EGR2 antibody - C-terminal region (P100880_P050)
- Known as:
- EGR2 (anti-) - C-terminal region (P100880_P050)
- Catalog number:
- p100880_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- EGR2 antibody - C-terminal region (P100880_P050)
Related genes to: EGR2 antibody - C-terminal region (P100880_P050)
- 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 antibody - C-terminal region (P100880_P050)
Related articles to: EGR2 antibody - C-terminal region (P100880_P050)
- Rare earth elements (REE), such as gadolinium (Gd) and erbium (Er), are increasingly recognised as emerging environmental contaminants due to their widespread use in industrial processes, electronics, and medical imaging applications. Despite their extensive presence in aquatic ecosystems, little is known about their developmental toxicity. In this study, embryos were exposed to environmentally relevant concentrations of Gd and Er during critical early developmental stages. The assessed endpoints included survival, malformations, growth (body length), and heart rate. Both Gd and Er caused significant sublethal effects, including increased axial malformations, reduced growth, and altered cardiac activity. To explore potential mechanisms of toxicity, the expression patterns of key developmental genes (, , , , , ) and pro-inflammatory cytokines (, , ) were analysed using Real-Time PCR. The results showed dysregulation of gene expression, indicating disruption to pathways involved in morphogenesis and neurodevelopment. Elevated reactive oxygen species levels suggested that oxidative stress was a contributing factor. Raman spectroscopy confirmed biochemical changes affecting proteins, lipids, and nucleic acids, providing evidence of cellular stress and metabolic imbalance. Overall, our findings demonstrate that even low-level exposure to Gd and Er can impair amphibian embryonic development and disturb molecular homeostasis. These results emphasise the ecological risks of REE pollution and highlight the importance of ongoing environmental monitoring and long-term toxicological research. - Source: PubMed
Publication date: 2026/03/24
Fogliano ChiaraDi Marino SimonaRusciano GiuliaVignola FrancescaPetito AdrianaVenditti PaolaCretì PatriziaMotta Chiara MariaAvallone BiceScudiero RosariaCarotenuto Rosa - Tau neurofibrillary tangles are a hallmark of several neurodegenerative diseases called tauopathies, including frontotemporal dementia and Alzheimer's Disease. Ongoing clinical trials for tauopathies seek to reduce Tau in the brain through immunotherapy, antisense oligonucleotides, and siRNA. codes for Tau, therefore understanding how the gene is regulated and the effect of genetic variation at its regulatory elements is likely to have high relevance for tauopathies. We screened a ∼3 Mb region including the locus using 2 different massively parallel reporter assay (MPRA) strategies in KOLF2.1J h-NGN2 neurons and HEK293FT cells, identifying previously unannotated cis-regulatory elements (CREs). Using CRISPR interference (CRISPRi) in mixed neuron cultures, we identified a new CRE for , as well as 2 CREs for another nearby gene of interest, . Known genetic variation from the Alzheimer's Disease sequencing project was tested in a separate MPRA at the top CREs near the gene, identifying variants with altered regulatory effects including those at previously identified CREs for . Using a saturation mutagenesis screen of a 2,000 bp region encompassing the promoter, we assessed regulatory effects of each possible single nucleotide variant in this region. We identified several neuron-specific regulatory variant effects at this region, including a high confidence binding site for the transcription factors EGR2, ZBTB14, and TCLF5 at a region of high MPRA activity and genetic conservation. - Source: PubMed
Publication date: 2026/03/09
Hauser Rebecca MLimbo Henry LBrazell J NicholasMoyers Belle ALauzon Shelby NBarinaga Erin AJohnston S QuinnRogers Brianne BTaylor Jared WCochran J Nicholas - Serotonergic psychedelics have attracted considerable interest as promising therapeutic agents. However, the molecular mechanisms linking their acute hallucinogenic-like effects to longer-lasting neuroplastic responses remain incompletely understood, partly because of the scarcity of native neural models suitable for mechanistic studies. Here, we developed a neural stem cell-derived in vitro model capable of differentiating into neuronal and glial lineages and, after characterization, used it to investigate the molecular pharmacology of serotonergic psychedelics. A panel comprising tryptamines, phenethylamines and ergolines, including psychedelic compounds and selected non-psychedelic analogues, was evaluated alongside ketamine and TrkB agonists. Endpoints included dendritogenesis, synaptogenesis, immediate-early gene induction, BDNF expression and lactate production. TrkB silencing