Ask about this productRelated genes to: EGR1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: EGR1 Blocking Peptide
- Common regulatory and coding variants may influence type 2 diabetes (T2D) risk by altering gene regulation or protein function. Identifying these variants and their associations with disease risk may inform disease control strategies. This study prioritized candidate variants by integrating two-group comparative genotyping with in-silico structural and dynamic analyses. - Source: PubMed
Publication date: 2026/05/06
Rezaei Seyyed Amin SeyyedKohkalani MoeinMehri MaghsoudDerakhshan Sima MansooriZanchi Fernando BertonCaceres Rafael AndradeAmirfiroozi Akbar - Hepatic fibrosis induced by Schistosoma japonicum (S. japonicum) infection is a major global public health concern. Centrosomal protein 72 (CEP72), a key regulator involved in maintaining cellular architecture and integrity, is significantly upregulated during the progression of hepatic fibrosis; however, its specific biological function in this pathological process remains largely elusive. This study was designed to elucidate the novel biological role of CEP72 in liver fibrosis, with a particular focus on the pathogenesis of S. japonicum-induced hepatic fibrosis. - Source: PubMed
Publication date: 2026/05/05
Fang QianMei GuangboZhao XuejunXu WeijiaLi ShanshanWang YinanMao ZheZhang JiaxiLiu KejunFeng JiayiYang WenjuanQiu XuebingKuang NaJiang HongLi XiaoqingZhou RuiDong HuifenMing Zhenping - Acute kidney injury (AKI) is a fatal condition with high morbidity and mortality rates. Recent studies indicated that ferroptosis is implicated in the pathogenesis of AKI. This suggests that ferroptosis inhibitors deserve more attention as AKI therapeutic options. We explored the comparative effectiveness of liproxstatin-1 (Lip-1) and N- acetyl cysteine (NAC) in mitigating ferroptosis in lipopolysaccharides (LPS)- induced AKI. Herein, mice were exposed to a single intraperitoneal (IP) injection of 10 mg/kg LPS. They were treated either by 10 mg/kg Lip-1 or NAC (total 3 doses of each drug over 6 days). Serum urea, creatinine and malondialdehyde, along with tissue EGR-1, GPX-4 and iron, were assessed. Histological, immuno-fluorescence and ultrastructural studies were conducted as well. Our results elucidated that; Lip-1 possesses significant antiferroptotic effects that modulated the three cornerstones of ferroptosis; MDA, GPX-4 and iron. Additionally, it downregulated EGR-1 and PERK, and upregulated GB3P1, affecting the cellular pathways that relate ferroptosis to endoplasmic reticulum stress (ER stress), stress granules (SGs) formation and lysophagy. The antiferroptotic actions of NAC were less remarkable. In conclusion, our study presents a foundation for therapeutic options directed against ferroptosis in AKI, advocating application of Lip-1 or NAC, with a specific focus on Lip-1. - Source: PubMed
Publication date: 2026/05/02
Ibrahim Heba FThabet Eman HAssem SaraAbd El Mottelib Lobna M M AAbd El-Kader Sara BakrKhan Mohammed SaroshRostom Dina - Large vessel vasculitides (LVV), including giant cell arteritis (GCA) and Takayasu arteritis (TAK), share common features such as inflammation of large sized arteries but differ in several key aspects, including age of onset and pathogenic mechanism. This narrative review gives an update of recent insights into pathogenesis of GCA and TAK, and discusses emerging targeted therapies based on these insights. It highlights omics-based signatures, ULK3 and SLAMF7 in GCA, EGR1 in TAK, alongside genetic and somatic risk factors such as clonal haematopoiesis (DNMT3A/TET2) linked to relapse and ischaemic vision loss in GCA, and the IL6R-p.Asp358Ala variant as a predictor of reduced interleukin (IL)-6 receptor blockade response. Common mechanisms include CD4⁺ T-cell, monocyte/macrophage, and B-cell infiltration with activation of IL-6, JAK/STAT/interferon, and IL-17 pathways. Giant cell arteritis is characterised by GM-CSF-driven macrophages and disrupted programmed cell death (PD)-1/PD-L1 checkpoint regulation, while TAK shows dominance of CD8⁺ T cells and tumour necrosis factor (TNF)-α signalling. Interleukin-6 receptor inhibitors (e.g., tocilizumab) show robust efficacy in GCA but with notable non-responders; the JAK inhibitor upadacitinib demonstrated efficacy in a Phase III study, whereas IL-17 blockade (secukinumab) yielded inconsistent results. In TAK, TNF inhibitors and tocilizumab are comparably effective; early data suggest Janus kinases (JAK) inhibitors promote remission, imaging improvement, and glucocorticoid sparing. Mavrilimumab (GM-CSF receptor blockade) is promising in GCA. Recent studies have increasingly focused on short-term glucocorticoid therapy in combination with biologic agents. Advances in biomarker research, including investigation of the IL-6 receptor and IL-17A gene polymorphisms, may enable more targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/04
Reisch MyriamThiel JensBosch Philipp - Human speech likely arose from regulatory changes for speech-related brain regions, yet causal variants and mechanisms remain unclear. is a prime candidate, showing specialized expression in vocal learning circuits of human and zebra finch brains and carrying a promoter deletion linked to autism spectrum disorder (ASD) with language dysfunction. Here, we perform integrative analyses with cross-species brain single-cell multi-omic data and the more complete genomes of the Vertebrate Genomes Project. We identify a human-specific CCG insertion in the promoter, creating a human-unique CCG-repeated motif. This motif is fixed in both archaic and modern humans but is disrupted by rare clinical variants that exhibit language-related phenotypes and autism. Binding motif models predicted, and reporter assays reveal that this human allele drives stronger -dependent transcription than its chimpanzee allele. Genome-wide, 107 other genes have core promoters with the identical motif; enriched for postsynapse and implicated in ASD, including . At the promoter, an ASD-causative CCG-repeated variant enhances -dependent promoter activity, and its activating effects are predicted in human brain regions using AlphaGenome. Our findings suggest that small variations in the number of CCG repeats in promoters can exert a large regulatory effect on complex traits and their associated disorders. - Source: PubMed
Publication date: 2026/04/24
Lee ChulDavenport Matthew HJarvis Erich D