c_Myc
- Known as:
- c_Myc
- Catalog number:
- 11-433-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- c_Myc
Related products to: c_Myc
9E10 c-mycActin regulatory protein CAP-G,Actin-capping protein GCAP39,Capg,Macrophage-capping protein,Mbh1,Mouse,Mus musculus,Myc basic motif homolog 1Ad-hOKSiM Human Oct4, Klf4, Sox2, and c-MycAd-hOKSiM/Human Oct4, Klf4, Sox2, and c-MycAd-mMKOS c-Myc-F2A-Klf4-T2A-Oct4-E2A-Sox2Ad-mMKOS-GFP c-Myc-F2A-Klf4-T2A-Oct4-E2A-Sox2, GFP tagAd-mMKOS-GFP/c-Myc-F2A-Klf4-T2A-Oct4-E2A-Sox2, GFP tagAd-mMKOS/c-Myc-F2A-Klf4-T2A-Oct4-E2A-Sox2Agarose Immobilized Goat anti-c-mycAgarose Immobilized Goat Anti-c-mycAgarose Immobilized Goat anti-c-myc PolyclonalAgie-bp1,Angiotensinogen gene-inducible enhancer-binding protein 1,DNA-binding protein AGIE-BP1,Hivep2,Human immunodeficiency virus type I enhancer-binding protein 2 homolog,Mibp1,MIBP-1,Myc intron-bialpha c-Myc antibodyalpha c-Myc antibodyalpha c-Myc antibody Polyclonal Antibodies Primary antibodies Related articles to: c_Myc
- Intermediate-risk neuroblastoma patients older than 18 months, with non- amplified, International Neuroblastoma Risk Group Staging System localized, unresectable or International Neuroblastoma Staging System stage 3 tumors, and unfavorable histology have inferior outcomes compared with other intermediate-risk patients. This study aimed to identify genetic prognostic biomarkers within this rare subgroup. - Source: PubMed
Publication date: 2026/07/01
Hartley Hannah EFong Fang ChyiGabriel Alem SStevenson Louise KBeckett EmilyAllinson Lisa MGoodman AngharadPotts AaronWhittle EmilyBarford RubyLamparelli AliceHerd FionaMazzocco KatiaPezzolo AnnalisaMorini MartinaArdito MartinaEva AlessandraOgnibene MarziaFischer MatthiasAckermann SandraRosswog CarolinaHero BarbaraSmith Graham RUnsworth Adrienne AMcCorkindale MichaelGeorge Sally LTall JenniferMolenaar Jan JMatser YvetteLangenberg KarinTytgat GodelieveNoguera RosaBerbegall Ana Pde Mora Jaime FontCombaret ValériePierron GaelleMühlethaler-Mottet AnnickSchoumans JacquelineTchinda JoëlleBanzola IrinaJeison MartaHameiri-Grossman MichalBeiske Klaus HAuger NathalieVan Roy NadineBasta Nermine OMcNally Richard J QTaschner-Mandl SabinePapadakis VassiliosDi Cataldo AndreaWheeler KateBermúdez Jose DBeck-Popovic MajaSegura VanessaCanete AdelaSchleiermacher GudrunTweddle Deborah A - Thymidylate synthase (TS) is a key enzyme in thymidylate biosynthesis and an established target of chemotherapeutics such as 5-fluoro-2'-deoxyuridine (5FdUR) and raltitrexed (RTX). Inhibition of TS disrupts the dUTP:dTTP balance, leading to uracil misincorporation, triggering futile base excision repair cycles, DNA strand breaks, and ultimately cell death. Interestingly, when the main uracil-DNA repair pathway is inhibited, treatment with TS-inhibitory drugs still leads to cell death. Beyond its catalytic role, TS also binds RNA, autoregulating its own translation and interacting with transcripts such as p53 and c-Myc, thereby linking TS activity to broader post-transcriptional regulatory networks. These interactions, together with regulation by miRNAs and lncRNAs, suggest that TS inhibition may provoke cellular responses extending beyond DNA metabolism. To explore these mechanisms, we investigated the transcriptomic effects of TS inhibition with either 5FdUR or RTX in wild-type HCT116 and two HCT116-derived cell lines with different capacities in base excision and mismatch repair pathways. Both drugs induced DNA damage responses yet displayed distinct transcriptional signatures. A strong 5FdUR-biased induction of mRNAs corresponding to p53-related pathways was detected in all cell lines and further validated with qPCR and Western blot. Moreover, co-immunoprecipitation coupled to sequencing revealed direct RNA partners of TS, highlighting its possible post-transcriptional regulatory role. Our findings underscore the multifaceted impact of TS inhibition, linking enzymatic disruption to RNA-level regulation and revealing drug-specific differences in cellular responses. - Source: PubMed
Publication date: 2026/07/01
Holub EszterSzajkó Milda BlankaFelföldi AnnaVértessy Beáta GBékési Angéla - Osteoarthritis (OA) is a leading cause of chronic pain and disability in the elderly. The lack of sensitive diagnostic methods for early OA remains a major clinical challenge. Synovial fluid contains exosomes (SF-exosomes) that carry disease-specific biomolecules, making them promising targets for early diagnosis. However, efficient isolation of SF-exosomes with high purity is technically demanding. This study aimed to develop phosphatidylserine-based molecularly imprinted polymers (P-MIPs) for the efficient enrichment of SF-exosomes and to discover potential protein biomarkers for early OA diagnosis using proteomic analysis. P-MIPs can specifically recognize phosphatidylserine on the extracellular vesicle membrane, thereby achieving highly selective enrichment of extracellular vesicles. P-MIPs were synthesized via a reverse microemulsion system. The binding capacity, specificity, and enrichment efficiency of P-MIPs were characterized. SF-exosomes from 6 OA patients and 6 healthy controls were enriched using P-MIPs and analyzed by LC-MS/MS proteomics. Differentially expressed proteins (DEPs) were subjected to