EDC3

Last update 08 May 2025

Basic Info

Synonyms

EDC3, enhancer of mRNA decapping 3, Enhancer of mRNA-decapping protein 3

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Introduction

Binds single-stranded RNA. Involved in the process of mRNA degradation and in the positive regulation of mRNA decapping. May play a role in spermiogenesis and oogenesis.

100 Clinical Results associated with EDC3

100 Translational Medicine associated with EDC3

0 Patents (Medical) associated with EDC3

Literatures (Medical) associated with EDC3

31 Dec 2025·Epigenetics

Normal bronchial field basal cells show persistent methylome-wide impact of tobacco smoking, including in known cancer genes

Article

Author: Gera, Shweta ; Spivack, Simon D ; Patel, Dhruv ; Marsh, Ava ; Shah, Chirag ; Peter, Yakov ; Khulan, Batbayar ; Dobkin, Jay ; Ye, Kenny ; Liao, Will ; Waldman, Spencer ; Okorozo, Aham ; Shi, Miao Kevin ; Sadoughi, Ali ; Vijg, Jan ; Siddiqui, Taha ; Desai, Aditi

Lung carcinogenesis is causally linked to cigarette smoking, in part by epigenetic changes. We tested whether accumulated epigenetic change in smokers is apparent in bronchial basal cells as cells of origin of squamous cell carcinoma. Using an EM-seq platform covering 53.8 million CpGs (96% of the entire genome) at an average of 7.5 sequencing reads per CpG site at a single base resolution, we evaluated cytology-normal basal cells bronchoscopically brushed from the in situ tobacco smoke-exposed 'bronchial epithelial field' and isolated by short-term primary culture from 54 human subjects. We found that mean methylation was globally lower in ever (former and current) smokers versus never smokers (p = 0.0013) across promoters, CpG shores, exons, introns, 3'-UTRs, and intergenic regions, but not in CpG islands. Among 6mers with dinucleotides flanking CpG, those containing CGCG showed no effect from smoking, while those flanked with TT and AA displayed the strongest effects. At the gene level, smoking-related differences in methylation level were observed in CDKL1, ARTN, EDC3, CYP1B1, FAM131A, and MAGI2. Among candidate cancer genes, smoking reduced the methylation level in KRAS, ROS1, CDKN1A, CHRNB4, and CADM1. We conclude that smoking reduces long-term epigenome-wide methylation in bronchial stem cells, is impacted by the flanking sequence, and persists indefinitely beyond smoking cessation.

01 Mar 2025·Veterinary Microbiology

EDC3 protein of P-body suppresses PRRSV proliferation and functions by upregulating MyD88

Article

Author: Li, Changhong ; Wang, Yiran ; Deng, Qiaomu ; Wen, Guilan ; Yang, Hongxing ; Hu, Xuan ; Zhao, Jing

Porcine reproductive and respiratory syndrome virus (PRRSV) causes significant economic losses to the swine industry worldwide. Despite numerous studies on this virus, the molecular mechanisms underlying PRRSV infection remain unclear. Enhancer of mRNA decapping 3 (EDC3) is a crucial scaffold protein for P-body assembly that stimulates mRNA decapping by alleviating self-inhibition of the DCP1/2 decapping complex. In this study, we investigated the impact of EDC3 on PRRSV proliferation, as well as its influence on three key adaptor proteins of the innate immune system: Toll-like receptor interleukin-1 receptor domain-containing adaptor inducing interferon-β (TRIF), mitochondrial antiviral signaling protein (MAVs), and myeloid differentiation factor 88 (MyD88). Western blotting and quantitative real-time PCR assays showed that EDC3 overexpression in both Marc-145 and PAM-CD163 cells significantly inhibited transcription of the PRRSV N gene and expression of the N protein. Conversely, knockdown of EDC3 expression in these cells significantly promoted the transcription of the PRRSV N gene and expression of the N protein. Furthermore, our results demonstrated that EDC3 overexpression significantly enhanced the expression of MyD88, whereas the inhibition of EDC3 expression led to a reduction in this process. In contrast, EDC3 did not effectively promote the increase in protein levels of TRIF and MAVs. In conclusion, the P-body EDC3 protein suppresses PRRSV proliferation and function by upregulating MyD88. This work is the first to report the mechanism of action of EDC3 against PRRSV, providing ideas for studying antiviral innate immunity.

01 Nov 2024·Molecular Biology of the Cell

Med13 is required for efficient P-body recruitment and autophagic degradation of Edc3 following nitrogen starvation

Article

Author: Friedson, Brittany ; Hanley, Sara E. ; Cooper, Katrina F. ; Willis, Stephen D.

The Cdk8 kinase module (CKM), a conserved, detachable unit of the Mediator complex, plays a vital role in regulating transcription and communicating stress signals from the nucleus to other organelles. Here, we describe a new transcription-independent role for Med13, a CKM scaffold protein, following nitrogen starvation. In Saccharomyces cerevisiae, nitrogen starvation triggers Med13 to translocate to the cytoplasm. This stress also induces the assembly of conserved membraneless condensates called processing bodies (P-bodies) that dynamically sequester translationally inactive messenger ribonucleoprotein particles. Cytosolic Med13 colocalizes with P-bodies, where it helps recruit Edc3, a highly conserved decapping activator and P-body assembly factor, into these conserved ribonucleoprotein granules. Moreover, Med13 orchestrates the autophagic degradation of Edc3 through a selective cargo-hitchhiking autophagy pathway that utilizes Ksp1 as its autophagic receptor protein. In contrast, the autophagic degradation of Xrn1, another conserved P-body assembly factor, is Med13 independent. These results place Med13 as a new player in P-body assembly and regulation following nitrogen starvation. They support a model in which Med13 acts as a conduit between P-bodies and phagophores, two condensates that use liquid-liquid phase separation in their assembly.

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