ETS_1
- Known as:
- ETS_1
- Catalog number:
- 000416A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ETS_1
Related genes to: ETS_1
- Gene:
- CNMD NIH gene
- Name:
- chondromodulin
- Previous symbol:
- MYETS1, LECT1
- Synonyms:
- CHM-I, CHM1, BRICD3
- Chromosome:
- 13q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-18
- Date modifiied:
- 2016-10-20
- Gene:
- ETS1 NIH gene
- Name:
- ETS proto-oncogene 1, transcription factor
- Previous symbol:
- EWSR2
- Synonyms:
- FLJ10768, ETS-1
- Chromosome:
- 11q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- ST11 NIH gene
- Name:
- suppression of tumorigenicity 11 (pancreas)
- Previous symbol:
- -
- Synonyms:
- PETS1
- Chromosome:
- 3p
- Locus Type:
- phenotype only
- Date approved:
- 1998-10-14
- Date modifiied:
- 2011-02-10
Related products to: ETS_1
Adenovirus E1A enhancer-binding protein,E1AF,E1A-F,ETS translocation variant 4,ETV4,Homo sapiens,Human,PEA3,Polyomavirus enhancer activator 3 homolog,Protein PEA3Bos taurus,Bovine,E74-like factor 1,ELF1,ETS-related transcription factor Elf-1Bos taurus,Bovine,E74-like factor 5,ELF5,ETS-related transcription factor Elf-5Bos taurus,Bovine,EHF,ETS domain-containing transcription factor,ETS homologous factorBos taurus,Bovine,ETS translocation variant 1,ETV1Bos taurus,Bovine,ETS2,Protein C-ets-2Bovine E74-like factor 1 (ets domain transcription factor) (ELF1) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine E74-like factor 5 (ets domain transcription factor) (ELF5) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine ets homologous factor (EHF) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine ETS homologous factor(EHF) ELISA kitBovine ETS homologous factor(EHF) ELISA kit SpeciesBovineBovine ETS translocation variant 1(ETV1) ELISA kitBovine ETS translocation variant 1(ETV1) ELISA kit SpeciesBovineBovine ets variant 1 (ETV1) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine ets variant 6 (ETV6) ELISA kit, Species Bovine, Sample Type serum, plasma Related articles to: ETS_1
- It remains unclear whether super-enhancers (SEs) can drive expression of circular RNAs (circRNA) in gastrointestinal cancers (GI cancers). We first identified circRREB1 as a novel SE-driven circRNA in GI cancers and HNRNPL as the RNA binding protein controlling circRREB1 biogenesis. Indeed, SE-driven HNRNPL leads to high circRREB1 expression in GI cancers, which is regulated by transcription factor MAZ. circRREB1 could promote invasion and metastasis of cancer cells in vitro and in vivo. Mechanistically, circRREB1 binds to the SRSF3-XRN1-YTHDC2 complex in cytoplasm, destabilizes the mA-modified CD44 mRNAs, and, thus, enhances metastasis of cancer cells. Consistently, high circRREB1 levels in malignant tissues are associated with poor patient prognosis. Although showing no impacts on tumor growth in nude mice, circRreb1 accelerates tumor proliferation in immunocompetent mice. Interestingly, circRreb1 elevates Ets1 expression through a competing endogenous RNA mechanism, up-regulates Cxcl2 expression and secretion, drives myeloid-derived suppressor cells (MDSCs) infiltration to tumors and contributes to formation of immunosuppressive tumor microenvironments. In line with this, depletion of MDSCs abrogates the oncogenic effects of circRreb1 in vivo. Notably, circRREB1 silencing synergizes with anti-PD1 therapy to activate antitumor immunity, offering novel insights into circRNA-mediated cancer epigenetics and promising therapeutic targets. - Source: PubMed
Publication date: 2026/05/15
Zhang LongYu XinyuanGong ChenglongHan LinyuLi CanZhang XuetingHan PengxiaoYang YantingHuo YanfeiZhang NashaYang Ming - Following acute viral infection, naïve CD4+ T cells differentiate into T helper 1 (Th1) and T follicular helper (Tfh) cells. The transcription factor Ets1 represses Tfh cell formation and function following protein immunization; however, whether Ets1 regulates Tfh differentiation in viral infection is unclear. Here, we demonstrate that during acute viral infection, conditional deletion of Ets1 in CD4+ T cells impairs germinal center (GC) Tfh differentiation and function, resulting in diminished GC B-cell responses, reduced IgG2c class switching, and impaired antibody production. Mechanistically, Ets1 deficiency results in aberrant upregulation of Blimp1 to negatively impact early Tfh and GC Tfh cell differentiation in a cell-intrinsic manner. Early Tfh differentiation is partially restored by knockdown of Blimp1 in Ets1-deficient T cells. In contrast, during protein immunization where Blimp1 is not highly expressed, Ets1 is not required to repress expression of CD25 and Blimp1 in early Tfh cells, and Ets1 deficiency results in a cell-intrinsic enhancement in GC Tfh differentiation. Collectively, these results demonstrate that Ets1 is a positive regulator of GC Tfh cell differentiation and function during viral infection, highlighting a context-dependent role for Ets1 in GC Tfh cell responses. - Source: PubMed
