FOXM1 antibody
- Known as:
- FOXM1 (anti-)
- Catalog number:
- orb135525
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FOXM1 antibody
Related genes to: FOXM1 antibody
- 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 antibody
Related articles to: FOXM1 antibody
- 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
Miyashita AzusaFukushima Satoshi - Postoperative cognitive dysfunction (POCD) is a common post-anesthesia complication that seriously impairs patient prognosis. Microglial M1/M2 polarization imbalance is a key link in POCD development. Forkhead box M1 (FOXM1) is downregulated in sevoflurane (SEV)-induced cell models, but whether it affects microglial M1/M2 polarization remains unreported. qRT-PCR and Western blot were employed to detect the mRNA and protein levels. Flow cytometry was used to evaluate the expression of M1 markers and M2 markers in microglia. ELISA was employed to detect inflammatory factors. Cellular oxidative stress status and mitochondrial membrane potential (MMP) were assessed using commercial kits. GO functional annotation and KEGG pathway enrichment analyses were performed on the top 500 protein-coding genes downstream of FOXM1. Bioinformatic prediction, ChIP assay, and dual-luciferase reporter assay were used to verify the regulatory relationship between FOXM1 and regulator of G protein signaling 10 (RGS10). SEV treatment significantly decreased FOXM1 expression in HMC3 cells (P < 0.001, P < 0.01). FOXM1 overexpression alleviated SEV-induced M1/M2 polarization imbalance, reduced inflammation (lowered inflammatory factors), and mitigated oxidative stress (with reduced ROS/MDA, increased SOD/GSH-Px, and ameliorated MMP depolarization). GO/KEGG analysis revealed FOXM1 downstream genes were enriched in pathways like MAPK and TNF signaling pathways. FOXM1 bound to the RGS10 promoter and enhanced its transcription. RGS10 silencing reversed the ameliorative effects of FOXM1 overexpression on SEV-induced cellular changes (M1/M2 polarization, inflammation, oxidative stress, and MMP). FOXM1 regulates RGS10 via direct binding to its promoter, thereby modulating microglial M1/M2 polarization, inflammation, and oxidative stress. This study identifies the FOXM1-RGS10 axis as crucial for SEV-induced microglial dysfunction, providing experimental evidence for POCD mechanism elucidation and potential target screening. - Source: PubMed
Publication date: 2026/08/20
Zhang ChenLiu XiufengLiu Juan