EGR2, affinity purified antibody, goat, 100 ug.
- Known as:
- EGR2, antigenic enriched (anti-), caprine, 100 ug.
- Catalog number:
- GT41010-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- EGR2 affinity purified antibody goat 100 .
Related genes to: EGR2, affinity purified antibody, goat, 100 ug.
- 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, affinity purified antibody, goat, 100 ug.
Related articles to: EGR2, affinity purified antibody, goat, 100 ug.
- 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 - This study aimed to investigate the effects of early-life oral supplementation with 6'-sialyllactose (6'-SL) on neurobehavioral development in mice and the potential mechanisms involving the microbiota-gut-brain (MGB) axis. Neonatal mice received daily oral gavage of saline or 6'-SL from birth to postnatal day (PND) 21. Behavioral tests (Y-maze, open field, light-dark box, forced swim test) were conducted from PND 37-41. Fecal metagenomics and short-chain fatty acid (SCFA) levels were assessed, and brain gene expression was analyzed by RNA sequencing and reverse transcription quantitative real-time PCR (RT-qPCR) at PND 21 and PND 42. Our findings revealed that 6'-SL supplementation enhanced cognitive function in growing mice, as evidenced by improved performance in the Y-maze test. Early-life 6'-SL supplementation exerts profound and sustained regulatory effects on the gut microbiota and SCFA. At PND 21, 6'-SL enriched Akkermansia muciniphila and elevated acetate, isobutyrate, and isovalerate, while suppressing Enterococcus. At PND 42, Akkermansia muciniphila and Escherichia were further enriched, while Alistipes and Duncaniella were inhibited. Meanwhile, acetate, isobutyrate and propionate levels remained elevated. Notably, these changes were observed not only at the end of the intervention but also persisted at PND 42, indicating a sustained long-term effect of 6'-SL supplementation. In contrast, most myelin genes were altered only to a small extent at PND 21, compared with their marked upregulation in the PFC at PND 42 (Mbp, Mog, Olig1, Sox10, Egr2, Vegfa). Correlation analysis revealed that the abundance of Akkermansia muciniphila was positively correlated with isobutyrate levels, Escherichia showed a positive correlation with propionate levels, while Enterococcus was negatively correlated with acetic acid. These SCFA were positively associated with myelin gene expression. Further, these genes were positively associated with cognitive performance, suggesting their potential involvement in cognitive function. Thus, 6'-SL enhances spatial cognition in early-life mice through a mechanism involving gut microbiota and SCFA modulation, subsequent upregulation the transcription of prefrontal myelination-related gene. This study provides novel insights into the mechanisms by which 6'-SL regulates early brain development via the MGB axis and offers critical theoretical support for nutritional supplementation strategies in infancy. - Source: PubMed
Publication date: 2026/09/17
Yang MingxinLuo YatingWu SimouJia WenChen HongruHe FangCheng Ruyue - Peripheral nerve transection requires surgical treatment, although functional recovery remains incomplete. Here, we developed a biofunctional nanocomposite nerve interface combining an ion-covalent gelatin methacryloyl (GelMA)/Laponite hydrogel with engineered thermostable fibroblast growth factor-2 (FGF-2) to recreate a regenerative microenvironment. Laponite incorporation (2%-2.5% w/v) precisely modulated the hydrogel network, providing shear-thinning behavior, enhanced viscoelasticity, microporosity, a twofold increase in compressive modulus, controlled degradation, injectability, and three-dimensional (3D) bioprintability. Functionalization with thermostable FGF-2 enabled sustained release while preserving bioactivity, promoting Schwann cell viability, metabolic activity, cytoskeletal organization, and upregulation of nerve growth factor receptor (NGFR), glial cell line-derived neurotrophic factor (GDNF), early growth response protein 2 (EGR2), octamer-binding transcription factor 6 (OCT6), and SRY-box transcription factor 9 (SOX9). Nerve interfaces consisting of a basal polycaprolactone (PCL) layer and a biofunctional GelMA (10%)/Laponite (2%) hydrogel containing FGF-2 (1 µg mL ) were fabricated by 3D bioprinting followed by visible-light crosslinking. In a rat neurotmesis model, FGF-2-functionalized wraps significantly improved motor function, electrophysiological recovery, Schwann cell activity (S100 calcium-binding protein), neurofilament organization and myelination (FluoroMyelin), and muscle preservation. Collectively, this work introduces a 3D-bioprinted, cell-instructive nerve interface integrating mechanical neuroprotection with sustained neurotrophic signaling to enhance peripheral nerve regeneration. - Source: PubMed
Publication date: 2026/09/04
Rodriguez-Sanchez Diego NJoshi AkshatSafari Saeedde Carvalho Leticia A MMuller Kevin SKim UijinCartarozzi Luciana PKamaraj MeenakshiErmis Meneksede Barros Natan Rde Oliveira Alexandre L R