MYBL2 antibody - N-terminal region (P100748_P050)
- Known as:
- MYBL2 (anti-) - N-terminal region (P100748_P050)
- Catalog number:
- p100748_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MYBL2 antibody - N-terminal region (P100748_P050)
Related genes to: MYBL2 antibody - N-terminal region (P100748_P050)
- Gene:
- MYBL2 NIH gene
- Name:
- MYB proto-oncogene like 2
- Previous symbol:
- -
- Synonyms:
- BMYB, B-MYB
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: MYBL2 antibody - N-terminal region (P100748_P050)
Related articles to: MYBL2 antibody - N-terminal region (P100748_P050)
- - Source: PubMed
Publication date: 2026/09/30
Ha Jin WoongKim Sang YeanJeon SoyoungNa Min JeongYoon Jung HwanNam Suk Woo - T helper 17 (Th17) cell differentiation is governed by a complex transcriptional network centered on the lineage-specifying factor RORγt, accompanied by STAT3, IRF4, and SMAD2/3. However, the complete repertoire of transcriptional regulators controlling Il17a gene transcription and Th17 commitment remains incompletely defined. Here, we identify zinc finger protein 335 (ZFP335) as a critical regulator of Th17 differentiation. Mechanistically, ZFP335 directly binds and activates the Mybl2 promoter, and the resulting MYBL2 protein cooperates with RORγt to drive Il17a transcription. Genetic ablation of Zfp335 attenuated imiquimod-induced psoriasis-like skin inflammation and diminished Th17 cell responses in vivo. Notably, Mybl2 deficiency phenocopied these protective effects. Collectively, these findings establish a ZFP335-MYBL2-IL17A transcriptional axis that governs Th17 differentiation and identify this pathway as a potential therapeutic target for Th17-mediated inflammatory diseases. - Source: PubMed
Li WenhuaYang BiaoYuan NingWang XinJia XiaoxuanSu YanhongZhang XiaoranZhang TianzheGao YangLiu JunRen YuyingSong JiapengYang XiaofengLei LeiZhang Baojun - Hub genes associated with non-small cell lung cancer (NSCLC) were identified through bioinformatics screening. In vitro experiments analyzed the potential mechanisms by which these genes regulate tumor malignant phenotypes and macrophage polarization. Differentially expressed genes were identified from The Cancer Genome Atlas (TCGA)-NSCLC and GSE32175 datasets, followed by protein-protein interaction (PPI) network analysis to screen hub genes. The effects of MYB Proto-Oncogene Like 2 (MYBL2) on NSCLC progression and macrophage polarization were evaluated using in vitro models. The regulatory relationship between MYBL2 and C-C motif chemokine ligand 2 (CCL2) was investigated by Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays, and rescue experiments were performed to validate the role of the MYBL2-CCL2 axis. Bioinformatics screening identified BUB1B, CDCA2 and MYBL2 as key hub genes with high expression in NSCLC, among which MYBL2 was significantly upregulated in NSCLC cells. Functional experiments confirmed that MYBL2 silencing markedly inhibited the malignant proliferation, migration and invasion of NSCLC cells. Tumor cell MYBL2 knockdown effectively reversed M2-like polarization and promoted M1-like polarization in the co-culture system. Mechanistically, MYBL2 directly bound to the CCL2 promoter region to enhance CCL2 transcriptional activity and upregulate CCL2 expression in NSCLC cells. Exogenous CCL2 supplementation significantly rescued the inhibitory effect of MYBL2 knockdown on macrophage M2-like polarization, verifying the mediating role of CCL2 in this regulatory axis. MYBL2 is strongly expressed in NSCLC cells and is associated with enhanced malignant phenotypes. It may affect macrophage M2-like polarization by upregulating CCL2, thus participating in NSCLC immune microenvironment remodeling. - Source: PubMed
Publication date: 2026/09/10
