcription factor EGR2, a master regulator of myelin gene expression, and of the myelin protein MPZ correlates with demyelination. To evaluate the therapeutic potential of DNM2 supplementation, post-symptomatic intrathecal delivery of AAV9-DNM2 driven by the Schwann cell-specific MPZ promoter was performed at 4 weeks. Although DNM2 expression increased in peripheral nerves (∼1.9-fold), no significant improvements were observed across behavioural, electrophysiological, structural or molecular parameters. Together, these findings establish the mouse as a robust preclinical model, recapitulating key features of -Charcot-Marie-Tooth, and provide crucial insight into the biological and temporal constraints that must guide future therapeutic strategies for -Charcot-Marie-Tooth. - Source: PubMed
Publication date: 2026/09/01
Goret MarieArbogast ThomasLaporte Jocelyn - This study discovers the high expression of EGR2 in neuropathic pain (NP) and further explores the molecular mechanism of EGR2-mediated inflammatory response of spinal microglia. GSE92718 was obtained from the GEO database to screen differentially expressed genes in NP. A chronic constriction injury (CCI) model was established in male C57BL/6J mice. EGR2 shRNA was intrathecally injected into CCI mice, followed by RT-qPCR, Western blot, ELISA, and immunofluorescence to detect inflammatory response and microglial activation. An in vitro inflammatory cell model was established by inducing BV-2 cells with 100 ng/mL LPS. The binding between EGR2 and MRTO4 was predicted through bioinformatics and verified by dual luciferase and ChIP assays. EGR2 was the most significantly differentially expressed gene in NP. EGR2 expression was upregulated in spinal cord tissues of male CCI mice, mainly in microglia and neurons. EGR2 shRNA alleviated CCI-induced mechanical allodynia and thermal hyperalgesia, inhibited pro-inflammatory cytokines and microglial activation. EGR2 transcriptionally activated MRTO4 expression. LPS induced BV-2 cell activation and inflammatory response. Overexpression of EGR2 increased pro-inflammatory cytokines and Iba-1 + positive cells in LPS-stimulated BV2 cells, while the addition of sh-MRTO4 rescued the trend. In conclusion, EGR2 gene is significantly upregulated in the spinal cord tissues of male CCI mice. EGR2 facilitates LPS-induced inflammatory responses in microglia by transcriptionally activating MRTO4 expression, suggesting that this signaling pathway may participate in NP-associated spinal inflammation. - Source: PubMed
Publication date: 2026/09/21
Cheng FangKaya Olchy Louange PandyShrestha AekrajAdjei Dennis AmofahLi Hai-YingJiang Li-Xue - Malignant peripheral nerve sheath tumor (MPNST) carries the highest excess mortality of the cancers associated with neurofibromatosis Type 1, and usually arises from a neurofibroma. We asked whether the transcriptomic differences that distinguish MPNST from neurofibroma reproduce across independent cohorts, and whether a compact score derived from them transports between platforms. We meta-analyzed five public discovery cohorts of primary nerve-sheath tissue (113 MPNST, 79 neurofibromas; 3 platforms) and held out a sixth, independently generated cohort. Neurofibroma and MPNST tissue differed at 1489 genes in two opposing themes: up-regulated mitotic machinery (TOP2A, EZH2, AURKA) and loss of Schwann-cell identity (the transcription factors SOX10 and EGR2, and the myelin genes PMP2 and MPZ). These differences were reproducible. Among the significant genes assayed in all five cohorts, almost all changed in the same direction in everyone, and 93.3% of those detectable in the held-out cohort agreed in direction. Leave-one-cohort-out re-derivation of the pipeline gave a mean AUC of 0.90 across five folds (per-fold 0.84 to 0.97). CD276 (B7-H3) was selectively up-regulated, whereas CD274 and PDCD1LG2 were not. The myelin marker PMP2, a readout chosen retrospectively after the held-out results were known, separated MPNST from neurofibroma in that cohort but left atypical and conventional neurofibromas unseparated (AUC 0.67, p = 0.10). A program score derived without the discovery cohort carrying survival data was associated with shorter survival there, an exploratory single-cohort association. The composition of a compact score varied with platform and preprocessing, so no fixed single-sample classifier is warranted. - Source: PubMed
