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)
- 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 - Small cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy characterized by rapid proliferation, early dissemination, and limited durable benefit from current chemoimmunotherapy. Although immune checkpoint blockade has modestly improved clinical outcomes, the regulatory logic linking malignant cell states to the tumor immune microenvironment remains incompletely understood. Here, we applied an integrative single-nucleus transcriptomic framework to dissect tumor cell heterogeneity, regulatory programs, and immune-stromal communication networks in SCLC. - Source: PubMed
Publication date: 2026/08/04
Jia HonglingAn YongxuanChen BingZhang YuqiXu YifeiGuan FeilongWu QianSun LiliLi YajingBi JunjieJi XiuliQiu Zhanjun - Hypoxia-induced reprogramming of glutamine metabolism and ferroptosis resistance serve as pivotal factors that drive the progression of solid tumors and contribute to therapeutic resistance. However, the potential interaction between these processes remains inadequately understood. Elucidating the regulatory mechanisms linking these pathways is essential for developing effective therapies for solid tumors. This study demonstrated that HIF-1α promotes the expression of UBASH3B in hepatocellular carcinoma (HCC), resulting in ferroptosis resistance mediated by glutamine metabolism. Mechanistically, HIF-1α-driven UBASH3B dephosphorylated MYBL2 at Y15, leading to MYBL2 stabilization and a reprogramming of glutamine metabolism that modulates ferroptosis resistance. Specifically, MYBL2 augmented the transcriptional activity of SPSB4, which facilitated the K48-linked polyubiquitination and degradation of GLUD1, a key enzyme in glutamine metabolism, at residue K191. This degradation inhibited glutamine-driven oxidative phosphorylation (OXPHOS). Furthermore, UBASH3B played a crucial role in macrophage polarization and T-cell inhibition by promoting CXCL8 expression, which contributed to immunosuppression. Finally, we found that targeting UBASH3B in HCC cells using ZIF-8-Cu@siRNA@HA nanoparticles (ZCSH NPs) enhanced the efficacy of anti-PD-1 in combination with lenvatinib treatment. In summary, our study uncovers a novel interaction between hypoxia, glutamine metabolic reprogramming, and immune suppression in HCC progression, positioning UBASH3B as a promising therapeutic target for overcoming hypoxia-induced treatment resistance. - Source: PubMed
Publication date: 2026/08/06
Pan Guo-QiangZhang Shao-PengWang XiQu YingLiu Xue-FengYan Yu-ChuanLi TaoDong Zhao-Ru - Osteosarcoma (OS) is an aggressive bone cancer that most commonly affects children and young adults. OS exhibits a high degree of genomic complexity, as well as cellular plasticity, and dynamic transcriptional regulation is suggested to contribute to treatment resistance and metastasis. Cell lines are well characterised as models to advance our knowledge on OS biology. HOS and U2OS cells have increased invasiveness and higher migratory ability compared with MG63. In this study, we employed a tandem array of consensus transcription factor response elements (catTFREs) proteomic approach to characterise transcription factor (TF) regulatory networks related to OS aggressiveness. We mapped 7355 proteins and enriched 504 TFs and coregulators. When we integrated proteomics with cell line specific gene expression, H3K27ac marked enhancers and chromatin accessibility, we classified the TFs and coregulators common for HOS and U2OS and specific for the individual cell lines. We demonstrate that RUNX2 and MYBL2 are specifically enriched in HOS and U2OS. RUNX2 and MYBL2 exhibited an increase in expression in metastatic compared to primary OS tumours and may be linked to cell aggressiveness. ETV5, TBX15, and USF1 were among TFs specific to the lower migratory cell line MG63 and these genes were more expressed in primary OS tumours. Our analysis provides a comprehensive understanding of the transcriptional drivers that shape OS cell line regulatory landscapes and may have implications as markers pending further validation. - Source: PubMed
Publication date: 2026/07/29
Thang Nguyen XuanMartinsen EmilyAbdelhalim MohamedTran The TrungLedsaak MaritRogne MarieThiede BerndEskeland Ragnhild