abolished dendritogenic responses to serotonergic psychedelics, ketamine and TrkB agonists, whereas 5-HT receptor silencing selectively impaired serotonergic psychedelic-induced plasticity and altered TrkB-dependent responses. Most serotonergic compounds also increased synaptogenesis and induced and expression, although ligand-specific differences were evident, particularly for psilocin and the phenethylamines DOI and Ariadne. Uncoupling of G or G protein-dependent signaling differentially modified neuroplastic and transcriptional responses, indicating a ligand and endpoint dependent contribution of both pathways. Serotonergic psychedelics further induced a 5-HT receptor dependent lactate response that was generally sensitive to disruption of either G or G protein coupling. Taken together, these findings support a model in which serotonergic psychedelics recruit an integrated 5-HT -TrkB signaling network with distinct structural, transcriptional and metabolic outputs, and establish this neural stem cell-derived system as a valuable platform for screening and dissecting the signaling basis of psychedelic action. - Source: PubMed
Publication date: 2026/03/23
Taddei-Tardón MarcoMedina-Rodríguez LidiaMaltman Jessica LHudson SarahPotukanuma SritanviJiménez Javier HidalgoMartín-Guerrero Sandra MGonzález-Maeso JavierLópez-Giménez Juan F - The basic leucine zipper ATF-like transcription factor 3 (BATF3) has been implicated in the pathogenesis of type 1 diabetes mellitus (T1DM), where it may influence immune regulation and pancreatic β-cell homeostasis. Nevertheless, the upstream molecular mechanisms governing BATF3 expression remain largely undefined. Bioinformatic analyses of GEO and UCSC databases were conducted to identify transcription factors potentially regulating BATF3 (GEO: GSE9006 PBMC microarray; newly diagnosed T1D, n = 43; healthy controls, n = 24). Clinical samples (PBMC, n = 30) from T1DM patients and healthy controls were analyzed by qPCR to assess BATF3 and candidate transcription factor expression. Lentiviral transduction and siRNA-mediated knockdown were applied to examine BATF3 regulation and its impact on CD8⁺ T-cell function. Transcription factor-promoter interactions were validated using dual-luciferase reporter assays and ChIP-qPCR. EGR1, EGR2, EGR3, and c-MYC were identified as differentially expressed transcription factors in GSE9006, with c-MYC emerging as the central regulator. Clinical analysis demonstrated significantly elevated expression of c-MYC and BATF3 in T1DM patients compared with healthy controls (n = 30, p < 0.05). In vitro assays confirmed that c-MYC binds to the BATF3 promoter region approximately 1-2 kb upstream of the transcription start site, thereby promoting BATF3 transcription, enhancing CD8⁺ T-cell proliferation, and inhibiting apoptosis (CD8⁺ T cells isolated from PBMCs of healthy children). ChIP-qPCR further localized the primary c-MYC binding site to the - 1,214 to - 1,203 bp region relative to the BATF3 transcription start site. c-MYC, a critical regulator of BATF3, is markedly elevated in T1DM patients. By driving BATF3 transcription, it promotes CD8⁺ T-cell expansion and limits apoptosis, jointly contributing to pediatric T1DM pathogenesis. These observations highlight the c-MYC-BATF3 axis as a mechanistic pathway relevant to pediatric T1DM and a potential biomarker framework. - Source: PubMed
Publication date: 2026/03/25
Zhao YingTang ZhichengTao YingZhao SihuiDing QijieYang Weixia - Excessive activation of interleukin-17-producing helper T (T17) cells can cause autoimmune tissue inflammation. However, how T17 cells enhance their pathogenicity within target tissues and whether destabilized regulatory T cells contribute to pathogenic T17 cell populations remain unclear. Using a T17 cell-dependent autoimmune arthritis model, we demonstrated that T17 and regulatory T cells did not undergo significant mutual plasticity, based on lineage-tracing and T cell receptor (TCR) repertoire analyses. Single-cell RNA sequencing of joint CD4 T cells revealed three phenotypically distinct T17 clusters, ranging from a CD103⁺ Tcf1 stem-like state to a CD200⁺ Egr2 highly pathogenic state. The phenotypic transition to the CD200⁺ pathogenic state was not a default progression driven by inflammatory cues, but rather a highly selective process mediated by tissue-restricted secondary TCR engagement within inflamed joints. Our findings delineate the heterogeneity and pathogenic potential of arthritogenic T17 cells, highlighting secondary autoimmune TCR signaling as a critical regulatory determinant of their developmental trajectories that may serve as a therapeutic target for autoimmune arthritis. - Source: PubMed
Publication date: 2026/03/23
Takeuchi YusukeOhara DaiyaWatanabe HitomiNishimura YujiIwasaki TakeshiHori ShoheiKawamoto HiroshiKato HirokiKondoh GenMorinobu AkioMimori TsuneyoHirota Keiji