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
- Chimeric antigen receptor (CAR)-T cell therapy demonstrates remarkable clinical efficacy, yet limited persistence and functional exhaustion impede durable responses. While memory-like phenotypes are associated with sustained CAR-T function and improved clinical outcomes, the underlying molecular mechanisms of CAR-T cell memory maintenance remain incompletely defined and we still lack actionable strategy to sufficiently promote CAR-T cell memory formation. Here, we identified that Karyopherin Subunit Alpha 2 (KPNA2)-mediated MYC nuclear import robustly enhanced CAR-T cell memory and antitumor function. In clinical CAR-T cell products, KPNA2 expression and MYC pathway activation are correlated with superior therapeutic potency. Overexpressing MYC showed negligible effect on CAR-T cell function due to insufficient nuclear import; in contrast, incorporating KPNA2 in CAR-T cells facilitated MYC nuclear import, augmented memory formation, enhanced cytotoxicity and antitumor activity both in vitro and in vivo. Such functional improvement was not associated with risks of transformation in KPNA2-overexpressing CAR-T cells. Mechanistically, our integrated transcriptomic and epigenomic analyses revealed that KPNA2 increased MYC occupancy at memory-associated gene loci, upregulating T cell memory programs. Furthermore, virtual drug screening identified the small molecule TMS which potentiates KPNA2-MYC interaction. TMS treatment of CAR-T cells enhanced MYC nuclear accumulation, promoted memory-oriented transcriptional profiles, and improved antitumor potency in preclinical models. These findings established KPNA2-MYC interaction as a pivotal mechanism governing CAR-T cell memory formation, providing genetic and pharmacological strategies to advance therapeutic T cell design and manufacturing. - Source: PubMed
Publication date: 2026/10/08
Han ShiKong DelinYang ChenYe FangYue JuanWang KexinZheng HaiqiongMo ZhuomaoLiang XinghuaHu KejiaWang JianyuJiang PengleiLi XiaZhang MengZeng XiangjunChen YijinYang LinWang YanyanShao MiQian PengxuHu YongxianHuang HeWang Dongrui - Persistent infection with high-risk human papillomavirus (HPV) is the principal etiologic driver of cervical cancer. However, HPV status and E6/E7-mediated disruption of the p53/RB axis do not fully explain why HPV-associated lesions differ in persistence, malignant progression, therapeutic response, and relapse. This review examines how host chromatin architecture and related transcriptional programs may contribute to the stabilization of malignant cell states following HPV-mediated checkpoint disruption. We discuss evidence linking HPV persistence and integration to epigenetic permissiveness, three-dimensional genome organization, enhancer-promoter rewiring, cohesin dynamics, and WAPL-associated chromatin regulation. Particular attention is given to how these mechanisms may influence MYC/E2F-centered proliferative output and cooperate with context-dependent signaling and tumor microenvironmental adaptation to contribute to treatment tolerance and resistant malignant states. We also consider how chromatin-informed biomarkers, public datasets, perturbation-guided prioritization, authenticated cervical cancer cell lines, organoids, and patient-derived models can be used to evaluate therapeutically relevant vulnerabilities. By integrating viral oncogenesis with host genome regulation and adaptive resistance, this review proposes a conceptual and experimentally testable framework for stratifying HPV-driven cervical cancer and prioritizing candidate intervention nodes. - Source: PubMed
Publication date: 2026/10/08
Kumagai KatsuyoshiSuzuki YasuhiroKitahara KeiChiba AyumiYajima Hiroaki - Hormone receptor-positive (HR+)/HER2-negative metastatic breast cancer that progresses on CDK4/6 inhibitors (CDK4/6i) and endocrine therapy (ET) faces a major therapeutic challenge, and chemotherapy is frequently used despite its modest clinical benefit. Paclitaxel is commonly used in this setting; however, intrinsic and acquired resistance substantially limit the depth and durability of response. Polo-like kinase 1 (PLK1) is a key mitotic regulator implicated in resistance to taxanes and ET/CDK4/6i. We evaluated whether PLK1 inhibition with onvansertib enhances paclitaxel activity in HR+ breast cancer models with intrinsic or acquired ET/CDK4/6i resistance, testing