PEA3 _ HIP EMSA Kit
- Known as:
- PEA3 _ HIP EMSA Kit
- Catalog number:
- AY1228
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PEA3 _ HIP EMSA Kit
Related genes to: PEA3 _ HIP EMSA Kit
- Gene:
- ETV4 NIH gene
- Name:
- ETS variant 4
- Previous symbol:
- -
- Synonyms:
- E1A-F, E1AF, PEA3
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-27
- Date modifiied:
- 2016-02-25
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- Colorectal cancer (CRC) remains a major health threat with poor prognosis in advanced stages. The transcription factor ETV4 (ETS translocation variant 4) has been implicated in various cancers, but its specific role, prognostic value, and mechanisms in CRC, particularly concerning the tumor immune microenvironment, are not fully understood. - Source: PubMed
Publication date: 2026/04/15
Meng RuipengWang ShilongShe ZhanfeiWang HuaimingWu BoQiao YuChen PengyuanNargerel Yang XiaofengWang Liang - CIC::DUX4 sarcoma (CDS) is a rare cutaneous and deep soft tissue tumor in the differential diagnosis of small round blue cell sarcomas. CDS, by definition, is negative for rearrangements in EWSR1, and has been reported to have strong nuclear WT1 expression and ETV4 expression in most published cases so far. We herein report a case of challenging CDS diagnosed by genomic profiling, with weak, focal cytoplasmic WT-1 positivity, positive staining for CD56, CD138 (subset), and CD4 (subset). This case highlights the challenges involved in evaluating cutaneous small round blue cell tumors based on morphology and immunohistochemistry alone, especially in the presence of an atypical immunophenotype. - Source: PubMed
Publication date: 2026/03/31
Jiang JaniceSay BrandonBrown RyanneRieger KerriCharville Gregory WNarala SaisindhuSaleem AtifNovoa Roberto - Pigs are one of the most important livestock species for providing meat products in the world. Deciphering the genetic architecture of feed efficiency-related traits is beneficial to improve the genetic progress of these traits and save the total cost of pork production. However, the genetic architecture of feed efficiency-related traits remains unclear. - Source: PubMed
Publication date: 2026/02/27
Lin ChangguangChen QiuyongLiu YaxuanCai WeiHuang TaoZhou YiLin JinyuZhou LunjiangChen Xinzhu - Colorectal cancer (CRC) lethality is largely driven by liver metastasis and the associated tumor microenvironment (TME). This study identifies ETS variant transcription factor 4 (ETV4) as a central integrator of oncogenic signaling, metabolism, and stromal remodeling. In CRC cells, hepatocyte growth factor (HGF)/MET signaling induces ETV4 via an ERK1/2-p65 pathway. ETV4, in turn, directly activates MET and asparagine synthetase (ASNS), creating a positive feedback loop that amplifies MET signaling and elevates intracellular asparagine (Asn). Tumor-derived Asn acts as a paracrine signal that induces inflammatory cancer-associated fibroblast (iCAF) like activation in hepatic stellate cells (HSCs) and promotes iCAF polarization in primary CAFs, leading to enhanced HGF secretion that further stimulates MET tumor cells. Genetic and pharmacologic disruption of this axis attenuates CRC growth and metastatic traits in vitro and in mouse models. Notably, combined inhibition of HGF/MET signaling and Asn metabolism produces greater antitumor activity than either monotherapy. Together, these data delineate an HGF/MET → ETV4 → MET/ASNS → asparagine → iCAFs and iCAF-like HSCs → HGF circuit that links signal amplification, metabolic reprogramming, and niche conditioning, and provide a rationale for therapeutic strategies co‑targeting HGF/MET and Asn pathways in advanced CRC. - Source: PubMed
Publication date: 2026/03/20
Fu DujiangZhang MeijiaCai MaopingWang MiaoHuang ZiaoLin ZeshengLiu YixinQian WangChen GuopengLiang YuxingWei DongyiXie JingYan PichengQu YuanyuanWei Yongchang - Enhancers, as cis-regulatory elements, play pivotal roles in transcriptional homeostasis. The abnormality in enhancers is highly associated with various diseases, including osteoporosis. However, the landscape of active enhancers underlying bone diseases remains incomplete. By conducting an integrative analysis of transcriptome and ChIP-seq data, we identify enh11 as an active enhancer during osteoblastogenesis. CRISPR/Cas9-mediated deletion of enh11 inhibits cell differentiation of pre-osteoblast MC3T3-E1 cells. The osteoblast-specific knockout of enh11 reduces bone formation and decreases bone mass in mice. In addition, Etv4 is identified as the downstream target of enh11. Functional experiments both in vitro and in vivo validate that Etv4 promotes osteogenesis and bone formation. Mechanistically, enh11 upregulates the expression of Etv4 to promote osteogenesis, probably via binding to the transcription factor Stat3. These findings not only deepen our comprehension of the molecular mechanisms of enh11 underlying bone formation but also highlight enh11 and Etv4 as promising therapeutic targets for osteoporosis. - Source: PubMed
Publication date: 2026/03/17
Zhang JunyouWang QilinCheng ZhuoyuLiu JiaxinLiu QianQi SihanChen ZhihengDuan YingyingLiu ZhaoshuoJia JieLi Chunyan