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
- Airway epithelial cells contribute critically to the initiation of allergic airway inflammation via the release of alarmins such as interleukin-33 (IL-33). Nevertheless, the intracellular regulatory networks governing epithelial alarmin release remain inadequately defined. Although autophagy has been implicated in epithelial stress adaptation and the transcription factor early growth response 1 () is promptly induced upon allergen challenge, it remains uncertain whether contributes to IL-33 release as a representative indicator of epithelial activation through autophagy-associated processes. In this study, human bronchial epithelial BEAS-2B cells were exposed to house dust mite (HDM) extract. expression was manipulated using gain- and loss-of-function strategies. Autophagy-associated alterations were evaluated by monitoring LC3B, p62, and PI3K-III (Vps34) levels, together with immunofluorescence microscopy. IL-33 release into culture supernatants was quantified by ELISA as a functional readout of epithelial activation. Pharmacological interference with autophagy was employed to examine functional engagement. An HDM-driven murine model was utilized to assess in vivo correlates. Publicly accessible transcriptomic datasets were interrogated in an exploratory manner to characterize epithelial stress signatures linked to this axis. HDM treatment upregulated in airway epithelial cells, concomitant with autophagy-associated alterations and enhanced IL-33 release. Forced expression coincided with elevated LC3B-II levels, diminished p62 accumulation, and increased PI3K-III abundance, whereas silencing produced reciprocal effects. Pharmacological suppression of autophagy attenuated IL-33 release and inhibition of Class III PI3K blunted the overexpression-driven increase in IL-33 release. In HDM-challenged mice, colocalization of EGR1 and LC3B was observed in lung tissue sections. Exploratory transcriptomic profiling further suggested that allergen provocation may elicit a coordinated epithelial stress response characterized by inflammatory and metabolic pathway enrichment. The results show that is associated with epithelial autophagy-related alterations under allergic stimulation, and these changes are accompanied by augmented release of the alarmin IL-33. These observations support a conceptual framework wherein -linked autophagy-associated processes may contribute to epithelial stress responses during early inflammatory events in allergic airway disease. Elucidation of the precise molecular underpinnings and causal relationships awaits further investigation. - Source: PubMed
Publication date: 2026/09/25
Wang XinyangRen JieZhao YanLuo Zhengxiu - This study evaluated whether a protein-protein interaction (PPI) network-based approach can link in vitro exposure-induced gene expression signatures to human disease modules. - Source: PubMed
Publication date: 2026/09/26
Tomonaga TaisukeIida MidoriIzumi HirotoMorimoto ShinyaNakamura YukikoTakeshita Jun-IchiMorimoto ToshikiHigashi HidenoriYatera KazuhiroMorimoto YasuoNishida Chinatsu - Regular bathing is a common habit worldwide, yet bath additives have been characterized almost exclusively at the physiological level, while their molecular effects on human cells remain largely unexplored. We previously showed by RNA sequencing (RNA-seq) that the complex bath additive Karada Totonou ProBath (KTPB) induced the expression of and hyaluronic acid synthase genes in human keratinocytes and fibroblasts, which represent the vascular endothelial growth factor (VEGF)-producing side of the cutaneous angiogenic axis; whether the VEGF-receiving endothelium responds to KTPB was unknown. Here, human vascular endothelial cells were exposed to KTPB and profiled by RNA-seq, and cytotoxicity was assessed using resazurin and Hoechst assays. KTPB altered gene expression in a time-dependent manner, and the differentially expressed genes were classified into three clusters with distinct temporal profiles: a late-repressed cluster, a transiently induced cell cycle-associated cluster, and a late-induced cluster enriched for blood vessel development and VEGFA-VEGFR2 signaling. The angiogenesis-related genes , , and were markedly upregulated, peaking at 1-2 h. KTPB showed no detectable cytotoxicity in this cell model at any of the tested concentrations, which spanned the recommended use range. These results indicate that KTPB elicits an angiogenesis-associated transcriptional program in vascular endothelial cells without compromising viability and highlight transcriptomics' value for characterizing bath additives. - Source: PubMed
Publication date: 2026/09/01
Otani NorihiroNguyen Kieu D MMaehara KiyoshiWan JiaweiHirokawa AtsushiSugasawa Takehito - Life has evolved under continuous exposure to solar light, and the emergence of the eye during the Cambrian period is thought to have accelerated biological diversification. Beyond vision, light acts as a biological regulator of metabolism and tissue organization. To elucidate ocular disease mechanisms and develop new therapies, we have investigated how light is sensed by the eye and coupled to physiological and pathological responses. This review reexamines the eye as a photoreceptive organ and summarizes recent advances showing how light input governs retinal metabolism, refractive development, and visual restoration. First, we describe how retinal light reception is linked to oxygen-dependent metabolic control. As one of the most oxygen-demanding tissues, the retina relies on hypoxia-inducible factor (HIF) signaling to coordinate angiogenesis, mitochondrial metabolism, fibrosis, and neuronal survival. Beyond pathological neovascularization, disrupted light-metabolic coupling contributes to neurodegeneration and subretinal scarring. Screening of natural compounds identified HIF regulators with therapeutic efficacy, and optical approaches were developed to detect hypoxia-induced intraocular cytokines noninvasively. Second, we show that environmental light regulates ocular growth in ways beyond image formation. Violet light activates nonvisual photoreception via OPN5-expressing retinal ganglion cells, engaging an OPN5-EGR1 pathway that preserves choroidal thickness and suppresses axial elongation through coordinated retina-brain-choroid-sclera interactions. Third, we demonstrate that light itself becomes therapeutic through optogenetic visual restoration. Chimeric rhodopsins confer high-sensitivity light responsiveness to surviving inner retinal neurons and have recently entered first-in-human clinical evaluation for advanced retinitis pigmentosa. These findings establish photobiology as a unifying framework for translational ophthalmology. - Source: PubMed
Publication date: 2026/09/23
Kurihara Toshihide - Myocardial ischemia-reperfusion (I/R) injury is a major cause of cardiac dysfunction, but the mechanisms linking metabolic stress to regulated cardiomyocyte death remain incompletely defined. N6-methyladenosine (mA), the most abundant internal modification of eukaryotic mRNA, is installed by the methyltransferase-like 3 (METTL3)-containing writer complex and regulates RNA fate. Here, we investigated whether METTL3-mediated mA modification contributes to PANoptosis-like cardiomyocyte death during I/R injury. In mouse myocardial I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) models, global mA levels and METTL3 expression were markedly increased. Lactate accumulation was associated with p300-dependent H3K18 lactylation (H3K18la) enrichment at the promoter, suggesting a metabolic-epigenetic mechanism for METTL3 transcriptional upregulation. Functionally, METTL3 promoted PANoptosis-related death signaling, strengthened the association of ZBP1 with PANoptosis-related components, and aggravated infarction, adverse remodeling, and cardiac dysfunction, whereas METTL3 deletion or pharmacological inhibition with STM2457 was protective. Mechanistically, METTL3 enhanced mA modification of mRNA, thereby increasing EGR1 expression through YTHDF1-mediated translational regulation and IGF2BP2-mediated mRNA stabilization. EGR1 further activated transcription, and EGR1 restoration partially reversed the protective effects of METTL3 deficiency. These findings identify a lactate-H3K18la-METTL3-EGR1-ZBP1 axis that drives PANoptosis-like cardiomyocyte death and suggest METTL3 inhibition as a potential strategy against I/R-induced cardiac injury. - Source: PubMed
Publication date: 2026/09/21
Li LinnanGao JinfengZhang XiaoxueDai KunmingCheng HaoMa JianyingGe Junbo