across six cell lines and eight patient-derived xenograft models, including paclitaxel-resistant tumors. The combination synergistically inhibited cell viability in vitro and improved antitumor efficacy in xenograft models. Notably, the combination induced tumor regression across all paclitaxel-resistant models, with complete responses in more than half of treated animals in three of five models, and deep, durable regressions in paclitaxel-sensitive models, markedly outperforming either agent alone. Mechanistically, the combination exacerbated mitotic stress, disrupted spindle architecture, suppressed proliferative and cell-cycle-associated transcriptional programs, and promoted proteasome-dependent c-MYC degradation, resulting in enhanced apoptotic cell death in vitro and in vivo. Importantly, genetic modulation of c-MYC expression altered the apoptotic response, establishing c-MYC downregulation as a key mediator of the observed antitumor efficacy. Collectively, these findings support PLK1 inhibition as a mechanistically rational strategy to potentiate taxane efficacy and overcome resistance in advanced HR+/HER2-negative breast cancer. - Source: PubMed
Publication date: 2026/10/08
Sreekumar SreejaGonzalez Migdalia EKlein DavisEblimit ZeenaMontaudon ElodieCroucher Peter J PDerrien HéloïseSourd LauraWu Chu-ChiaoSmeal TodMarangoni ElisabettaRidinger Maya - Resistance limits the clinical efficacy of RAS inhibitors. We applied chemical and genetic screens and identified the AXL receptor tyrosine kinase as a driver of resistance to RAS-ERK inhibition. We determined that combination treatment with the AXL inhibitor bemcentinib (AXLi) together with the RAS(ON) multi-selective tri-complex inhibitor RMC-7977 (RASi) or the ERK-selective inhibitor SCH772984 (ERKi) significantly enhanced growth suppression in human -mutant pancreatic and lung cancer models. Combined AXLi and RASi treatment of human -mutant pancreatic cell line-derived xenograft tumors synergistically suppressed ERK activation and MYC expression, and caused tumor regression. Analyses of immunocompetent mouse allograft pancreatic tumor models revealed a largely tumor cell-intrinsic response to inhibitor treatment. We identified an unexpected mechanism whereby KRAS inhibition upregulated the AXL ligand GAS6, activating AXL but inducing an AXL-dependent adaptive resistance mechanism wherein AXL antagonizes RASi efficacy. Our observations support concurrent AXL inhibition as a strategy to enhance RAS inhibitor clinical efficacy. - Source: PubMed
Publication date: 2026/08/11
Ching Yan MingNarayanan ShruthiKlomp Jeffrey AIsermann TamaraLoewe SinaChang Wen-HsuanWaters Andrew MNicewarner Peña Sheila RBaldelli ElisaEdwards A ColeBörding TeresaYang RunyingGoodwin Craig MGautam PrsonPonz-Sarvisé MarianoHorst DavidSeamon KyleZhuang YongxianTran LinhJiang JingjingSingh MallikaWennerberg KristerPetricoin Emanuel FBryant Kirsten LStalnecker Clint AEarp H SheltonCox Adrienne DSers ChristineVicent SilvestreDer Channing JPapke Bjoern - The core transcriptional regulatory program governed by a small set of master transcription factors is pivotal for establishing context-specific cellular features. Here, we report the roles of master factor MYC in actively regulating cancer-type specific super-enhancer activity and orchestrating a super-enhancer-dependent core transcriptional regulatory circuitry consisting of MYC, ETS2, and FOXP1 in colorectal cancer. The core regulatory module selectively promotes the transcription of super-enhancer-controlled genes in cooperation with co-activator BRD4, and perturbing the core circuitry factors sensitizes colon cancer cells to BET inhibition. LGR5, a key stemness gene, is activated in colorectal cancer at least in part by a circuitry-controlled distal super-enhancer, which is a frequently gained super-enhancer in colorectal cancer and required for metastasis propagation. These findings reveal a hierarchical transcription regulatory network in colorectal cancer, pinpoint distal enhancer as an important fuel for LGR5 overexpression in cancer, and provide insights for precisely targeting detrimental transcription events in therapy. - Source: PubMed
Publication date: 2026/09/08
Ye MinWang ShilanChen YonghengMa HongchaoYing YingMa WenlongShi LiangMa CanjieLiu XianmingWu WeitaoFordil BushraJia MinGeng RuZhang XinyingSong XiaomanLin TianleWang MaolinZhu Wei-GuoShu Xing-Sheng