FOXM1
- Known as:
- FOXM1
- Catalog number:
- ARP39518_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- FOXM1
Related genes to: FOXM1
- 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
Related articles to: FOXM1
- - Source: PubMed
Publication date: 2026/06/06
Peng JunyaJiang RuiTu JiajuanLiu WanliPing LuDun RuikangZhang WenyuChen HaoShi YihongPan XuJia PanpanLi MengjieWang WenjingLiu LuluHong XiafeiZhang YuhanLiu YuanhaoLv KeXu QiangWang WeibinLiao QuanHan XianlinDai MenghuaZhang TaipingGuo JunchaoWang WenzeTian XiuyunYuan ChunhuiHao ChunyiWu HuanwenWu JianhuiWu WenmingLin ZhixiangZhao Yupei - Mitosis entry is tightly regulated by a complex network of mechanisms involving epigenetic modifications, signaling pathways, transcriptional control, and structural changes. Although substantial progress has been made in understanding these processes individually, the mechanisms integrating chromatin dynamics with mitotic regulators are still not fully understood. Here, we identify a functional antagonism between the deacetylase SIRT2 and the acetyltransferase MOF in the G-M transition and mitotic progression. This interplay, which involves MOF deacetylation by SIRT2, regulates key histone marks, including H4K16ac (histone 4 lysine-16 acetylation) deacetylation and H4K20me1 (histone 4 lysine-20 monomethylation) deposition, condensin II loading, and the stability of the key mitotic regulator PLK1, and contributes to the FOXM1-mediated transcriptional control of mitosis. Our findings reveal a previously unrecognized layer of regulation in G-M progression with possible impact in cancer, highlighting the intricate cross-talk between chromatin dynamics and mitotic control and providing important insights into chromosomal stability. - Source: PubMed
Publication date: 2026/06/19
Espinosa-Alcantud MaríaSima NúriaFernández-Duran IreneMarazuela-Duque AnnaMartínez-Cebrián GerardGuitart-Solanes AnnaGámez-García AndrésMartínez-Redondo PalomaBosch-Presegué LaiaVazquez Berta NPaños LuisBech Joan JosepThomas TimMartinez-Balbás Marian AVoss Anne KKrüger MarcusSerrano LourdesOlivella MireiaCuartero Sergide la Torre CarolinaVaquero Alejandro - High-mobility group (HMG) protein families are critical regulators of chromatin structure and gene expression in breast cancer. This study systematically evaluates their expression patterns, genetic interactions, and clinical relevance. - Source: PubMed
Shariff Ehtesham AhmedAzharuddin AhmedAbu-Zaid RatebAl-Wathinani AhmedAlenazy Eid BasheerSharieff Raiyan Ehtesham Ahmed - CDK4-selective inhibitors are emerging as promising anticancer agents. Relative to dual CDK4/6 inhibitors, CDK4-selective inhibitors have the potential to retain efficacy while improving tolerability. However, the therapeutic value and mechanistic consequences of selectively targeting CDK4 in prostate cancer remain largely undefined. Here, we investigated the anti-tumour activity and mode of action of the CDK4 inhibitors AU2-94 and atirmociclib across diverse prostate cancer models. - Source: PubMed
Publication date: 2026/06/17
Safaroghli-Azar AvaCroft TravisMekonnen Laychiluh BLenjisa JimmaDickel MajaShrestha Raj KSita SamyuktaChoo NicholasRoach MichaelBasnet Sunita K CLawrence Mitchell GSelth Luke AWang Shudong - Keloid is a refractory fibroproliferative skin disorder with unclear molecular pathogenesis. Here, we delineated FOXM1's role in regulating BMP4/Smad1/5/8 signaling and keloid fibroblast (KF) behavior via integrated bioinformatics and experiments. Bioinformatics analysis of GSE145725 identified differentially expressed genes and co-expression modules. PPI network analysis and module-trait correlation pinpointed BMP4 as a central hub gene. KnockTF 2.0 prediction and luciferase assays confirmed FOXM1 directly binds BMP4 promoter sites to repress its transcription. In vitro assays showed BMP4 overexpression inhibited KF proliferation, migration, and extracellular matrix synthesis by activating Smad1/5/8 phosphorylation. FOXM1 overexpression abrogated these effects via reduced Smad1/5/8 phosphorylation, which was validated by functional rescue experiments. In summary, our findings unravel a novel FOXM1-BMP4-Smad1/5/8 regulatory circuitry in keloid pathogenesis, providing new mechanistic insights and highlighting FOXM1 as a promising therapeutic target for this recalcitrant disorder. - Source: PubMed
Publication date: 2026/05/14
Zhang LuyangLiu AnzhuXue YiJi YiWang GedunSun LetianShi Ting