Ask about this productRelated genes to: MSI2 antibody
- Gene:
- MSI2 NIH gene
- Name:
- musashi RNA binding protein 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q22
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-29
- Date modifiied:
- 2016-10-24
Related products to: MSI2 antibody
Related articles to: MSI2 antibody
- Neuroblastoma (NB) is the most common extracranial solid tumor in children and is characterized by marked clinical heterogeneity and poor prognosis. MYCN amplification drives NB tumorigenesis through epigenetic reprogramming and is frequently accompanied by a copy-number gain of the long arm of chromosome 17 (17q). Epigenetic dysregulation of enhancer landscapes-particularly large regulatory elements termed super‑enhancers (SEs), which are enriched for H3K27ac and bound by lineage-specific master transcription factors (TFs)-establishes distinct NB cellular identities and states. These SE domains demarcate oncogenes that function as critical regulators of cell proliferation and apoptosis. Therefore, SE-driven genes represent tumor vulnerabilities, offering selective therapeutic opportunities. - Source: PubMed
Publication date: 2026/05/16
Zhang XiYang YangZhang MengzhenFan KaisiHuang ZhaorongZhang YangKong LingkaiChen QinmingTan RongyingZhang ShimengYu DaiyueXiong XiaozheWu Kai - In vertebrates, two genes, Musashi1 (Msi1) and Musashi2 (Msi2), encode for highly similar Musashi protein paralogs. The Musashi proteins are known to bind to 3'-UTRs and control translation. In photoreceptor cells, the Musashi proteins promote the inclusion of photoreceptor-specific alternative exons by binding to the proximal downstream of their introns. While the Musashi proteins are expressed in various cell types, their role in regulating splicing appears to be confined to photoreceptor cells, where the two proteins have exceptionally high expression levels. To test if the photoreceptor-specific role of MSI1 and MSI2 in splicing is due to their expression levels in photoreceptor cells, we generated combined Msi1 and Msi2 knockouts that progressively reduced the number of Musashi alleles in photoreceptor cells. We analyzed the splicing of photoreceptor-specific exons in the Cc2d2a, Cep290, Prom1, and Ttc8 genes and the function of photoreceptor cells in the knockouts. We found that a single allele from either Msi1 or Msi2 is sufficient to maintain photoreceptor function and support high inclusion levels of the photoreceptor-specific exons. - Source: PubMed
Publication date: 2026/05/14
Jeong BohyeStoilov Peter - Cervical cancer (CC) remains a major cause of cancer-related mortality in women. This study aimed to clarify the oncogenic role and underlying mechanism of Importin-7 (IPO7), a nuclear transport protein, in CC progression. - Source: PubMed
Publication date: 2026/04/29
Zhou WanzhenXu QinyangQiu TianWang JuanChen JingJiang RongzhenTeng YinchengMa LiBai YunZhang Rui - To investigate the role and molecular mechanisms of the RNA-binding protein MATR3 in myocardial fibrosis of atrial fibrillation (AF). Expression of MATR3 and MSI2 in AF patients was analyzed using GEO datasets (GSE79768, GSE14975, GSE31821). Human atrial fibroblasts (HAFs) induced by Angiotensin II (Ang-II) were used as an in vitro cellular model of myocardial fibrosis. Expression and interactions of MATR3, METTL3, and MSI2 were validated by qRT-PCR and Western blot. The binding between MATR3 and METTL3 was confirmed by co-immunoprecipitation (Co-IP). The mA modification level of MSI2 mRNA was detected by methylated RNA immunoprecipitation (MeRIP-qPCR). Cell proliferation, migration, and fibrotic phenotypes were evaluated by CCK-8, EdU, scratch, and Transwell assays, as well as detection of fibrosis markers. An Ang-II-induced mouse model of atrial fibrosis was constructed, and the in vivo effects of MATR3 were verified by HE staining, Masson's trichrome staining, and molecular detection. Analysis of GEO datasets showed that both MATR3 and MSI2 were highly expressed in AF patients. Ang-II treatment significantly upregulated the expression of MATR3 in HAFs, while knockdown of MATR3 inhibited Ang-II-induced proliferation, migration, and pro-fibrotic phenotypic changes in HAFs (reducing the expression of α-SMA, collagen I/III). Mechanistically, MATR3 interacted endogenously with METTL3 and stabilized the METTL3 protein by inhibiting proteasomal degradation. METTL3 mediated the mA modification of MSI2 mRNA, enhancing its stability and promoting its expression. MSI2 exerted a pro-fibrotic effect by activating the Wnt/β-Catenin pathway. In vivo experiments confirmed that silencing MATR3 downregulated the expression of METTL3 and MSI2, inhibited the activation of the Wnt pathway, and alleviated Ang-II-induced atrial fibrosis in mice. MATR3 promotes myocardial fibrosis and exacerbates AF by regulating METTL3-mediated mA modification of MSI2 mRNA to activate the Wnt/β-Catenin pathway. Targeting MATR3 may represent a potential therapeutic strategy for AF. - Source: PubMed
Publication date: 2026/03/18
Wei ZihanLi JingDai PinjiQian ChengLi Xiaoli - Clonal hematopoiesis of indeterminate potential (CHIP) is a precursor condition characterized by the expansion of blood cell clones harboring somatic mutations originating in hematopoietic stem cells (HSCs). Since individuals with CHIP face a high risk of developing myeloid malignancies, targeting CHIP clones could provide a viable strategy for leukemia prevention. Despite its clinical significance, the mechanisms underlying CHIP predisposition and progression remain poorly understood. Recent genome wide association studies (GWAS) have identified several non-coding genetic loci that are strongly associated with CHIP; however, their underlying mechanisms still remain unknown. We hypothesize that risk variants in these non-coding loci modulate enhancer elements active in HSCs. To test this, we selected 1,374 non-coding variants from 51 loci associated for CHIP risk in the UK Biobank and screened them for regulatory activity using a Massively Parallel Reporter Assay (MPRA). We performed our lentiviral MPRA screen in MUTZ-3 cells, a human hematopoietic cell line relevant to HSCs, which express CD34 surface marker and are dependent on HSC-specific transcription factors. Using a MPRA library of ~73,000 constructs in CD34+ fraction of MUTZ-3 cells, we identified 87 variants representing 32 GWAS loci. We used targeted genome editing to demonstrate endogenous enhancer activity across 3 MPRA variants that affect the transcription of NKD2, FLT3, and MSI2. Our functional studies on MSI2 indicate that presence of higher levels of MSI2 mediated by CHIP risk allele enhances the clonal expansion of TET2 knockout hematopoietic stem and progenitor cells, providing a mechanistic link whereby non-coding genetic variants can influence the expansion of mutant CHIP clones. - Source: PubMed
Publication date: 2026/01/23
Nguyen TrieuJeejan JessicaIwasaki TakeshiKales SusanChakraborty JoyeetaYanase ChieShekhar ArunaKwasniak DominikaHegde AditiVoit RichardStengel KristyIto KeisukeTewhey RyanNandakumar Satish