Elf3 antibody - middle region (ARP31639_P050)
- Known as:
- Elf3 (anti-) - middle region (ARP31639_P050)
- Catalog number:
- arp31639_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Elf3 antibody - middle region (ARP31639_P050)
Related genes to: Elf3 antibody - middle region (ARP31639_P050)
- Gene:
- ELF3 NIH gene
- Name:
- E74 like ETS transcription factor 3
- Previous symbol:
- ESX
- Synonyms:
- EPR-1, ESE-1, ERT
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-12
- Date modifiied:
- 2016-10-05
Related products to: Elf3 antibody - middle region (ARP31639_P050)
Related articles to: Elf3 antibody - middle region (ARP31639_P050)
- E74-like ETS transcription factor 3 (ELF3) has been implicated in various tumorigenesis and inflammatory diseases. However, its expression profile and role in lung adenocarcinoma (LUAD) remain poorly defined. In the present study, through comprehensive clinical and experimental analyses, we aim to clarify the association between overexpression in LUAD tissues and poor prognosis. Functional assays reveal that knockdown inhibits the proliferation, migration, and invasion of LUAD cells, while ELF3 overexpression enhances these functions. Pathway enrichment analysis indicates that ELF3 influences the metabolic processes of LUAD. Mechanistically, ELF3 exerts oncogenic effects by regulating the transcription of hexokinase 2 (HK2) and glucose transporter type 1 (GLUT1). High-throughput screening reveals that dacinostat, by targeting the active site of the ELF3 protein, attenuates the glycolytic, proliferative, and metastatic abilities of LUAD cells. Additionally, ubiquitin-specific peptidase 18 (USP18) strengthens the stability of the ELF3 protein and influences the malignant biological behavior of LUAD through ELF3. In conclusion, the USP18/ELF3/HK2 and USP18/ELF3/GLUT1 axes play critical roles in glucose metabolism, proliferation, and metastasis of LUAD cells. Dacinostat inhibits the malignant progression of LUAD by targeting ELF3, providing strong evidence for developing novel therapeutic strategies targeting ELF3. - Source: PubMed
Zeng YuYi YeranZhang QinfenLi LiZhao XiaoheJin HaixiaHuang ZiqiGuo ShiweiWang QiyuShen MengLi BaihuiYang LiliZhao Weipeng - Breast cancer remains a leading cause of cancer-related mortality in women, largely due to metastasis and treatment resistance. ELF3, an ETS transcription factor, has been linked to cancer progression; however, the mechanisms regulating its activity remain incompletely understood. ELF3 expression and its association with patient survival were analyzed using GEO datasets and the Kaplan-Meier Plotter platform. Functional studies were performed using ELF3 knockdown in breast cancer cell lines, followed by WST-1 assays and crystal violet staining. Protein-protein interactions were evaluated using co-expression analysis, immunofluorescence, split luciferase complementation, GST pull-down, and yeast two-hybrid assays. Cycloheximide chase assays were conducted to assess ELF3 protein stability. A panel of small molecules was screened to identify inhibitors of the ELF3-HSP27 interaction, and a lead compound was further validated using biochemical and functional assays. Antitumor activity was evaluated in a xenograft mouse model. High ELF3 expression was associated with poorer overall survival in breast cancer patients. HSP27 was identified as a binding partner that stabilizes ELF3 protein, thereby promoting breast cancer cell proliferation. A novel small-molecule inhibitor disrupting the ELF3-HSP27 interaction suppressed cancer cell growth in vitro and reduced tumor growth in vivo. The ELF3-HSP27 interaction represents a previously unrecognized contributor to breast cancer progression, and its disruption provides a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/05/08
