Ask about this productRelated genes to: Meis3 Blocking Peptide
- Gene:
- MEIS3 NIH gene
- Name:
- Meis homeobox 3
- Previous symbol:
- -
- Synonyms:
- MRG2, DKFZp547H236
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2018-11-16
Related products to: Meis3 Blocking Peptide
Related articles to: Meis3 Blocking Peptide
- Esophageal squamous cell carcinoma (ESCC) demonstrates pronounced ethnic disparities, being prevalent in Asian populations. However, the genetic mechanisms underlying this disparity remain poorly understood. This study aims to characterise the functional contribution of the regulatory variant rs113671272 in alkylglycerone phosphate synthase (AGPS) to ESCC susceptibility and prognosis in Chinese cohorts. - Source: PubMed
Publication date: 2026/04/07
Fang XumengDeng JiayingLiu MingTan WenWang MengyunWu YuannaZhao Kuaile - Hypertrophic cardiomyopathy (HCM) is a prevalent genetic cardiac disorder characterized by myocardial hypertrophy and diastolic dysfunction. While traditionally attributed to sarcomeric mutations, recent studies have highlighted the pivotal contribution of immune dysregulation and stromal-immune interactions in its pathophysiology. However, the molecular drivers bridging structural remodeling and immune activation remain poorly defined. - Source: PubMed
Publication date: 2025/10/22
He JinchenZhou ZehuaKong DejunZhu HengLiu ChunmeiWang YuyuanWu TianqiChen JinfengLiao YanWu Qi - Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, with high molecular heterogeneity contributing to its poor prognosis. Among potential biomarkers, is associated with aggressive tumor behavior and poor patient outcomes. However, the transcriptional mechanisms governing expression in GC remain largely unexplored. This study aimed to systematically investigate the upstream regulatory landscape of and its role in tumor progression. By integrating multicohort transcriptomic data (n = 945), we inferred consensus transcriptional regulatory networks (TRNs) and identified six putative transcription factors (PRRX1, TWIST1, SNAI2, MEIS3, VENTX, and EGR2) as robust regulators of . The functional enrichment analysis revealed that these regulators are involved in the epithelial-mesenchymal transition (EMT) and extracellular matrix remodeling, key processes associated with tumor invasion and metastasis. Experimental validation using chromatin immunoprecipitation (ChIP) assays indicated the direct and differential binding of TWIST1 and SNAI2 to the promoter, supporting their roles as key regulators of expression in GC. Our findings provide a mechanistic link between expression and EMT transcriptional programs, offering insights into its association with a poor prognosis. By integrating bioinformatic predictions with experimental demonstration, this study not only improves our understanding of regulation but also provides a framework for dissecting the transcriptional networks governing aggressive tumor phenotypes. These results contribute to a broader understanding of GC progression and may inform future therapeutic strategies targeting EMT-related pathways in GC. - Source: PubMed
Publication date: 2025/05/11
Rohan PauloCruz Dos Santos EvertonAzevedo Pedro LeiteOliveira da Conceição JessicaAbdelhay ElianaBinato Renata - The AXL receptor tyrosine kinase is implicated in various cancers, and its expression is linked with poor survival and resistance to therapy. In this review, we overview the complexity of AXL receptor signaling, emphasizing the distinctions between the AXL isoforms. Recent studies have identified a third AXL isoform, AXL3, which lacks the growth arrest-specific 6-binding domains found in AXL1 and AXL2. This unique structure of AXL3 suggests alternative activation and signaling mechanisms. Activation of AXL1/2 typically occurs through ligand binding, dimerization, and phosphorylation, leading to downstream signaling via pathways including PI3K/AKT, MAPK/ERK, JAK/STAT, and NF-κB. Unlike other oncogenic kinases, in which overexpression and overactivation can be attributed to genomic alterations, AXL upregulation is generally caused by nongenetic mechanisms. Analysis of the promoter region of AXL3 reveals potential binding sites for transcription factors such as KLF16 and MEIS3, which are linked to oncogenic pathways. AXL signaling in cancer promotes cell survival, proliferation, migration, and immune evasion. Therefore, inhibiting AXL by therapeutic approaches has been explored with varying results. Elucidating the functions and regulatory mechanisms of the different AXL isoforms is imperative for developing effective targeted therapies that improve outcomes in AXL-driven cancers. - Source: PubMed
Eriksen Gjerstad MayAehnlich PiaGelebart PascalMc Cormack Emmet - Immune checkpoint blockade (ICB) therapies, particularly anti-PD-1, benefit only a limited subset of colorectal cancer (CRC) patients. G-protein signaling modulator 1 (GPSM1) is implicated in immunity and oncology, yet its role in regulating the CRC tumor microenvironment (TME) and contributing to anti-PD-1 resistance remains poorly understood. - Source: PubMed
Publication date: 2025/02/25
Chen YangJia HuiqingZhang XiangyanZhao HanXiao YujingLi NaYao YifanXing Xiaoming