TGT3 EMSA Kit
- Known as:
- TGT3 EMSA Kit
- Catalog number:
- AY1249
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- TGT3 EMSA Kit
Related genes to: TGT3 EMSA Kit
- 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
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- Osteoarthritis (OA) is characterized by progressive cartilage degradation accompanied by limited intrinsic repair capacity. Stromal vascular fraction (SVF) transplantation has demonstrated potential for regenerating damaged joint tissue; however, the pathological microenvironment impairs SVF stemness, thereby limiting therapeutic efficacy. Herein, we developed a bioinspired hydrogel formed via the cross-linking of hyaluronic acid-grafted dopamine and a fibroblast growth factor 2-mimetic peptide-modified RADA16-I. This injectable hydrogel combined excellent gelation performance with multifunctionality, particularly in enhancing SVF proliferation and chondrogenic differentiation. The hydrogel activated forkhead box M1 (FOXM1) - mediated epigenetic reprogramming, enhancing DNA repair capacity and increasing chromatin accessibility at pluripotency loci. In a rat OA model, combined hydrogel and SVF transplantation significantly enhanced articular cartilage regeneration and ameliorated OA symptoms. This study provides preliminary evidence showing that a biomaterial-mediated epigenetic reprogramming strategy improves recovery in OA, highlighting the therapeutic potential of the novel hydrogel for stem cell-based regenerative medicine. - Source: PubMed
Publication date: 2026/04/20
Hou WaifangChen YongfengXiao LongyouQi WeiDu TianshuSun QiangXue BoruiZhao QingheXie PengfeiYe ZiHan FeiGuo LingliJiao YangZhang RanranJia HongHuang XiaoGuo JianweiWang PengWang HuayiWang YuanruiChen WenjingWu HainingHe LiuminZhang Dawei - Nasopharyngeal carcinoma (NPC) is a highly aggressive malignancy. Given conventional therapy limitations, exploring non-apoptotic pathways like ferroptosis is crucial. Tryptophan (Trp) metabolic reprogramming is a key mechanism by which NPC cells evade ferroptosis by maintaining redox homeostasis. In this study, we investigated the anti-NPC activity of rAnguillin, a novel recombinant peptide derived from Anguilla anguilla, and elucidated the molecular mechanisms by which it induces ferroptosis via the FOXM1/PABPC1L axis. rAnguillin (7009 Da) was prepared via prokaryotic expression, with its primary sequence verified by LC-MS/MS. Notably, rAnguillin significantly inhibited NPC cell proliferation (IC = 3.306 μM at 24 h) and suppressed xenograft tumor growth in vivo in a dose-dependent manner. Mechanistically, as validated by CETSA and site-directed mutagenesis, rAnguillin directly interacted with the transcription factor FOXM1, triggering its ubiquitin-proteasome-dependent degradation. The downregulation of FOXM1 inhibited the transcriptional activation of PABPC1L, subsequently leading to the inactivation of the JAK2-STAT1 signaling axis. This cascade significantly suppressed the expression of rate-limiting enzymes such as IDO1, thereby depleting the tryptophan metabolic flux and the antioxidant protective effects of its metabolite, 3-hydroxyanthranilic acid (3-HAA). Ultimately, this disruption of redox homeostasis triggered robust ferroptosis, as evidenced by TEM and inhibitor rescue experiments. Taken together, this study demonstrates that rAnguillin induces ferroptosis in NPC cells by targeting FOXM1 for degradation, which subsequently suppresses the FOXM1-PABPC1L-JAK2/STAT1-tryptophan metabolism axis. These findings provide a promising therapeutic strategy and a potent drug candidate for the treatment of NPC. - Source: PubMed
Publication date: 2026/04/13