Liu YiJung SehyunHwang Soo-YeonJo HyunjiBang YunjeeLee YunaShin Jae-HoNa YounghwaKwon Youngjoo - Exosomes are nanosized extracellular vesicles (30-150 nm) secreted by most cell types, carrying various biomolecules that reflect the physiological or pathological state of their cells of origin. Owing to their molecular diversity and stability in bodily fluids, exosomes have emerged as promising tools in precision medicine. Diabetic kidney disease (DKD), affecting approximately 30-40% of individuals with diabetes, remains the leading cause of end-stage kidney disease worldwide. Current diagnostic tools, including albuminuria and estimated glomerular filtration rate, lack sensitivity and specificity for early detection and dynamic monitoring of disease activity. Emerging evidence indicates that urinary exosomes derived from glomerular cells, particularly podocytes, provide an insight into intrarenal pathobiology, reflecting real-time cellular injury and key disease-associated changes. Given the central role of podocytes in maintaining the glomerular filtration barrier and their early involvement in DKD, podocyte-derived urinary exosomes hold potential and may enable earlier intervention and more personalized therapeutic strategies. Beyond their biomarker potential, exosomal protein and microRNA cargo such as Regucalcin, Elf3, PHYD1, miR-155, miR-21, miR-29, actively participate in key pathogenic processes, including inflammation, fibrosis, oxidative stress, and metabolic dysregulation, thereby contributing to DKD progression. This review synthesizes current evidence providing mechanistic insights on urinary exosomes and their cargo as emerging biomarkers in DKD, highlighting their translational potential in advancing precision nephrology. In addition, we also discuss the current challenges in clinical implementation of exosome-based biomarkers into routine clinical practice for the diagnosis of DKD. - Source: PubMed
Publication date: 2026/05/22
Haripriya VAnandh UrmilaDinda Amit KumarKalita Bhargab - Gallbladder cancer (GBC), an aggressive disease with limited treatment options, occurs mainly in low-income and middle-income regions of Asia and Latin America. We analysed whole-exome sequencing data from 262 GBC tumour-normal sample pairs from Chilean, Chinese, Indian, Japanese and South Korean patients to investigate differences in GBC mutation profiles according to geographic location and genetic ancestry. - Source: PubMed
Publication date: 2026/05/21
Gárate-Calderón ValentinaKumar RajivMarcelain KatherineZollner LindaBoekstegers FelixBarajas OlgaLoader DenisseRivera María TeresaMorales Erikde Toro GonzaloCaglevic ChristianShibata TatsuhiroLorenzo Bermejo Justo - Sepsis is a prominent cause of mortality worldwide, attributed to the overactivation of the immune system. Ginseng is a medicinal plant with strong biological effects, yet the mechanism underlying its limited bioavailability and robust biological activity remains poorly understood. Here, our data revealed that ginseng-derived vesicle-like nanoparticles (GDVLNs) exhibit high biocompatibility and can be rapidly absorbed and distributed to various extraintestinal organs. Moreover, GDVLNs effectively protect against multiple organ dysfunction caused by sepsis in an RNA-dependent manner, as evidenced by the retention of protection after protein degradation, but loss of protective effect following lipid extraction administration and RNA degradation. Furthermore, through de novo miRNA sequencing, we identified pgi-MIR6136a-p3 as the most abundant species-specific miRNA in GDVLNs. We found that GDVLNs deliver pgi-MIR6136a-p3 into macrophages, thereby alleviating sepsis-induced multiple organ injury. Mechanistically, pgi-MIR6136a-p3 derived from GDVLNs inhibits systemic inflammation against sepsis by directly targeting ELF3 and suppressing the activation of the NF-κB signaling. Lastly, we validated that GDVLNs-derived pgi-MIR6136a-p3 also suppresses ELF3/NF-κB signaling in human monocyte-derived macrophages. These findings reveal a novel molecular mechanism that GDVLNs derived pgi-MIR6136a-p3 regulate innate immunity across kingdoms and provide a promising translational therapeutic strategy for sepsis. - Source: PubMed
Publication date: 2026/05/20
Zhang Fang-LingWu Tian-ShengZhou Hong-BinMa JinWu Zhi-QingChen Sai-NanMa KeLi Yi-HaoChen Xiao-ShuTan Wan-YueWang Yuan-XingLiang Pian-PianZhao Xiao-ShanLiu Ke-XuanHuang Huan-Sen