Ask about this productRelated genes to: ETV3 antibody
- Gene:
- ETV3 NIH gene
- Name:
- ETS variant 3
- Previous symbol:
- -
- Synonyms:
- PE-1
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2016-10-05
Related products to: ETV3 antibody
Related articles to: ETV3 antibody
- - Source: PubMed
Publication date: 2026/04/28
Mansilla-Polo MiguelAndreu-Lapiedra RafaelValle Irene Luna-DelSuch-Taboada EsperanzaÉvole-Buselli Montserrat - The midnolin-proteasome pathway represents a crucial ubiquitin-independent protein degradation mechanism. However, its precise interactome, including both degradative substrates and nondegradative interactors, remains largely uncharacterized due to the limitations of conventional approaches. To address this, we developed a robust multiplexed photo-cross-linking platform for comprehensively profiling the midnolin interactome. This platform uniquely integrates two distinct chemical biology strategies: first, the genetic encoding of a photo-cross-linking unnatural amino acid into midnolin's Catch domain and second, the use of a residue-selective photo-cross-linker, enabling the covalent capture and subsequent proteomic profiling of protein-protein interactions. Using this platform, we successfully identified numerous midnolin interactors, including several newly identified degradative substrates (e.g., ETV3, JUN, PRKD1, FN3KRP) and multiple nondegradative binding interactors, significantly expanding its known interactome repertoire. Collectively, our research establishes an innovative platform for investigating the context-dependent interactome of the midnolin system. This platform offers unprecedented insights into midnolin's multifaceted roles in ubiquitin-independent degradation and diverse cellular processes. Furthermore, leveraging this platform to explore midnolin interactome across various biological contexts holds significant potential. It could accelerate the development of next-generation strategies for degrading pathogenic proteins and aid in the discovery of therapeutic targets, particularly for those undruggable targets that resist conventional ubiquitin-dependent approaches. - Source: PubMed
Publication date: 2026/03/12
Xu YaliZhao WensiFu JingjingLiu ZihaoNie Hui-JunZhang JunGuo JingliTan MinjiaChen Xiao-Hua - Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, yet the functional impact of noncoding variants on enhancer activity remains largely unexplored. In this study, we adapted and applied two high-throughput techniques, SNP-STARR-seq and Methyl-STARR-seq, to systematically evaluate the influence of 30,790 noncoding SNPs and more than 134,000 CpG sites on enhancer activity in primary and metastatic CRC cells. We identified 922 SNPs and 487 CpG-containing elements modulating enhancer activity in primary cells and found 3136 SNPs and 3008 methylation-sensitive elements with metastasis-specific regulatory effects. Multi-omics integration linked these variants to target genes, and CRISPR editing validated their roles in driving tumorigenic and metastatic phenotypes. Furthermore, we identified two CRC-specific hypermethylated loci, cg08640619 and cg25982657, as exceptional tissue-based early detection biomarkers (AUC > 0.96). Mechanistically, hypermethylation at cg08640619 disrupts RUNX2 binding, leading to inhibition of and . Our study provides a comprehensive platform for understanding how genetic and epigenetic variants disrupt transcriptional programs in CRC, offering insights into disease susceptibility and identifying potential diagnostic and therapeutic targets. - Source: PubMed
Publication date: 2026/02/20
Chen ErfeiYang QiqiDai HaoyangChen YixinZhang YihuiWang QianglongHou RongrongChen MingWang JieXie QianwenSun WenjuNing Yong-QiangFan LigangYan Jian - Dendritic cells (DCs) facilitate the maintenance of immunological tolerance in the steady state. We report that transcription factor Etv3 is preferentially expressed in mature DCs, including tissue-derived migratory DCs (migDCs), and facilitates their homeostatic maturation and CCR7-dependent migration. Mice with global or DC-specific deletion of Etv3 manifested the expansion of CD25 regulatory T (T) cells, spontaneous activation of conventional T cells, and multiorgan T cell infiltration. Etv3 deficiency exacerbated TLR7-driven systemic lupus erythematosus (SLE)-like disease, supporting the reported genetic association of human with SLE. Etv3-deficient migDCs up-regulated multiple costimulatory molecules, including OX40 ligand (OX40L/TNFSF4), whose blockade partially rescued the T cell abnormalities. These results identify Etv3 as an essential regulator of the tolerogenic function of DCs and implicate it in the regulation of human autoimmunity. - Source: PubMed
Publication date: 2026/02/12
Adams Nicholas MMartinez-Krams DanielEsteva EduardoRa Ai CAlexiou Allegra IliadiJin HuaYun Tae JinTellaoui Rayan SleimanMudianto TennyVollmer EmilyNovikova EkaterinaTan YanjunHuntley WilliamKrichevsky OlegDolgalev IgorIzmirly PeterBuyon Jill PMoreira Andre LLund Amanda WReizis Boris - - Source: PubMed
Publication date: 2025/11/15
Rallapalle VyshnaviToral-Orduno JenniferShukla BrindaGraham LaurenKole LaurenBhambhvani PradeepHarada ShukoSaha AditiBailey LucySokolowski DanielRavindran AishwaryaGoyal Gaurav