Perkins BryantFuchs BryceNguyen Nguyen XWilliams Matthew AHale J Scott - Cancer progression is influenced by the dynamic interplay between tumor cells and the surrounding stromal microenvironment. Therapy-induced senescence (TIS) of stromal fibroblasts represents a common outcome of anticancer treatments, contributing to tumor progression through the senescence-associated secretory phenotype (SASP). While SASP cytokines promote cancer malignancy, the contribution of secreted metabolites from senescent cells remains poorly understood. Here, we investigate the role of senescent stromal metabolism in regulating prostate and ovarian cancer cell invasion. Conditioned media (CM) from TIS-induced human prostate (HPFs) and ovarian fibroblasts (HOFs) promote enhanced invasion of cancer cells. Invasion is partially preserved after exposure to boiled CM, suggesting a role for heat-stable metabolic factors. Metabolomic profiling of senescent fibroblasts-derived CM reveals a significant increase in Glutamine (Gln) levels, identifying senescent stromal fibroblasts as a previously unrecognized source of extracellular Gln in the tumor microenvironment (TME). Exposure of cancer cells to senescent CM increases Gln uptake, together with upregulation of the transporter SLC1A5 and increased intracellular Gln. This metabolic adaptation is associated with increased malignant phenotype including epithelial-to-mesenchymal transition (EMT) and stemness features. Extracellular Gln depletion, pharmacological inhibition of glutaminase-1 (GLS1) in cancer cells, or Gln synthetase (GS) silencing in fibroblasts markedly impair senescent fibroblasts CM-induced invasion, EMT markers expression, and stemness features in cancer cells. Stromal-derived Gln is associated with increased cancer cell invasion through activation of a redox-dependent NRF2/ETS1 signaling axis. Analysis of patient-derived transcriptomic datasets further suggests chemotherapy-associated upregulation of Gln metabolism and expression. These findings identify senescent stromal-derived Gln as a key metabolic driver of prostate and ovarian cancer aggressiveness and reveal a TIS-associated metabolic vulnerability that could be explored in future preclinical studies. - Source: PubMed
Publication date: 2026/04/24
Lori GiuliaMancini CaterinaPaffetti CaterinaDesideri DayanaPranzini EricaSanti AliceLeri ManuelaBiagioni AlessioBenelli MatteoSpatafora PietroManicone Fedele MariaSorbi FlaviaLeo AngelaFambrini MassimilianoSerni SergioMagherini FrancescaTaddei Maria Letizia - Recent studies have advanced understanding of chromosomal organization and its role in gene regulation, yet most analyses focus on short-range interactions (<2 Mb), limiting insight into broader architecture. The relationships between topologically associating domains (TADs), sub-TAD loops, cross-TAD interactions, and chromosomal compartmentalization remain poorly understood. Here, using high-resolution Hi-C analysis, we identify extensive multi-megabase and interchromosomal interactions (metaloops) in T lymphocytes that organize into meta-TAD associations (metadomains). These metaloops connect distal promoters and regulatory elements of genes functionally important in T cells, including Ctla4, Ikzf2, Il2ra, Ets1, and Foxo1. Reanalysis of mouse and human datasets confirms their reproducibility and dependence on superenhancers. Genome-wide clustering reveals three distinct interchromosomal hubs, including a superenhancer-enriched hub linked to T cell-specific gene activation. Integrative analysis of regulatory genomics data identifies factors associated with short- versus long-range interactions. This study introduces a broadly applicable computational framework and reveals features of T cell genome organization. - Source: PubMed
Publication date: 2026/05/07
Dolsten GabrielWang Zhong-MinHuang XiaoSong SusieWilson Michael JBing Xin YangKe WenfanCafiero Thomas RNelson Amy NFernando SebastianPloss AlexanderSchedl PaulLevine Michael SViny Aaron DRudensky Alexander YPritykin Yuri - Clear cell renal cell carcinoma (ccRCC) is a common and aggressive form of kidney cancer with VHL mutations present in > 50% of cases. These mutations lead to dysregulation of hypoxia-inducible factors (HIFs) and activation of oncogenic pathways, making VHL-deficient ccRCC a challenging target for therapy. In this study, we identified cc-885, a molecular glue degrader, as a selective inhibitor of VHL-deficient ccRCC. cc-885 promotes ubiquitination and degradation of transcription factor ETS1, which cooperates with EPAS1 (HIF-2α) to drive tumorigenesis. We demonstrated that cc-885 selectively targeted the p51 and p42 isoforms of ETS1, disrupting p27/p51 balance and suppressing ETS1 transcriptional activity. Moreover, combining cc-885 with an EPAS1 inhibitor, belzutifan, significantly enhanced the anti-tumor efficacy. Our findings provide a novel and precise therapeutic strategy for VHL-deficient ccRCC by targeting ETS1 degradation and disrupting the ETS1-EPAS1 complex. - Source: PubMed
Publication date: 2026/05/06
Yang TaoweiLi QihaoYe KunLiu KezhiZhou MiChen MinyuLiao LicanHuang KangboWang ZhuDeng QiongWang JieyanJin MeiyuChen XuLiang HuiZhang JiaxingLuo Junhang