Sun QiongMeng JingMcGowan RochelleHodge BelindaShan DanielMiller NicolasShi Weiwei - Glioblastoma (GBM) is among the most aggressive primary brain tumors, marked by rapid proliferation, therapeutic resistance, and profound intratumoral heterogeneity. Epigenetic regulators such as lysine-specific demethylase 1A (KDM1A) and histone deacetylase 2 (HDAC2) are aberrantly expressed in resistant GBM subpopulations and strongly correlate with poor clinical outcomes. Here, we assessed the therapeutic potential of MPT0G521, a dual KDM1A/class I HDAC inhibitor, in disrupting epigenetic regulation and cell cycle progression. Bioinformatic analyses of resistance-associated gene profiles (temozolomide and 2 Gy radiation) and single-cell transcriptomic datasets from distinct tumor regions revealed enrichment of KDM1A and HDAC2 in high-cycling GBM clusters, particularly at invasive margins prone to recurrence. Functional assays demonstrated that MPT0G521 potently inhibited proliferation of both parental and temozolomide-resistant GBM cells, inducing G2/M arrest and apoptosis. Transcriptomic profiling further identified significant downregulation of centrosome integrity genes (FSD1, KIFC1), spindle regulators (TUBB, STMN1, KIF2C, KIF15), kinetochore components (AURKB, CDCA8, SPAG5), and G2/M checkpoint mediators (CENPF, MYBL2, CCNF, MYT1, CDC25A), resulting in disrupted mitotic progression. Mechanistically, MPT0G521 increased histone H3 methylation and acetylation, validating its dual inhibitory activity against KDM1A and class I HDACs. Collectively, these findings indicate that MPT0G521 disrupts the G2/M activation and mitotic machinery, thereby suppressing proliferative and resistant GBM subpopulations. This dual epigenetic strategy holds strong promise for overcoming GBM heterogeneity and reducing recurrence. - Source: PubMed
Publication date: 2026/09/02
Wu An-ChihChuang Jian-YingLiu Jr-JiunSalim Enrica AngelinaWu Ming-HsiaoJing Shih-WeiHsu Tsung-IChang Kwang-YuChang Wen-ChangThakur AmandeepLiou Jing-PingLo Wei-Lun - B-MYB (MYBL2) is a transcription factor of the MYB family that plays critical roles in cell cycle progression, proliferation, and survival. Through the DREAM-MMB-FOXM1 network, B-MYB coordinates the expression of genes required for mitosis and cytokinesis (G2/M genes), while genes required for DNA replication during S phase are regulated by E2F-DP complexes. Initially identified as a regulator of normal cell cycle processes, B-MYB has emerged as a key oncogenic driver across multiple cancer types. This review addresses the physiological roles of B-MYB, the mechanisms underlying its oncogenic activation, and its contributions to tumorigenesis and clinical relevance as a prognostic biomarker and potential therapeutic target. Aberrant activation of B-MYB, driven by gene amplification, transcriptional upregulation, or post-translational modification, is reported as a recurrent feature of aggressive cancers. The consequences of B-MYB overexpression, including uncontrolled proliferation, genomic instability, apoptosis evasion, epithelial-to-mesenchymal transition, therapy resistance and metabolic reprogramming, further underscore B-MYB as a central oncogenic driver. Clinically, B-MYB overexpression correlates with poor prognosis, advanced disease and chemoresistance across multiple malignancies. Thus, we aim to emphasise the biological roles of B-MYB in physiological and cancer mechanisms, alongside the growing evidence establishing it as both a biomarker of disease and a potential therapeutic target. While previous reviews have addressed isolated aspects of B-MYB biology, this review provides a comprehensive and updated integration of recent mechanistic advances (A-MYB/B-MYB functional redundancy and YAP/TAZ-TEAD crosstalk) and the therapeutic potential of non-canonical DNA structures at the B-MYB promoter. We further review current trends and methodologies for targeting B-MYB and outline new perspectives for future therapeutic research. - Source: PubMed
Publication date: 2026/08/31
Miranda AndréOliveira Paula AMergny Jean-LouisCruz Carla