MYNN antibody - middle region (ARP33160_T100)
- Known as:
- MYNN (anti-) - middle region (ARP33160_T100)
- Catalog number:
- arp33160_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MYNN antibody - middle region (ARP33160_T100)
Related genes to: MYNN antibody - middle region (ARP33160_T100)
- Gene:
- MYNN NIH gene
- Name:
- myoneurin
- Previous symbol:
- -
- Synonyms:
- SBBIZ1, ZBTB31, ZNF902
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-26
- Date modifiied:
- 2016-10-24
Related products to: MYNN antibody - middle region (ARP33160_T100)
Related articles to: MYNN antibody - middle region (ARP33160_T100)
- Rearrangements involving MECOM at chromosome 3q26.2 are recurrent in myeloid neoplasms, classically represented by inv(3)(q21q26.2) and t(3;3)(q21;q26.2), which reposition the GATA2-distal haematopoietic enhancer and drive aberrant EVI1 overexpression. However, the full structural and mechanistic diversity of MECOM rearrangements (MECOM-r) is yet to be explored. We retrospectively analysed 97 cases with cytogenetically defined MECOM-r and identified 12 with complex rearrangements using GTG-banded karyotyping and tri-colour interphase/metaphase fluorescence in situ hybridisation analyses. These 12 cases demonstrated remarkable structural heterogeneity. The abnormalities encompassed translocations, inversions, insertions, duplications, and deletions, which often coexisted within the same specimen as multiple rearranged subclones. Insertional events emerged as a distinct mechanism of MECOM activation. These encompassed insertions of MYNN and/or MECOM into chromosomes 1 and 6, insertion of chromosome 8 segment into MECOM, and inverted insertions between homologous chromosome 3 segments. Recurrent breakpoints at 3q21 across multiple cases, together with localised copy number imbalances frequently involving the MYNN and GOLIM4 loci at 3q26.2, underscore the architectural fragility of these two regions. Co-occurring abnormalities such as -5/del(5q), -7/del(7q), and TP53 loss were common, reflecting a permissive genomic background for chromosomal reassembly. Our findings expand the mechanistic landscape of MECOM-r beyond canonical inv(3)/t(3;3), establishing 3q21 and 3q26.2 as structural 'hotspots' and genomic instability hubs. Distinct from fusion-driven oncogenes such as KMT2A, MECOM activation results from enhancer hijacking and regional structural remodelling, leading to EVI1 overexpression and clonal evolution in myeloid malignancies. - Source: PubMed
Publication date: 2026/07/03
Wang Jia-ChiOo EmmaEnriquez ElmonLivingston Nathan - This study aimed to investigate the role and mechanism of the transcription factor myoneurin (MYNN) in the pathogenesis of pulmonary arterial hypertension (PAH). In vitro, hypoxia-treated human and mouse pulmonary artery smooth muscle cells (PASMCs) exhibited reduced MYNN expression. Functional studies demonstrated that knockdown of MYNN promoted the proliferation and migration of PASMCs under normoxic conditions, whereas overexpression of MYNN effectively suppressed hypoxia-induced abnormal proliferation and migration of PASMCs. Mechanistically, MYNN directly binds to the promoter region of the PDLIM1 gene and promotes its transcription. Downregulation of MYNN led to decreased PDLIM1 expression, thereby releasing the inhibition on NF-κB and ultimately driving the pathological proliferation and migration of PASMCs. This study reveals MYNN/PDLIM1/NF-κB signaling axis in hypoxia induced PASMC proliferation and migration, and establishes MYNN functions as a protective transcription factor, thereby revealing a promising new therapeutic approach for PAH. - Source: PubMed
Publication date: 2026/08/06
Guo XinmengGao ChaoLi LingxueLi YutingFu JiaGong TingFeng FanCao ShukunFeng MingyueHuang YudiaoJiang XudongQi JingXing YanZheng Xiaodong - To investigate the effects of hexavalent chromium exposure on lncRNA TERC and its target genes MYNN and SERPINC1 in BEAS-2B cells, and their roles in hexavalent chromium-induced malignant transformation. In September 2022, BEAS-2B cells were treated with different concentrations of hexavalent chromium, and the mRNA expression levels of lncRNA TERC, MYNN and SERPINC1 were detected by qPCR. After knockdown or overexpression of lncRNA TERC via transfection, the cells were exposed to hexavalent chromium and the gene expression changes were measured. Long-term continuous exposure to 0.5 μmol/L hexavalent chromium was performed, and malignant phenotypes were assessed by morphological observation, wound healing assay, plate colony formation assay and soft agar colony formation assay. In malignantly transformed cells, the effects of lncRNA