FOXM1 Blocking Peptide, Blocking Peptides
- Known as:
- FOXM1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-1409
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- FOXM1 Blocking Peptide Peptides
Related genes to: FOXM1 Blocking Peptide, Blocking Peptides
- 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 Blocking Peptide, Blocking Peptides
Related articles to: FOXM1 Blocking Peptide, Blocking Peptides
- A better understanding of the response of granulosa cells to exogenous hormone stimulation and how this impacts the complex interplay between the granulosa cells and the oocyte is crucial for the optimal management of infertile couples seeking IVF treatment. - Source: PubMed
Publication date: 2026/06/10
Medica AlexaKim Matthew EHung Wei-TingSohni AbhishekDuleba AntoniTan KunWilkinson Miles F - In the mammalian cerebellum, three types of astroglial cells-Bergmann glial cells (BGs), inner granule cell layer (IGL) astrocytes, and white matter (WM) astrocytes-arise in postnatal timing from two types of progenitors: Bergmann glia-like progenitors (BGLPs) and astrocyte-like progenitors (AsLPs). In contrast to AsLPs, which are commonly observed in other brain regions, BGLPs have not been well studied. Here, we investigate differentiation abilities, gene expression profiles and differentiation control mechanisms of BGLPs at postnatal stages. BGLPs and AsLPs decrease in number as development progresses from postnatal day 0 (P0), and are almost absent by P10. By utilizing an electroporation-based method to BGLPs, we found that P6 BGLPs differentiate into BGs and IGL astrocytes, but not into WM astrocytes, consistent with a previous report. However, P0 BGLPs were observed to differentiate into not only BGs and IGL astrocytes, but also WM astrocytes and a small number of molecular layer inhibitory neurons. By conducting spatial transcriptomic analysis with over 5000 probes (Xenium), we successfully identified distinct clusters corresponding to BGLPs at P0 and P6, respectively, and genes preferentially expressed in P0 and P6 BGLPs. In addition, upstream regulatory analysis using Enrichr identified Foxm1 and Nfia as candidate regulators that affect stage-specific properties of BGLPs. in vivo knockdown and overexpression experiments further demonstrated that precise regulation of Foxm1 and Nfia expression is important for proper progeny production from postnatal BGLPs. This study gives insights into understanding molecular nature and differentiation ability control of BGLPs during postnatal cerebellar development. - Source: PubMed
Suyama KyokaAdachi TomaMizuno MinamiJi KaiyuanIsogai ErikoHasegawa IkukoNishitani KayoSone MasakiMiyashita SatoshiOwa TomooHoshino Mikio - Therapy resistance remains a major obstacle to successful cancer treatment and is driven by complex interactions between tumor-intrinsic adaptive mechanisms and signals originating from the tumor microenvironment. Among the molecular regulators implicated in these processes, the transcription factor FOXM1 has emerged as a key mediator of DNA damage repair, cell cycle progression, and stress adaptation. Although FOXM1 has traditionally been studied as a regulator of intracellular signaling pathways, accumulating evidence suggests that its functions extend beyond canonical transcriptional control. In this review, we analyze current knowledge on the mechanisms regulating FOXM1 expression and activity and discuss how FOXM1 contributes to therapy resistance. We propose that FOXM1 should be viewed not merely as a regulator of individual oncogenic pathways but as a systems-level coordinator that integrates intracellular stress adaptation with microenvironment-driven resistance mechanisms. Particular attention is given to the FOXM1 interactome, complemented by an analysis of protein interaction data from BioGRID. We also discuss emerging evidence implicating FOXM1 in intercellular communication. To identify potential links between FOXM1 signaling and extracellular vesicle cargo, we analyzed the overlap between FOXM1 target genes and proteins identified in extracellular vesicle proteome databases. These emerging regulatory networks may represent previously underappreciated contributors to therapy resistance. - Source: PubMed
