EGR1 EMSA Probe Set
- Known as:
- EGR1 EMSA Probe Set
- Catalog number:
- AY1303P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- EGR1 EMSA Probe Set
Related genes to: EGR1 EMSA Probe Set
- Gene:
- EGR1 NIH gene
- Name:
- early growth response 1
- Previous symbol:
- -
- Synonyms:
- TIS8, G0S30, NGFI-A, KROX-24, ZIF-268, AT225, ZNF225
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-11
- Date modifiied:
- 2016-10-05
Related products to: EGR1 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: EGR1 EMSA Probe Set
- Aging is often regarded as the last chapter of development. There is growing evidence that aging and development are mechanistically linked. Here we describe a genetic switch involving EZH2 and EGR1 as opposing regulatory nodes that appears to connect aging and development across human tissues. We show that this switch defines two distinct states in fibroblasts: a proliferative (EZH2-high/EGR1-low) state and a non-proliferative and extracellular matrix-expressing (EGR1-high/EZH2-low) state. During replicative aging, cells shift from the proliferative state to the non-proliferative state and targeting either regulatory node-by overexpressing EZH2 or suppressing EGR1-rejuvenates aged fibroblasts. We provide evidence that this switch is involved in the transition from neural progenitor cells to matured neurons during brain development and becomes destabilized during aging, partially reversing the gene expression program established during development. We observed that this same switch becomes blurred and biased towards EGR1-high/EZH2-low state during the aging of muscle stem cells and hematopoietic stem cells. Since genetic switches are widely used in development to establish and reinforce cellular identity, we propose that attenuation of developmental switches may underlie aging across diverse organs and tissues, and partially accounts for the erosion of the epigenetic landscape and the loss of cellular identity. - Source: PubMed
Publication date: 2026/07/30
Khetan NehaZheng JiashunDeng ChanghuiWu EvanLi Hao - Recent advances in neuropsychopharmacology have renewed interest in psychedelics and entactogens as potential treatments for brain disorders, owing to their rapid effects on neural plasticity, cognition, and affect. Classical serotonergic psychedelics primarily act as 5-HT2A receptor agonists with additional activity at 5-HT1A and other serotonin receptors, whereas entactogens such as MDMA enhance monoamine release through transporter interactions. These actions converge on glutamatergic circuits, intracellular signaling cascades and transcriptional programs that can remodel synaptic connectivity. At the cellular level, psychedelics and entactogens acutely induce immediate early genes, including c-Fos, EGR1 and NPAS4, which regulate downstream targets such as BDNF and Arc to promote neuritogenesis, dendritic spinogenesis and synaptogenesis in cortical and hippocampal networks. Complementary epigenetic changes in DNA methylation and histone acetylation may help sustain these transcriptional effects beyond the period of drug exposure. In parallel, these compounds modulate neuroimmune pathways via 5-HT2A and sigma-1-receptors, altering cytokine profiles and microglial activation in a context-dependent manner rather than exerting a uniform antiinflammatory class effect. Preclinical studies and early clinical trials suggest that psychedelics and entactogens can produce rapid and sometimes durable improvements in mood and anxiety symptoms and are being investigated for conditions such as major depressive disorder, post-traumatic stress disorder, obsessive-compulsive disorder, substance use disorder and selected neurodegenerative syndromes. However, most indications remain supported only by small or early-phase studies and evidence for disease modification, particularly in Alzheimer's disease-related dementia, is currently limited to mechanistic hypotheses and preclinical models. This review synthesizes current knowledge on the receptor-level, molecular, genetic and immunological mechanisms of psychedelics and entactogens, linking these processes to neuroplasticity and brain network reorganization. It also discusses emerging therapeutic evidence, safety considerations and evolving regulatory frameworks, highlighting critical knowledge gaps and priorities for future research. - Source: PubMed
Publication date: 2026/07/31
