EGR4
- Known as:
- EGR4
- Catalog number:
- Y213867
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- EGR4
Related genes to: EGR4
- Gene:
- EGR4 NIH gene
- Name:
- early growth response 4
- Previous symbol:
- -
- Synonyms:
- NGFI-C, PAT133
- Chromosome:
- 2p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-27
- Date modifiied:
- 2016-10-05
Related products to: EGR4
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- The polarization of tumor-associated macrophages (TAMs) toward an M2-like phenotype critically promotes acute myeloid leukemia (AML) progression. Building on the clinical observation that Caspase-1 (CASP1) expression is elevated in AML and correlates with M2 macrophage abundance, we identify a novel signaling axis in AML cells, involving CASP1 and the transcription factor early growth response protein 4 (EGR4), that orchestrates macrophage polarization. Knockdown (KD) of CASP1 in human AML cells (THP-1, MOLM-13) shifted their secretome, which consequently skewed macrophage polarization away from the M2 phenotype at multiple levels. Mechanistically, transcriptomic sequencing revealed that CASP1 KD significantly upregulated EGR4 expression. Crucially, EGR4 interference partially reversed the macrophage-polarizing effects of CASP1 KD, establishing EGR4 as an essential downstream effector. In a xenograft model using NOD/SCID mice—a defined system for studying human AML-macrophage crosstalk—CASP1 KD potently suppressed tumor growth. Immunohistochemical analysis revealed a remodeled microenvironment characterized by reduced proliferation (Ki67), upregulated EGR4, suppression of the M2-associated IL-10/p-STAT3 pathway and CD206, alongside a concomitant increase in M1-associated marker CD86. In conclusion, our integrated analysis delineates a novel AML cell-intrinsic pathway wherein CASP1 represses EGR4, thereby enabling an M2-like macrophage phenotype via the IL-10/p-STAT3 pathway. The identification of this CASP1-EGR4 axis identifies it as a promising therapeutic target for reshaping the immunosuppressive microenvironment in AML. - Source: PubMed
Publication date: 2026/02/27
Qian YiChen YueFeng Zu-XiZhu Xiao-FengZhang LiXiong HaoZhang Xiang-HuiBai JunLi Yan-HongWang Yu-XianLi Li-JuanZhang Lian-Sheng - Head and neck squamous cell carcinoma (HNSCC) exhibits a distinct sex disparity in incidence, with a higher incidence in males than females. Recent studies have suggested that this difference persists even after accounting for smoking and alcohol use, highlighting the need to elucidate the underlying biological mechanisms. In this study, we demonstrated that sex differences in HNSCC are androgen-dependent and identified androgen receptor (AR) signaling as a key regulator of the tumor immune microenvironment by modulating CD8⁺ T cell differentiation and function. Mechanically, early growth response 4 (EGR4) functioned as a direct downstream transcriptional effector of AR that induced CD8⁺ T cell dysfunction. Clinically, androgen deprivation therapy (ADT) was an effective therapeutic strategy in HNSCC, suppressing tumor growth in mice while improving intratumoral CD8⁺ T cell function. Moreover, combining ADT with immune checkpoint inhibitors led to improved antitumor efficacy. Together, these findings reveal ADT as a promising therapeutic approach to enhance the antitumor activity of sex-biased CD8⁺ T cells in HNSCC, which could inform the development of sex-biased immunotherapies for treating HNSCC patients. - Source: PubMed
Publication date: 2026/02/09
Wang QiyueTan ZhuoZheng ChuanmingXu JiajieLi QingHong ShiqinYu DilongHu XiaopingWang JiafengJiang LiehaoHuang PingZhang YiwenGe Minghua - Spermatogonial stem cells (SSCs) are essential for long-term spermatogenesis and hold therapeutic potential for treating male infertility. While rodent SSCs are well characterized, human SSCs remain poorly understood. Here, we screen antibodies against proteins encoded by genes enriched in specific subsets of human undifferentiated spermatogonia (uSPG) identified by single-cell RNA sequencing. We characterize four markers labeling distinct uSPG subsets: PIWIL4 marks primitive, quiescent uSPG; EGR4 