ELK1

Last update 08 May 2025

Basic Info

Synonyms

ELK1, ETS domain-containing protein Elk-1, ETS transcription factor ELK1

Introduction

Transcription factor that binds to purine-rich DNA sequences (PubMed:10799319, PubMed:7889942). Forms a ternary complex with SRF and the ETS and SRF motifs of the serum response element (SRE) on the promoter region of immediate early genes such as FOS and IER2 (PubMed:1630903). Induces target gene transcription upon JNK and MAPK-signaling pathways stimulation (PubMed:7889942).

100 Clinical Results associated with ELK1

100 Translational Medicine associated with ELK1

0 Patents (Medical) associated with ELK1

2,065

Literatures (Medical) associated with ELK1

01 Dec 2025·Molecular Biology Reports

STAT-3, ELK-1, and c- Jun contributes IL-6 mediated ADAMTS-8 upregulation in colorectal cancer

Article

Author: Sav, Feyza Nur ; Keskin, Saliha Derya ; Eroğlu, Kübra Paspal ; Alper, Meltem ; Köçkar, Feray ; Keleş, Yasemin

BACKGROUNDADAMTSs are extracellular matrix metalloproteinases that mainly process extracellular matrix components and closely related tumorigenesis. ADAMTS-8 is an anti-angiogenic member of the family and is dysregulated in common cancers. The tumor suppressor function of the ADAMTS-8 has been demonstrated in colorectal cancer. Although ADAMTS-8 plays a critical role in tumor progression, transcriptional regulatory features haven't been studied yet.MATERIALS AND METHODSThe human ADAMTS-8 promoter was cloned into the pMetLuc Reporter vector. Basal promoter activity and the effect of the IL-6 on ADAMTS-8 promoter activity were determined by transient transfection assays in SW480 cells. QRT-PCR and Western blot analyses assessed the impact of IL-6 on ADAMTS-8 mRNA and protein expressions. Functional binding of the specific transcription factors to the ADAMTS-8 promoter region was evaluated by ChIP qPCR and EMSA.RESULTSOur results demonstrated that the ADAMTS-8 promoter includes multiple binding sites for transcription factors that could be activated in the inflammatory pathways. IL-6 stimulation increased ADAMTS-8 promoter activity, also mRNA, and protein expressions. Pathway inhibition studies showed that IL-6-mediated induction of ADAMTS-8 was achieved through p38/MAPK, NF-κB, PI3K, and SAPK/JNK pathways. STATs, Elk-1, and c-Jun functionally bind to the ADAMTS-8 promoter region.CONCLUSIONIt can be concluded that inflammation is a strong positive regulator of the ADAMTS-8 gene.

01 May 2025·International Journal of Biological Macromolecules

Host genetic variation governs PCV2 susceptibility through CXCL13 and ELK1-mediated immune regulation

Article

Author: Shu, Yuelong ; Zhou, Zhong-Wei ; Cheng, Yijun ; Yang, Na ; Jiang, Yunliang ; Wang, Wenlei ; Liu, Gen ; Gao, Yizhen ; Sun, Yi ; Wu, Yan ; Sun, Litao ; Gao, Feng ; Li, Xiang

Pathogenic viruses can drive evolutionary adaptations in host biology, leading to diversified immune responses and variable susceptibility among individuals. This study examined how genetic variation in host regulatory regions impacts susceptibility to viral infections. Utilizing a porcine model, we identified the single nucleotide polymorphism (SNP) g.-1014G>A as a critical determinant of CXCL13 expression levels following PCV2 viral exposure. Structural analyses showed that the transcription factor ELK1 specifically recognized and bound to the g.-1014G allele, but not to the g.-1014A allele, through essential residues such as Arg65. This allele-specific binding led to differential CXCL13 expression, with the G allele associated with increased resistance to viral infection. Functional studies demonstrated that CXCL13 played a multifaceted role in antiviral immunity, including the inhibition of viral replication, modulation of immune-related pathways, and attenuation of virus-induced apoptosis. The CXCL13-mediated response involved the activation of the PI3K/Akt pathway, enhancing cell survival during viral challenges. This SNP-dependent regulation of a host factor represented a novel mechanism underlying genetic differences in viral susceptibility, with potential implications for developing broadly applicable antiviral strategies.

01 Apr 2025·Cancer Letters

CircMFN2/miR-361-3p/ELK1 feedback loop promotes glutaminolysis and the progression of hepatocellular carcinoma

Article

Author: Qiao, Liang ; Xie, Chenxi ; Wang, Xiaoqian ; Hao, Xiaopei ; Cui, Hong ; Li, Qingjun ; Han, Feng ; Qian, Xiangjun ; Wan, Baishun ; Yu, Haibo ; Wang, Zhengzheng ; Ji, Yang ; Zhang, Xiaokai ; Zhuang, Hao ; Wang, Li ; Yang, Nanmu ; Zhou, Jinxue

Current evidence indicates that circRNAs are involved in the development of multiple malignancies including hepatocellular carcinoma (HCC). However, the specific functions of circRNAs in HCC metabolism and progression and their underlying regulatory mechanisms remain unclear. We have identified a novel circRNA circMFN2, by bioinformatics analysis of circRNA microarray data from the GEO database. The levels of circMFN2 were assessed in HCC cell lines and tissues, and its clinical relevance was assessed. The effect of circMFN2 on HCC cells was evaluated in vitro and in vivo. The effect of ELK1 on glutaminolysis and HCC progression was also explored. Patients with HCC and high circMFN2 expression exhibited worse survival outcomes. Functionally, downregulation of circMFN2 repressed the proliferation, invasion, and migration of HCC cells in vitro, whereas ectopic expression of circMFN2 had the opposite effects. The effects of tumor enhancement by circMFN2 on HCC were confirmed by in vivo experiments. Mechanistically, circMFN2 acted as a sponge for miR-361-3p, leading to the upregulation of its target ELK1, whereas ELK1 was enriched in the MFN2 promoter to enhance the transcription and expression of MFN2, indirectly leading to the upregulation of circMFN2. Additionally, we found that circMFN2 promotes glutaminolysis in HCC by increasing ELK1 phosphorylation. We concluded that circMFN2 facilitates HCC progression via a circMFN2/miR-361-3p/ELK1 feedback loop, which promotes glutaminolysis mediated by the upregulation of phosphorylated ELK1. Therefore, circMFN2 not only serves as a potential prognostic indicator, but it could also serve as a therapeutic target for HCC. Further studies are warranted.

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ELK1

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