c_Myc
- Known as:
- c_Myc
- Catalog number:
- 000402A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- 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
- Pediatric acute myeloid leukemia (AML) is biologically distinct from adult AML and carries a poor prognosis. OVCA2, a serine hydrolase with context-dependent roles, has unknown function in AML. We aimed to investigate its role, regulation, and clinical significance in pediatric AML. - Source: PubMed
Publication date: 2026/04/28
Jiao WanyanCheng SaisaiYang XiaoLiu HaiyanTang XiaodongLi QianlongLi YingZhou Bi - Leucine-rich repeat-containing protein 59 (LRRC59) has been implicated in the pathogenesis of various human cancers, but its functional role and underlying molecular mechanisms in cervical carcinogenesis and progression remain unknown. In this study, LRRC59 expression was assessed in cervical cancer (CC) and normal cervical tissues using public databases and clinical specimens. Correlations between LRRC59 expression and clinical characteristics were analyzed using data from our institutional cohort and The Cancer Genome Atlas (TCGA). The functional effects of LRRC59 on CC cell proliferation, apoptosis, invasion, and migration were evaluated through in vitro assays and xenograft tumor models. Potential mechanisms were identified by integrated bioinformatics analysis and subsequently validated experimentally. LRRC59 was significantly upregulated in CC tissues, and elevated LRRC59 expression correlated with poor prognosis. Knockdown of LRRC59 suppressed CC cell proliferation, invasion, and migration, while promoting apoptosis. Mechanistically, LRRC59 knockdown downregulated total β-catenin, nuclear β-catenin, and the expression of downstream targets c-Myc and cyclin D1. Treatment with SKL2001, a Wnt/β-catenin pathway agonist, partially reversed the inhibitory effects of LRRC59 knockdown on proliferation, invasion, and migration, as well as its pro-apoptotic effect. Furthermore, LRRC59 knockdown led to reduced expression of Y-box binding protein 1 (YBX1). Collectively, these findings demonstrate that LRRC59 promotes CC progression likely via YBX1-mediated Wnt/β-catenin signaling, identifying LRRC59 as a promising prognostic biomarker and potential therapeutic target in cervical cancer. - Source: PubMed
Publication date: 2026/04/28
Zhu QianXu GuiqinWang TianmingDing ZhuyunLiu LianhuaLing LingYing Xiaoyan - Neuroblastoma remains a major cause of pediatric cancer mortality and although intensive multimodal treatment strategies have improved survival, they have also led to an increased risk of long-term treatment-related toxicities among survivors. This study aimed to evaluate the potential involvement of (Musashi) Msi1 in neuroblastoma oncogenesis and etoposide treatment response. - Source: PubMed
Cochran Elizabeth DQiao JingboMachchhar ArtiJacobson Jillian CMcCreery SullivanChung Dai H - Resistance to Bruton tyrosine kinase inhibitors (BTKi) is inevitable in mantle cell lymphoma (MCL). Cyclin-dependent kinase-9 (CDK9), a key regulator of oncogenic transcription, is a promising therapeutic target. Here we studied a selective CDK9 inhibitor, AZD4573, in MCL. Treatment with AZD4573 thwarted growth of both parental and ibrutinib-resistant MCL cell lines and primary MCL cells and downregulated expression of MYC and MCL1. However, CDK9 inhibition enhanced basal and maximal oxygen consumption rate, as well as increased production of ATP and reactive oxygen species in ibrutinib-resistant cell lines and primary MCL cells. While treatment with AZD4573 led to modest prolongation of survival in an ibrutinib-resistant MCL PDX mouse model, accompanied by downregulation of TNF/NF-B and mTORC1 signaling pathways in murine splenocytes, OxPhos was upregulated suggesting tumor metabolic reprogramming. Single-cell RNA Sequencing analysis of PBMCs from patients treated with AZD4573 on a clinical trial demonstrated sustained downregulation of MYC targets and OxPhos in malignant B-cells from a responding patient with MCL. Conversely, two refractory patients exhibited upregulation of MYC targets and OxPhos in PBMCs. OxPhos inhibitor IACS-010759 demonstrated synergy with AZD4573 in vitro. Thus, CDK9 inhibition exhibits activity in ibrutinib-resistant MCL and can be further enhanced by co-targeting of OxPhos. - Source: PubMed
Publication date: 2026/04/28
Roleder CarlyZhao XiaofanLam ViShen HaifengDominguez Edward CChen CanpingRodriguez-Rodriguez SoniaWang LiliPhillips TycelXia ZhengDanilov Alexey V - Germline BRCA1/2 pathogenic variant (PV) carriers have elevated young-onset breast cancer risk. To define the pretreatment genomic landscapes of young-onset gBRCA-associated breast cancer, we evaluated 136 treatment-naïve tumors diagnosed before age 50 (92.6% ≤40): gBRCA1 86(63.2%); gBRCA2 50(36.8%) in the prospective POSH study, and 66 noncarriers from The Cancer Genome Atlas. Using whole exome sequencing, we analyzed somatic variation, allele-specific loss of heterozygosity (asLOH), homologous recombination deficiency (HRD), and single-base substitution signatures (SBS). gBRCA1(93%) and gBRCA2(96%) breast cancers had high rates of asLOH, but differed significantly in average HRD scores (57.4 ± 1.3 vs 43.7 ± 1.5, P < 0.0001) and median SBS composition (%): SBS1 (aging-associated) 12.9 vs 7.3, P = 0.013; SBS18 (reactive oxygen species [ROS]-associated) 1.4 vs 0, P = 0.007; and SBS3 (HRD-associated) 27.3 vs 42.6, P = 0.002. Compared to gBRCA2 tumors, gBRCA1 tumors with asLOH were significantly enriched for alterations in Hallmark ROS, DNA repair, and epithelial-mesenchymal transition pathways. In ER-positive, HER2-negative tumors from gBRCA1/2 carriers compared to noncarriers, we found significant enrichment of RB1 (OR:6.3;95%CI:2.8-15.4;padj = 0.001), TP53 (OR:4.6;95%CI:1.9-12.1;padj = 0.017), FAT1 (OR:3.9;95%CI:1.84-8.7;padj = 0.013), and MYC (OR:4.0;95%CI:1.8-9.1;padj = 0.017) SNV/indels/CNVs, associated with CDK4/6i resistance. Together, these findings demonstrate significant differences between gBRCA1 and gBRCA2-associated breast cancers, and preexisting CDK4/6i resistance mechanisms supporting prospective trials with individualized therapy for gBRCA1 vs gBRCA2 carriers, and comparing PARPi to CDK4/6i for ER-positive gBRCA1/2-associated breast cancer. - Source: PubMed
Publication date: 2026/04/28
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