TERC knockdown or overexpression on target gene expression and cell migration were evaluated. For inter-group data comparisons, if the data follow a normal distribution with homogeneous variances, one-way ANOVA is employed, followed by pairwise comparisons using the SNK test. After 24 h exposure to 0.75 and 1 μmol/L hexavalent chromium, the mRNA expression levels of MYNN and SERPINC1 increased with the elevation of concentration (<0.05). After exposure to 0.5 μmol/L hexavalent chromium for 1-7 d, the expression levels of both genes showed an overall upward trend with prolonged duration. Knockdown of lncRNA TERC significantly decreased SERPINC1 expression (<0.05), while overexpression of lncRNA TERC elevated the expression of both MYNN and SERPINC1 (<0.05). After long-term exposure to 0.5 μmol/L hexavalent chromium for 60 passages, the cells exhibited malignant phenotypic changes, with increased 48 h migration rate (<0.05) and higher soft agar colony formation rate than the control group [ (0.20±0.04) vs (0.09±0.03), <0.05]. The expression of TERC remained higher than that of the control group throughout the exposure (<0.05). In malignantly transformed cells, the expression levels of MYNN and SERPINC1 were elevated (<0.05). Knockdown of TERC decreased the expression of both genes and reduced cell migration (<0.05), whereas overexpression of TERC markedly increased the expression of both genes (<0.05) . Hexavalent chromium exposure induces alterations in MYNN and SERPINC1 expression in BEAS-2B cells, demonstrating concentration-and time-dependent effects. lncRNA TERC may promote cell migration by regulating the expression of MYNN and SERPINC1, playing a role in hexavalent chromium-induced malignant transformation. - Source: PubMed
Pan S MXu BQian Q QLi X DChen J FLou J LFeng L F - Clinical manifestations of aging spine, such as lumbar spinal stenosis, intervertebral disc degeneration, osteoporosis and sciatica, frequently co-occur, yet their shared genetic basis remains unclear. - Source: PubMed
Publication date: 2026/06/04
Chen JianquanZhong XingjieLi LipingFeng PeiyunDuan XiupingMai DiLiu LixiaXu Jianwen - Multiple sclerosis (MS) is a complex autoimmune disease with strong genetic components, but its genetic mechanisms remain largely underexplored. We aimed to pinpoint causal genes and evaluate their utility for MS risk prediction. We integrated MS genome-wide association study summaries with brain-derived splicing quantitative trait loci (sQTLs) and expression quantitative trait loci (eQTLs) via summary-data-based Mendelian randomization (SMR) and colocalization analyses to identify potential causal genes. Weighted gene coexpression network analysis (WGCNA) of the E-MTAB-5151 dataset identified MS-associated gene modules. LASSO regression determined the core gene signature. GO and KEGG enrichment analyses, immune infiltration, and gene set enrichment analysis (GSEA) explored the biological relevance. Using an independent protein quantitative trait loci (pQTL) dataset, key genes were further validated for pQTL-MS associations. SMR identified 28 sQTL genes and 66 eQTL genes for MS, 23 and 51 of which passed the colocalization tests, respectively. WGCNA identified three MS-associated modules, and their intersection with SMR genes prioritized 23 key genes. Functional enrichment analysis of the module genes and SMR genes highlighted the consistent involvement of immune-related pathways in MS, including lymphocyte activation and NF-κB signalling. LASSO regression established a 10–gene signature (ACP2, IL7, MYNN, RGS1, SAE1, SP140, TRAF3, TSPAN31, TYMP, and ZC2HC1A) with high predictive accuracy (AUC = 0.983 in internal validation; AUC > 0.70 across three external datasets). Immune infiltration analysis revealed a consistent immune cell expression pattern, in which the expression of MS risk genes was positively associated with naive CD4+ T cells and resting mast cells, but negatively associated with activated mast cells. In contrast, MS protective genes exhibited the opposite pattern. Furthermore, the integration of the MS genome-wide association study statistics validated ZC2HC1A and TRAF3 at the protein level. GSEA further linked both genes to the Hedgehog signalling pathway. Integrating genomic, transcriptomic, and proteomic data, we identified candidate causal genes for MS with robust evidence. ZC2HC1A and TRAF3 have emerged as promising biomarkers and mechanistic candidates for MS. Future follow-up functional studies are warranted to elucidate their molecular roles in MS pathogenesis. - Source: PubMed
Publication date: 2026/03/02
Chen MingZhao DuranFan HaipingZeng XiaojunZhang WeiLi LijuanLi Wei