Yuan QianhuiZhao YanZhou FuxinZhang YuebinJia XinyueYao JihongLv MeiWang JihongLv Li - Triple negative breast cancer (TNBC) is associated with poor prognosis and is mainly treated with chemotherapy-based regimens, often including carboplatin. Resistance to carboplatin is a common clinical issue that is either initially present or develops with treatment. Overcoming this resistance is a significant clinical challenge, which highlights the need for novel therapeutic strategies. We used a pooled shRNA screening approach with a chemoresistant TNBC patient-derived xenograft (PDX) cell (PDXC) line to identify targets whose knockdown would enhance the efficacy of carboplatin. This screening led to the identification of the ATR (ataxia telangiectasia and Rad3-related) gene as a key therapeutic vulnerability. Inhibiting ATR with BAY1895344 or AZD6738 re-sensitized carboplatin-resistant PDXCs and PDXs to carboplatin, resulting in an increase in DNA damage, and apoptosis. ATR inhibition prevents carboplatin-resistant cells from effectively engaging the S and G2/M checkpoints required for DNA repair, leading to mitotic catastrophe. We further identified that the addition of ATR inhibitors to carboplatin enabled FOXM1-targeted gene program leading to premature passage into mitosis. Moreover, targeting PKMYT1, a regulator of cyclin-dependent kinase 1 (CDK1) controlling the G2/M checkpoint, through knockdown or with the novel PKMYT1 inhibitor RP-6306, also enhanced carboplatin efficacy in our TNBC PDXC. Molecular factors associated with response to the ATR inhibitor/carboplatin combination included low RNA levels of PKMYT1. These results underscore the pivotal roles of ATR and PKMYT1 in mediating resistance to carboplatin in TNBC and support targeting these pathways to overcome carboplatin resistance in this disease. - Source: PubMed
Publication date: 2026/04/13
Guay JulietKuasne HellenChabot CatherineBozek KathrynMajedi YasaminBuchanan MargueriteAguilar-Mahecha AdrianaBareke EricUlmer BenjaminKong TimYang KangningLiao MinyanElebute OluwadaraGuo RuiningMonast AnieMorin GenevièveHuang SidongPark MoragBasik Mark - The high mortality of pancreatic ductal adenocarcinoma (PDAC) underscores the need for novel treatments. We investigated the potential role of human biofield therapy (BT) in modifying tumorigenic processes in murine and human PDAC cells through a series of in vitro and in vivo studies. - Source: PubMed
Yang PeiyingWei DaoyanChakraborty SharmisthaNguyen PhuongCusimano AndrewDeng DefengIqbal ShafaqmuhammadNelson MonicaCui MengDai JianliangGagea MihaiWagner RichardLi YishengCohen Lorenzo - Pancreatic cancer is a highly lethal disease characterized by rapid onset, aggressive progression, and limited treatment options. The involvement of FoxM1 in the TGF-β/Smad signaling pathway has been linked to pancreatic cancer progression; however, the mechanisms behind the cooperative regulation of TGF-β signaling by FoxM1 and Smad4 remain poorly understood. In this study, we utilized molecular cytology techniques, animal models, and human pancreatic cancer tissues to investigate the role of FoxM1 in Smad4 stabilization and its regulation of TGF-β signaling. Our findings reveal that FoxM1 inhibits ubiquitin-proteasome-mediated degradation of Smad4, resulting in its stabilization. Once translocated into the nucleus, Smad4 binds to the FoxM1 promoter region, inducing FoxM1 expression and forming a positive feedback loop. Furthermore, we observed significantly higher expression of this feedback loop in pancreatic cancer tissues compared to adjacent normal tissues, with markedly elevated levels in poorly differentiated tissues compared to well-differentiated ones. Therefore, the loop aberrantly activates the TGF-β pathway, driving pancreatic cancer progression. These findings uncover a novel mechanism of TGF-β pathway activation and provide potential new targets for the prevention and treatment of pancreatic cancer.This study elucidates that FoxM1 functions to impede the ubiquitin proteasome-mediated degradation of Smad4, consequently stabilizing it. Following nuclear translocation, Smad4 binds to the FoxM1 promoter region, initiating FoxM1 expression and establishing a positive feedback loop. This loop plays a pivotal role in promoting pancreatic cancer development and migration by aberrantly activating the TGF-β pathway. - Source: PubMed
Publication date: 2026/04/10
Ruan BanzhanWang BingshuZhang XiaodianLiu FujinWan ZhenlingChen YanWu JulanLuo ChunLu WenyanLu YandaZheng Shaojiang