bioinformatics analysis. The diagnostic value of hub genes was validated by ROC analysis in an independent cohort. The results showed that the binding capacity (Qmax) of P-MIPs was 129.71 µmol/g, and the cross-reactivity with sphingomyelin (SM), phenylphosphonic acid (PYP), and tyrosine phosphopeptides was less than 3.5%. The purity of enriched SF-exosomes was 82.6%. A total of 40 DEPs were identified, of which 28 were upregulated and 12 were downregulated in OA. PPI network analyses identified 10 hub genes: IL6, IL1B, MYC, CD4, MMP9, PTPRC, CXCL8, PPARG, ICAM1, and STAT3. ROC analysis showed that among the top five hub genes ranked by degree, MYC (AUC = 0.741) and IL6 (AUC = 0.735) exhibited good diagnostic performance. A combined biomarker panel comprising the top five hub genes achieved an even higher diagnostic accuracy, with an AUC of 0.899. The P-MIPs-based SF-exosome enrichment strategy is efficient and selective. MYC and IL6 are potential diagnostic biomarkers for early OA, and the identified DEPs provide insights into OA pathogenesis. Furthermore, this strategy can be extended for the recognition and enrichment of exosomes in other biological fluid matrices, facilitating the discovery of novel disease biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/07/01
Deng HualongJiang ChaoyongDeng HuaxinLi YaohuaZhang Baoliang - The tumor microenvironment (TME) limits durable antitumor immunity by impairing CD8 T cell responses. Memory like CD8 T cells are important for long-term immune control but are often restricted in the TME. Dendritic cells (DCs) are key regulators of T cell fate. Previous studies have shown that SHP1 in DCs fosters an immunosuppressive microenvironment and facilitates tumor immune escape. T cell factor-1 (TCF-1), encoded by Tcf7 gene, is required for central memory CD8 T cell (TCM) formation and is closely linked to canonical Wnt/β-catenin signaling. However, whether SHP1 in DCs regulates TCF-1 expression and TCM formation remains unclear. To investigate the role of DC intrinsic SHP1 in T cell immunity, SHP1 deficient DC2.4 cells and primary bone marrow derived dendritic cells (BMDCs) were co-cultured with OT-1 T cells to assess proliferation, TCM formation, cytotoxic activity, and TCF-1 expression. A DC-specific SHP1 knockout mice model was used to evaluate antitumor immunity in vivo, and Tcf7 or Ctnnb1 silencing was used to probe the TCF-1/Wnt/β-catenin axis. SHP1 downregulation in DCs markedly enhanced CD8 T cell proliferation, promoted the generation of CD62L CD44 central memory T cells, and potentiated B16-F10-OVA tumor cell killing, accompanied by increased TCF-1 expression in OT-1 T cells. In DC-specific SHP1 knockout mice, EO771 tumor growth was suppressed with concurrent increases in intratumoral IFN-γ and TCF-1 CD8 T cell frequencies. Mechanistically, we found that DC SHP1 regulates TCM formation via TCF-1, as silencing Tcf7 in OT-1 T cells abrogated this effect. SHP1-deficient DCs activated Wnt/β-catenin signaling in CD8 T cells, as shown by increased active β-catenin, total β-catenin, c-Myc and Cyclin D1, and a reduced phospho β-catenin/total β-catenin ratio. Critically, Ctnnb1 silencing in T cells abrogated the enhanced proliferation, TCM formation, and cytotoxic activity induced by SHP1-deficient DCs. DC-intrinsic SHP1 restrains central memory CD8 T cell formation via the TCF-1/Wnt/β-catenin axis. - Source: PubMed
Publication date: 2026/07/01
Li BingLu HuilinHuang JiayiLiang YushengYu WeizeWu ShunhongLei TingTan XiaomingZhang Yuan - Atypical teratoid/rhabdoid tumors (AT/RT) are the most common malignant brain tumors during infancy and associated with a dismal prognosis. The majority of patients suffer from tumor progression or recurrence, but underlying mechanisms remain unknown. To better understand such mechanisms, we performed single-nucleus RNA sequencing (snRNAseq) of eight paired primary tumors and recurrences. Tumor cells and cells of the tumor microenvironment (TME) were analyzed separately. Potentially therapy-resistant tumor cells were identified through the comparison of global gene expression profiles between primary and recurrent tumor cell populations using CIBERSORT. Histopathology, in vitro experiments, bulk RNA sequencing, and survival analysis were performed for validation. Paired primary and recurrent AT/RT showed significant differences in their gene expression profiles. Potentially therapy-resistant AT/RT-MYC tumor cells revealed changes in the extracellular matrix (ECM) as well as altered developmental processes and immune signaling pathways. Respective gene signatures were correlated with inferior survival in AT/RT-MYC patients. Tumor cells of relapsed AT/RT-MYC underwent partial epithelial-mesenchymal transition (pEMT), a feature that was confirmed by immunohistochemistry (IHC) and by analyzing AT/RT cells after standard therapy in vitro. Together, we identified potential mechanisms of tumor relapse and therapy resistance in AT/RT, which could be employed to improve therapy in future. - Source: PubMed
Publication date: 2026/07/01
Altendorf LeaAlthammer AntonRoy RajanyaHack Karolinede Faria Flavia WKoch ArendThaden VanessaSchoof MelanieSchuhmann Martin UHauser PeterJohann Pascal DHasselblatt MartinFrühwald Michael CKerl KorneliusSchüller Ulrich