EVI1 antibody - C-terminal region (ARP31659_P050)
- Known as:
- EVI1 (anti-) - C-terminal region (ARP31659_P050)
- Catalog number:
- arp31659_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- EVI1 antibody - C-terminal region (ARP31659_P050)
Related genes to: EVI1 antibody - C-terminal region (ARP31659_P050)
- Gene:
- MECOM NIH gene
- Name:
- MDS1 and EVI1 complex locus
- Previous symbol:
- MDS1, EVI1
- Synonyms:
- MDS1-EVI1, PRDM3, KMT8E
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-10
- Date modifiied:
- 2019-04-23
Related products to: EVI1 antibody - C-terminal region (ARP31659_P050)
Related articles to: EVI1 antibody - C-terminal region (ARP31659_P050)
- Congenital radioulnar synostosis (CRUS) is a forearm deformity caused by embryonic development disorder, characterized by limited forearm rotation, which can significantly impair patients' daily lives. The pathogenesis of CRUS has not been fully elucidated; with the advancement of whole-exome sequencing (WES) technology, a growing number of related gene mutations have been identified. - Source: PubMed
Publication date: 2026/02/26
Wang XiaoqingQu YuMa BingWang Hengbing - The gene MDS1 and EVI1 complex locus (MECOM) functions as a transcriptional regulator essential for development. Variants in MECOM have been recognized as pathogenic drivers, with well-established links to oncologic and hematopoietic disorders and increasing evidence for roles in cardiovascular diseases. Here, we examine the spectrum of MECOM variants and their connections to human diseases by integrating findings from genome-wide association studies (GWAS), expression quantitative trait loci (eQTL) analyses, and curated databases, together with single-case reports from whole-exome (WES) and whole-genome sequencing (WGS). Combining insights from both common and rare variants, we provide a comprehensive review of MECOM's genetic landscape and outline how specific alterations contribute to pathogenic mechanisms. We also highlight strategies targeting MECOM and the urgent need to investigate MECOM-associated single-nucleotide polymorphisms (SNPs) as both mechanistic drivers and potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/03
Chen JiayiVenkatesh AnirudhChen KaifuZhang Lili - Regulated in development and DNA damage response-1 (REDD1/DDIT4) is induced in response to environmental stress to restrain the mechanistic target of rapamycin complex 1 (mTORC1) signaling as an adaptive strategy to restore cellular homeostasis. Interestingly, REDD1/DDIT4 expression is upregulated in several tumor types including colorectal cancer, suggesting it may have a role in tumourigenesis. Here, we report that activating transcription factor 4 (ATF4)-dependent REDD1/DDIT4 expression is required for survival of colon tumor cells undergoing endoplasmic reticulum (ER) stress through the modulation of TRAILR2/DR5 gene expression. Our findings further demonstrate that resistance to ER stress-induced apoptosis in multicellular tumor spheroids (MCTS) is associated with constitutive expression of REDD1/DDIT4 and diminished mTORC1 activity. CRISPR/Cas9-mediated deletion of REDD1/DDIT4 markedly increases TRAILR2/DR5 expression and enhances apoptosis in spheroids exposed to ER stress. Interestingly, RNA sequencing analysis reveals that the loss of the transcriptional regulator EVI-1/MECOM in cells deficient in REDD1/DDIT4 amplifies the ER stress-induced upregulation of TRAILR2/DR5, leading to enhanced apoptosis. In summary, our findings underscore the crucial role of REDD1/DDIT4 in regulating TRAILR2/DR5-induced caspase-8 activation and apoptosis under chronic ER stress, by inhibiting mTORC1 activity and promoting EVI-1/MECOM-mediated suppression of TRAILR2/DR5 gene expression. - Source: PubMed
Publication date: 2026/03/28
Mora-Molina RocíoEl Yousfi YounesHagenlocher CathrinFernández-Farrán Francisco JavierRehm MarkusPalacios CarmenChristophorou Maria ALópez-Rivas Abelardo - - Source: PubMed
Birdwell Christine EFiskus WarrenMill Christopher PKadia Tapan MDaver NavalDiNardo Courtney DSasaki KojiDavis John ADas KaberiHou HanxiJain AntrixMalovannaya AnnaFlores Lauren BPourebrahim RasoulYuan SelinaSu XiaopingCeribelli MicheleBhalla Kapil N - Ecotropic viral integration site 1 (EVI1), encoded by the EVI1 gene on chromosome 3q26.2, is a dual-domain zinc finger transcription factor that functions as a potent proto-oncogene in a wide spectrum of hematological malignancies. Under normal physiological conditions, its expression is tightly regulated and restricted primarily to hematopoietic stem cells and specific embryonic tissues. However, aberrant overexpression of EVI1 is a hallmark of aggressive myeloid leukemias, including acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and the blast crisis of chronic myeloid leukemia (CML). The oncogenic activation of EVI1 occurs through diverse genetic mechanisms, most notably chromosomal rearrangements involving the 3q26 locus, such as inv(3)(q21q26.2) and t(3;3)(q21;q26.2), which juxtapose the EVI1 gene with potent enhancers like that of GATA2. Other mechanisms include the formation of oncogenic fusion genes (e.g., AML1-EVI1, ETV6-EVI1), enhancer hijacking, and retroviral insertional mutagenesis. Once overexpressed, EVI1 drives leukemogenesis through multifaceted molecular actions. It acts as a master transcriptional regulator, profoundly disrupting normal hematopoietic differentiation by repressing key lineage-specific transcription factors like RUNX1 and interfering with cytokine-induced maturation. Concurrently, EVI1 promotes cell survival and proliferation by modulating critical signaling pathways, including the potent inhibition of the tumor-suppressive TGF-β pathway and the activation of the pro-survival PI3K/AKT/mTOR cascade via PTEN suppression. EVI1 also cooperates with a multitude of other oncogenic lesions, such as MLL rearrangements, AML1 mutations, and activated RAS signaling, to accelerate disease progression. Clinically, EVI1 overexpression is one of the most robust independent indicators of poor prognosis, associated with therapy resistance and reduced overall survival. This review provides a detailed discussion of the mechanisms underlying EVI1's activation, its complex molecular functions in hematopoietic transformation, and its profound clinical implications in hematological malignancies. - Source: PubMed
Publication date: 2026/02/16
Hao YuchaoLiu JingLou JiachengYan Jinsong