Jin QuanyuGao ZhenxuanZhang ZeKong ChenchenLiu JiaxinAbudurezhake AermanKou LeiCai ShuguangYang WenqiangWang QiLi ZhitaoZhang Li - Taste 2 receptors (T2Rs) are known as receptors for sensing bitterness, but their gene expressions are observed in various extraoral tissues. T2Rs in adipocytes have attracted attention because bitter compounds influence lipid accumulation. However, the role of T2Rs in adipocytes has not been extensively investigated. This study investigated the functions of Tas2r108 and Tas2r126 in preadipocyte differentiation. Overexpression of Tas2r108 or Tas2r126 inhibited the differentiation of 3T3-L1 cells and mouse primary preadipocytes. Similarly, knockdown of Tas2r108 suppressed the differentiation of these cells. Consistent with the knockdown results, stimulation with T2R agonists during the differentiation of 3T3-L1 cells enhanced adipogenesis. Mechanistic analysis revealed that the suppressed differentiation by T2R overexpression involves the downregulation of Cebpb, while T2R knockdown involves the upregulation of Nr4a2 and Nr4a3 and downregulation of Egr2. Analysis with T2R agonists revealed that T2Rs in preadipocytes couple with inhibitory G-protein to downregulate intracellular cAMP concentrations, which works through ERK to enhance adipogenesis. These results demonstrate the regulation of adipocyte differentiation by T2Rs and suggest that bitter compounds enhance adipogenesis via T2Rs. - Source: PubMed
Publication date: 2026/09/19
Kato EisukeOshima ShotaAdachi YusukeImai Reitaro - Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of all heart failure cases worldwide, yet effective targeted therapies remain limited. Tectorigenin (Tec), a bioactive isoflavone derived from traditional Chinese medicine, exhibits diverse cardioprotective effects; however, its therapeutic potential and underlying mechanisms in HFpEF remain incompletely understood. This study aimed to investigate the effects of Tec on HFpEF and elucidate the underlying molecular mechanisms. A mouse model of HFpEF was established using the "two-hit" approach (high-fat diet + L-NAME). In vivo experiments included echocardiography, histological staining, treadmill testing, metabolic assessments, and molecular analyses. In vitro, neonatal rat ventricular myocytes (NRVMs) exposed to palmitic acid (PA) were used to model cardiomyocyte lipotoxicity. RNA sequencing, network pharmacology, molecular docking, surface plasmon resonance, pull-down assays, chromatin immunoprecipitation, and gene silencing were employed to elucidate the regulatory mechanisms. Tec attenuated HFpEF progression and retained therapeutic efficacy when administered after HFpEF establishment. In vitro, Tec alleviated PA-induced cardiomyocyte lipotoxicity. Mechanistically, Tec directly bound EGFR at the E762/M793 sites and inhibited its aberrant activation. Inhibition of EGFR signaling suppressed the downstream EGFR-EGR2 axis, thereby upregulating Acot1 and improving myocardial lipid metabolic homeostasis. Cardiac-specific Acot1 knockdown or pharmacological activation of EGFR markedly attenuated Tec-mediated improvements in cardiac function, remodeling, and myocardial lipid metabolism. Tec ameliorates HFpEF through the EGFR-EGR2-Acot1 axis, highlighting a potential therapeutic strategy for HFpEF. - Source: PubMed
Publication date: 2026/09/18
Wang Li-GuoLin KeYou Meng-ZhenLi Qin-FengWei Wen-JieLi HuiShi YiYan Yu-FengLi RanWang Mei-HuiXia Chun-LeiFu Guo-ShengXu Ya-Ting