Paul SampritiDubey SonalChandrasekharappa Mayur YergeriTiwari Prashant - Macrophage-enteric neuron dialog is crucial for intestinal homeostasis, but its specific role and underlying mechanism in inflammatory bowel disease (IBD) pathogenesis remain elusive. Here, we demonstrate that colonic macrophage-mediated extracellular matrix (ECM) remodeling orchestrates enteric neuronal maturation and dictates colitis progression. The depletion of Pcif1, recognized as a unique methyltransferase for mAm mRNA methylation, in macrophages attenuates colitis and protects enteric neurons from inflammation-driven degeneration. Specifically, Pcif1-deficient macrophages increase ECM accumulation, promoting their own extravasation into enteric neuronal plexuses and the maturation of enteric neurons, thereby curbing inflammation-driven neuronal injury and colitis progression. Mechanistically, Pcif1-mediated mAm modification inhibits the translation of Znf219 mRNA and represses the Znf219-Egr1 axis, a master transcriptional module that governs ECM remodeling. Finally, pharmacological blockade of PCIF1 promotes macrophage-mediated ECM deposition and suppresses colitis and neuronal loss. Our findings reveal a novel mechanism whereby ECM remodeling in macrophages drives enteric neuronal maturation and illuminate the mAm machinery as a promising therapeutic target for preventing neuronal loss in IBD patients. - Source: PubMed
Publication date: 2026/08/18
Ding ChenboZhao JiachenZhao TianXiao YeLi KaiLiu XiaoGe XuyangQin DemengHuang ZhiqianZhang YuLiu HuaDiao ZhiqingYe YouqiongFlavell Richard ALuo ChengChen ShijieYi ChengqiWang ZhengtingLi Hua-Bing - The postictal period, which immediately follows a seizure, is associated with several incapacitating symptoms or signs, such as psychosis, confusion, paresis, aphasia and memory loss. These symptoms can last from several minutes to even days and can have a negative impact on the quality of life for people living with epilepsy. However, there is a scarcity of data concerning the neurobiological mechanisms that mediate postictal amnesia and behavioural impairments. In the present study, we examined the impact of a single brief, self-limiting convulsive seizure induced by the chemoconvulsant pentylenetetrazol (PTZ) on trace fear learning. We found that PTZ administration produced a rapid but transient increase in hippocampal PI3K-Akt-mTOR signalling, with phosphorylation of Akt, mTOR, and ribosomal protein S6 peaking between 2 and 6 h post-seizure and returning to baseline by 24 h. This activation coincided with increased expression of plasticity-related markers, including Egr1 and PSD-95, and was associated with impaired memory in a hippocampus-dependent trace fear conditioning task. Administration of the mTORC1 inhibitor rapamycin 30 min post-seizure rescued the memory deficit. These findings suggest that postictal hyperactivation of mTOR signalling disrupts mechanisms of synaptic plasticity through excessive or unregulated protein synthesis, potentially saturating plasticity mechanisms and impairing new memory formation. Taken together, our results identify a critical role for aberrant mTOR signaling in mediating postictal cognitive dysfunction and suggest that targeted inhibition of mTORC1 may represent a therapeutic strategy for preserving memory after seizures. - Source: PubMed
Publication date: 2026/08/09
Fournier Neil MHorsey EmilyMaletta Teresa AnnEkins GillianBrandt LianneHuber Robert JLehmann Hugo - Angiogenesis is a hallmark of lung adenocarcinoma (LUAD) and a leading cause of mortality. Identifying potential therapeutic targets that modulate this process is of critical clinical importance. Here, we established a 12-gene risk-scoring model through bioinformatics screening and systematically delineated the molecular function of H2AC19, a previously poorly understood histone variant within this signature. Analysis of human LUAD specimens revealed elevated H2AC19 expression, which correlated positively with angiogenesis markers and advanced clinical stage and negatively with patient prognosis. Functional validation using CRISPR/Cas9 in patient-derived organoids (PDOs), cell models and xenografts demonstrated that H2AC19 promotes angiogenesis and tumor growth. Mechanistically, H2AC19 recruits p300 through its amino acid residues 24-88 to specifically augment H3K27 acetylation at the EGR1 promoter region, thereby triggering EGR1 transcriptional activation and subsequently promoting MMP-1-driven angiogenesis and progression of LUAD. Furthermore, we evaluated the therapeutic potential of lipid nanoparticles (LNP)-encapsulated siRNA targeting H2AC19, which significantly suppressed angiogenesis and LUAD progression. Collectively, our findings establish a critical role for H2AC19 in governing angiogenesis and highlight its potential as a promising therapeutic target for LUAD. - Source: PubMed
Publication date: 2026/07/08
Zuo FuwenYu JinlongLiu TongLiu XiaoruiYin JilongDing PengzhongPang YuhanLuo ZhengdongWang XiaofengGuo LingZhang YirongQi ShuangDu LutaoWang ZiyingYi FanZhang Xiaoshi