Publication date: 2026/06/10
Korolev Aleksei DBekbaeva Irina VShnaider Polina VShender Victoria O - : Vernodalin (VD) and crude extracts from leaves have previously demonstrated anticancer activity; however, their underlying molecular effects remain incompletely understood. This study investigated the anticancer activities of VD and extracts and characterized their associated molecular responses in breast (MDA-MB-231) and ovarian (A2780) cancer cells. : leaves were extracted with dichloromethane and ethyl acetate to obtain DEGE and EAGE, respectively. VD was isolated from EAGE and characterized by H-NMR and HPLC. Phytochemical profiles of the extracts were analyzed by GC-MS and HPLC. Cytotoxicity, clonogenic survival, cell cycle progression, migration, and protein expression were evaluated using MTT assay, colony formation assay, flow cytometry, wound healing assay, and Western blotting. : GC-MS analysis revealed distinct phytochemical compositions between DEGE and EAGE, although both extracts contained high levels of neophytadiene and phytol. VD, DEGE, and EAGE inhibited cell proliferation and migration in both cancer cell lines. VD suppressed proteins associated with cancer progression, including SMYD3, BRAF, MELK, FOXM1, Cyclin B1, MDR1/ABCB1, and MMP-9, with molecular responses differing between MDA-MB-231 and A2780 cells. DEGE and EAGE exhibited molecular regulatory patterns distinct from those of purified VD, suggesting contributions from multiple phytochemical constituents. : VD and crude extracts exhibit significant in vitro anticancer activity against breast and ovarian cancer cells and induce distinct molecular responses. The differential effects of DEGE and EAGE may be attributable to differences in their phytochemical constituents. - Source: PubMed
Publication date: 2026/06/11
Faisal MuhammadSukpondma YaowapaSangket JuntakarnTaraporn SiripornDokduang SirinapaGraidist Potchanapond - Abnormal shear stress is closely linked to the progression of intracranial aneurysms (IAs) and the apoptosis of middle layer of vascular wall. Insulin-like growth factor-1 (IGF-1) is crucial for vascular protection by inhibiting local vascular cell apoptosis; however, its involvement in the pathology of IAs remains unclear. Eight human IAs and 8 superficial temporal artery (STA) samples were collected for high-throughput sequencing to analyze the expression of IGF-1. IA mouse models were established to evaluate the effect of IGF-1 on the aneurysmal remodeling of the cerebral arteries. We conducted a comprehensive analysis of the Circle of Willis in mice using pathological and proteomic methods to assess the proliferation and apoptosis of vascular smooth muscle cells (VSMCs). Additionally, vessel perfusion was perfomed to evaluate the incidence of IAs in mouse model. In vitro, mouse VSMCs and endothelial cells (ECs) of aorta were extracted, and a co-culture model with a flow chamber was established to simulate a laminar flow environment. The relationship between wall shear stress (WSS) gradient and the expression of IGF-1 was explored. Then the proliferation and apoptosis of VSMCs, and the related signaling pathway was determined by CCK8, flow cytometry, immunoblotting analysis and chromatin immunoprecipitation. Both IGF-1 and IGF-1R was downregulated in human IAs. High WSS reduced VSMC IGF-1 expression, facilitated apoptosis in VSMCs, and suppressed their proliferation. Over expression of IGF-1 promoted VSMC proliferation and inhibited apoptosis both in vivo and in vitro. Moreover, increased IGF-1 expression reduced mouse IA incidence. Mechanistically, IGF-1 regulated high WSS-induced apoptosis and proliferation of VSMCs via the PI3K/AKT signaling pathway. Furthermore, elevated WSS was found to suppress the expression of FOXM1, which subsequently modulates the expression of IGF-1. High WSS downregulates the expression of IGF-1 in VSMCs, thereby inhibiting its proliferative and anti-apoptotic effects, which ultimately contributes to the IA progression via PI3K/AKT signaling pathway. Furthermore, FOXM1 played a role in this process by targeting IGF-1. - Source: PubMed
Publication date: 2026/06/25
Li Si-SiLu Zhi-WenLuo YinTang Hai-ShuangHong BoZhou YuLiu Jian-Min