marks uSPG at a proliferative crossroads; and PPP1R36 and NANOS3 label distinct proliferative subsets poised for differentiation. The most and least advanced subsets-PIWIL4+ and NANOS3+ cells-do not overlap. Comparative transcriptomics uncover candidate pathways involved in uSPG fate transitions, including RAS signaling. Using FSD1, a pan-uSPG cell-surface marker identified here, we purify the entire uSPG population and demonstrate that RAS signaling maintains the primitive uSPG state. These findings provide a framework for human uSPG identity, with broad implications for reproductive biology and regenerative medicine. - Source: PubMed
Publication date: 2026/01/23
Capponi ChiaraSmith ChristopherMedica AlexaHsieh Tung-ChinOrwig Kyle ETan Kun - Quick responses to viral infections, which are essential for controlling viral diseases, are typically mediated by interferons. Herpes simplex virus 1 (HSV-1) switches between lytic and latent infections in neurons. Here we show that host early growth response (Egr) genes (including Egr1-Egr4), which are not interferon-stimulated genes, are generally upregulated in HSV-1-infected neuronal cells and acutely infected mouse ganglia. Surprisingly, Egr1 upregulation is independent of previously reported pathways upstream of Egr1 expression but dependent on viral protein ICP0. EGR1, in turn, represses HSV-1 replication in neuronal cells. Recombinant HSV-1 expressing EGR1 exhibits reduced replication in mouse ganglia and brainstems in vivo. Mechanistically, EGR1 binds to sites within the viral latency-associated transcript (LAT) gene promoter to increase LAT expression, which is known to favor repression of viral lytic genes. Concurrently, EGR1 can stimulate the expression of host immune proteins IRF7 and ISG15, and IRF7 is required for the anti-HSV-1 function of EGR1. Interestingly, both EGR1 and IRF7 suppress HSV-1 replication independent of interferons. Furthermore, EGR2, EGR3, and EGR4 can enhance LAT and IRF7 expression too. In summary, EGR proteins are upregulated during HSV-1 infection and mediate interferon-independent antiviral responses through both viral and host targets. - Source: PubMed
Publication date: 2026/01/04
Wang ShuaishuaiHou FujunJin XunuoXiang YuhangPan Dongli - Propofol, a widely used intravenous anesthetic, has raised concerns regarding its potential neurotoxic effects on the developing brain. This study aimed to investigate the specific molecular mechanisms underlying propofol-induced neuronal damage during early development. Postnatal day 7 C57BL/6 J mice received a single intraperitoneal injection of propofol (50, 100, or 200 mg/kg) and hippocampal tissues were harvested 12 h post-exposure. Primary hippocampal neuronal cultures from mice embryos were exposed to propofol for 24 h. Genetic manipulations, including EGR4 and NPAS4 overexpression via plasmid transfection (in vitro) and adenovirus injection (in vivo), as well as NPAS4 knockdown using siRNA, were employed. Assessments included histopathology, apoptosis, cell viability, gene/protein expression, and transcriptional regulation. Propofol administration induced dose-dependent hippocampal neuronal injury in neonatal mice. Both in vitro (primary neurons) and in vivo (hippocampal tissue), ectopic overexpression of EGR4 via genetic manipulation significantly attenuated propofol-induced neurotoxicity. Mechanistically, EGR4 was found to directly bind to the NPAS4 promoter and positively regulate its transcription. Crucially, the anti-apoptotic effect of EGR4 overexpression was abolished upon NPAS4 knockdown. Our findings reveal a novel EGR4/NPAS4 transcriptional cascade through which propofol exerts its neurotoxic effects in the developing brain. Propofol downregulates EGR4 expression, leading to reduced NPAS4 transcription and subsequent neuronal apoptosis. While this pathway represents one potential mechanism of propofol-induced developmental neurotoxicity, it identifies EGR4 and NPAS4 as potential targets for therapeutic strategies aimed at mitigating anesthetic-related neuronal injury in the vulnerable developing brain. - Source: PubMed
Publication date: 2025/12/22
Han JingfeiCheng Hu