c_Myc EMSA Probe Set
- Known as:
- c_Myc EMSA Probe Set
- Catalog number:
- AY1283P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- c_Myc EMSA Probe Set
Related products to: c_Myc EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: c_Myc EMSA Probe Set
- Cancer stem cells (CSCs) are a therapy-refractory subpopulation that drives tumor persistence, recurrence, and metastasis. A defining characteristic of CSCs is their ability to reversibly exit the cell cycle and enter a quiescent state, thereby escaping cytotoxic therapies that primarily target proliferating cells. Although numerous reviews have examined CSC dormancy and quiescence, less attention has been devoted to recently identified regulators and to the molecular events associated with the transition into quiescence. This narrative review consolidates current knowledge on CSC-specific entry regulators, including the pRb/RBL2-E2F1/4-GCN5 axis, Fbxw7-c-Myc pathway, PML-PPARδ-FAO axis, ID1/ID3-p21 network, JARID1B-mediated G-like states, CDH1-SIRT5-Cyclin F axis, and AP-1/ETS network, alongside emerging evidence on epigenetic regulation, circadian influences, and immune-mediated signals. We critically evaluate the exhaustion hypothesis, delineate a therapeutic framework that distinguishes between prevention of quiescence entry, elimination of dormant CSCs, and forced reactivation, and identify key knowledge gaps. By integrating recent advances within a structured perspective, this review provides a framework for understanding how CSCs exploit quiescence for survival and therapy resistance and informs strategies to target this resilient population. - Source: PubMed
Ahmadi YasinAbdullah Trefa MAbolhasani SakhavatJalizi Amin - Chemoresistance, often driven by aberrant transcriptional and epigenetic mechanisms, remains a significant barrier to effective colon cancer therapy. This study introduces a dendrimer-based proteolysis-targeting chimera (PROTAC) system, JTP, generated by conjugation of polyamidoamine (PAMAM-G4) dendrimer with 4-hydroxythalidomide (an E3 ligase recruiter) and JQ1 carboxylic acid (a BRD4 inhibitor). The multivalent dendrimer scaffold increases local surface ligand density, promotes endocytic uptake and endosomal escape, and facilitates cytosolic engagement of BRD4 for proteasome-mediated degradation. In vitro, JTP effectively increased the chemosensitivity of CT26 colon cancer cells to chemotherapy, particularly to irinotecan, leading to enhanced DNA damage, cell cycle arrest in the S and G2/M phases, and apoptosis, as well as a synergistic reduction in oncoprotein expression. In vivo studies in orthotopic colon cancer-bearing mice demonstrated a prominent antitumor effect of JTP in combination with irinotecan, yielding marked inhibition of tumors and metastases and promoting long-term survival, with toxicity within a well-tolerated range. The in vivo studies also demonstrated the robust effects of JTP on reducing the expression of TFEB, c-Myc, β-catenin, Bcl-2, VEGFR2, IL-1β, TNF-α, HIF-1α, and vimentin by BRD4 elimination in tumor tissues. These findings demonstrate that combining JTP with epigenetic modulation offers an effective strategy to promote chemotherapeutic effects in colon cancer. - Source: PubMed
Publication date: 2026/09/17
Sharmila RamalingamIong Weng ChiLu I-LinSabu ArjunLo Chun-LiangShen Mina Ming-YinChiu Hsin-Cheng - To explore the molecular mechanisms by which ethionine induces neural tube defects (NTD) through regulating the lysine demethylase 5A (KDM5A)/trimethylated lysine 4 of histone H3 (H3K4me3) axis and modulating the Wnt/β-catenin signaling pathway. Specific pathogen-free adult male and female C57BL/6 mice (80 females and 35 males) were housed overnight in a 2∶1 female-to-male ratio. Vaginal plugs were examined the following morning to confirm pregnancy. Pregnant mice were randomly divided into two groups: the ethionine experimental group (ethionine group) and the control group. At embryonic day 7.5 (E7.5), the ethionine group received a single intraperitoneal injection of ethionine (500 mg/kg) to establish the NTD model, while the control group was injected with an equal volume of normal saline, with 21 mice in each group. At E10.5, pregnant mice were sacrificed and embryos were collected for observation and photography under a stereomicroscope. Brain tissues from embryos of both groups were harvested for transcriptome sequencing. The expression levels of KDM5A, H3K4me3, Wnt/β-catenin pathway components [β-catenin, transcription factor 4 (TCF4), axis inhibition protein 2 (Axin2), phosphorylated glycogen synthase kinase 3β (p-GSK3β)], and cell proliferation-related proteins [G1/S-specific cyclin-D1 (Cyclin D1), proliferating cell nuclear antigen (PCNA), Myc oncogene (c-Myc)] were assessed by Western blotting, real-time quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence. An additional KDM5A-specific inhibitor GSK-4J treatment group (GSK-4J group) and ethionine combined with GSK-4J treatment group (ethionine+GSK-4J group) were included to verify the regulatory role of the KDM5A/H3K4me3 axis. The pregnant mice in the GSK-4J group received intraperitoneal injection of GSK-4J (7 mg/kg) and the ethionine+GSK-4J group were injected with both 7 mg/kg GSK-4J and 500 mg/kg ethionine, with 12 mice in each group. Comparisons between the two groups were performed using independent samples t-test, one-way ANOVA was applied to evaluate the overall differences among multiple groups, and Tukey's honestly significant difference test was adopted for pairwise post-hoc comparisons. The ethionine treated group exhibited 48.79% (121/248) incidence of incomplete brain structure and morphological malformations, while the malformation rate in the control group was 3.73% (10/268), with a statistically significant difference (P<0.001). Compared with the control group, the ethionine group showed elevated KDM5A mRNA and protein levels, accompanied by reduced H3K4me3 modification levels (all P<0.001); protein expression of β-catenin, TCF4, and Axin2 were decreased (P<0.01, P<0.05), whereas p-GSK3β was increased (P<0.01). Following GSK-4J intervention, the expression of β-catenin, TCF4, and Axin2 was partially restored (all P<0.01), and the percentage of Cyclin D1-positive cells, as well as the expression of PCNA and c-Myc were increased (all P<0.05). Ethionine participates in NTD development by upregulating KDM5A to decreased H3K4me3 levels, inhibiting Wnt/β-catenin signaling pathway, and reducing neuroepithelial cell proliferation. Thus, targeting the KDM5A/H3K4me3 axis may provide a new strategy for the prevention and treatment of NTD. - Source: PubMed
Gao J JMu QZhang HZhang X BCao RZhang LGuo Y Y - Head and neck squamous cell carcinomas (HNSCCs) remain a significant clinical challenge due to treatment resistance and therapy-associated toxicity. Here, we evaluate the therapeutic potential and mechanism of action of AOH1996, a first-in-class small molecule that targets a cancer-associated isoform of proliferating cell nuclear antigen (caPCNA). Across HPV-positive and HPV-negative HNSCC models, AOH1996 induces robust cytotoxicity associated with mitotic arrest, multipolar mitosis, failed cytokinesis, cell-cell fusion, and DNA damage. Live-cell imaging reveals widespread mitotic catastrophe with limited successful mitotic progression. Notably, AOH1996 sensitivity correlates with c-Myc abundance, suggesting a potential biomarker of response. In vivo, AOH1996 suppresses tumor growth with minimal toxicity in xenograft models. Together, these findings establish AOH1996 as a promising therapeutic candidate that disrupts mitotic fidelity and induces cancer-selective cytotoxicity in HNSCC. - Source: PubMed
Rohlfes NicholasWallace Nicholas A - Lung adenocarcinoma (LUAD) remains molecularly heterogeneous, and many tumors lack clearly tractable vulnerabilities. We developed DepPrior, a computational framework that ranks candidate LUAD therapeutic targets by requiring concordant evidence of CRISPR dependency separability, molecular predictability, and cross-cohort expression/protein reproducibility. DepMap dependency scores were modeled from matched expression and copy-number features using linear and non-linear learners, and gene-level AUROC and R were combined into a heuristic DepScore. The final candidate set included FERMT2, CRKL, MYC, CHMP4B and related genes. The set formed a coherent tumor expression module in TCGA-LUAD, was strongly associated with proliferation-linked features, and showed rank-based concordance across GEO transcriptomic cohorts and CPTAC transcriptomic/proteomic resources. Five-fold cross-validation supported the ranking of non-linear models, although performance gains were moderate and should be interpreted as model-ranking evidence rather than as large effect-size proof. Orthogonal experiments in HCC827 cells showed modest but reproducible protein-level reductions after FERMT2 and CRKL knockdown, accompanied by a directionally stronger apoptosis-associated protein shift after combined suppression than after single perturbation. These findings support DepPrior as a reproducibility-oriented, hypothesis-generating approach for target nomination. Because cross-cohort expression concordance does not prove patient-tumor dependency conservation, and experimental validation was restricted to selected genes and cell-line systems without rescue or proliferation/clonogenic assays, the prioritized genes should be considered candidates for further perturbation, rescue, patient-derived model, and therapeutic tractability studies. - Source: PubMed
Publication date: 2026/08/27
Zhou FengWang ChengMo LizhiSun XuanZhang Ji