FOXM1 Monoclonal Antibody [5G10] 100 µg
- Known as:
- FOXM1 Monoclonal Antibody [5G10] 100 µg
- Catalog number:
- ABB-7277-100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- FOXM1 Monoclonal Antibody [5G10] 100 µ
Related genes to: FOXM1 Monoclonal Antibody [5G10] 100 µg
- Gene:
- FOXM1 NIH gene
- Name:
- forkhead box M1
- Previous symbol:
- FKHL16
- Synonyms:
- HFH-11, trident, HNF-3, INS-1, MPP2, MPHOSPH2, TGT3
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: FOXM1 Monoclonal Antibody [5G10] 100 µg
Related articles to: FOXM1 Monoclonal Antibody [5G10] 100 µg
- 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 - Despite advances in colorectal cancer (CRC) treatment, the chromosomal instability (CIN)-positive subgroup remains refractory to conventional therapies and immunotherapy. C2orf76, a poorly characterized gene identified as a CIN-linked candidate in CRC through bioinformatic analyses, has been associated with favorable prognosis and potential immune-related functions. However, its biological roles and underlying mechanisms in CRC remain largely unexplored. - Source: PubMed
Publication date: 2026/08/12
Zhang LiSong ZhuZhang PinjieJiang YuyuXiang YanWang ZetingDing YingyingRui BingZhou YangyangJiang JunfengCao ShuqiangLiu Xingguang - Cashmere goats are widely distributed in the cold, arid and semi-arid remote regions of northern China. Their main economic value is the production of precious cashmere fibers. The differentiation of second hair follicle (SHF) stem cells into hair follicle lineages plays a crucial role in SHF regeneration as well as in the morphogenesis and growth of cashmere fibers; however, its precise molecular mechanism is still unclear. In this study, we found that -methyladenosine (mA)-circHECA recruiting FUS promoted the differentiation of SHF stem cells into hair follicle lineages through stabilizing FOXM1 mRNA in SHF stem cells, thereby activating the NOTCH pathway in cashmere goats. Furthermore, we confirmed that the mA modification of circHECA is required for the FUS/FOXM1-mediated NOTCH signaling pathway to facilitate the differentiation of SHF stem cells into hair follicle lineages via transfecting circHECA mA-deficient mutants. Our results contribute to elucidating the functional mechanism of mA-circHECA in the differentiation of SHF stem cells into hair follicle lineages in cashmere goats. - Source: PubMed
Publication date: 2026/08/21
Zhang XinjiangZhu YuboShen JinchengXu RuqingBai ManFan YixingHui TaiyuZhang QiBai Wenlin - This study reports the design, synthesis, and biological evaluation of novel inhibitors targeting the epigenetic enzymes ALKBH2 and ALKBH5 as potential adjuvants to temozolomide therapy in glioblastoma. Given their critical role in DNA/RNA demethylation, tumor progression, and drug resistance, their inhibition represents a promising therapeutic strategy. Building on the previously identified lead compound MV1035, we employed structure-based drug design to develop new derivatives, including a second-generation series incorporating a fumarate hydrazide moiety to enhance binding affinity through interaction with both substrate- and cofactor-binding sites. Molecular docking studies predicted significantly improved binding for a set of new compounds but, due to multiple synthetic drawbacks, only a subset of the designed series was synthesized and evaluated biologically. MV3030 emerged as the most promising candidate. MV3030 demonstrated an inhibitory effect on ALKBH2 comparable to MV1035, also showing a more moderate inhibitory effect on ALKBH5. Notably, it exhibited intrinsic cytotoxicity in U87-MG cells and patient-derived glioma stem cells, whereas normal astrocytes exhibited markedly higher resistance to the treatment. Furthermore, MV3030 enhanced temozolomide efficacy and displayed favorable blood-brain barrier permeability both in silico and in vitro. Moreover, MV3030 modulated the FoxM1/Wnt/β-catenin axis. Overall, these findings identify MV3030 as a promising compound with the potential to overcome temozolomide resistance and improve glioblastoma treatment. - Source: PubMed
Publication date: 2026/08/12
Rivara MirkoMalacrida AlessioGhizzi MartinaBentivegna AngelaSica Francesco SaverioRe FrancescaMotta StefanoCallea LaraBonati LauraIncerti MatteoZuliani ValentinaNicolini Gabriella - Extramammary Paget disease (EMPD) is a rare epithelial malignancy that arises in the apocrine gland-bearing skin. Although localized intraepidermal EMPD generally follows an indolent clinical course, invasive EMPD is associated with lymph node metastasis, distant dissemination, and poor survival. Owing to its rarity, high-level evidence is limited and treatment strategies remain incompletely standardized, particularly for advanced disease. Recent advances in molecular profiling have revealed actionable therapeutic targets and created new opportunities for precision medicine. - Source: PubMed
Publication date: 2026/08/11
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