c_Myc
- Known as:
- c_Myc
- Catalog number:
- 000695A
- 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
- Protein arginine methyltransferase 5 (PRMT5) is overexpressed in B-cell lymphomas, including diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL). While PRMT5 is known to regulate multiple oncogenic pathways, including PI3K-AKT signaling, its role in lipid metabolism and ferroptosis, a regulated, iron-dependent cell death driven by lipid peroxidation, remains poorly understood. Here, we identify a novel role for PRMT5 in suppressing ferroptosis in DLBCL and MCL cells through upregulation of SLC7A11, which imports cystine for glutathione (GSH) biosynthesis. This effect is mediated by the AKT-MYC-ATF5 signaling axis. ATF5, a MYC-regulated transcription factor overexpressed in these lymphomas, induces SLC7A11 expression. In addition, ATF5 promotes the expression of ATF4, another key regulator of the ferroptotic response, which forms heterodimers with ATF5 to further reinforce this regulatory network. PRMT5 inhibition sensitizes lymphoma cells to ferroptosis inducers such as dimethyl fumarate (DMF), an electrophile that irreversibly depletes GSH via succination. Notably, combined treatment with the PRMT5 inhibitor GSK3326595 and DMF synergistically enhances anti-tumor activity in a patient-derived xenograft (PDX) model. These findings reveal a previously unrecognized PRMT5-ATF5-SLC7A11 axis that drives ferroptosis resistance in B-cell lymphomas and provide a strong rationale for targeting PRMT5 to potentiate ferroptosis-based therapies in relapsed or refractory disease. - Source: PubMed
Publication date: 2026/04/17
Liu YunxiaChen RuoyuGao XiaoyueZhu FenNi QinyuBates Paul DWu SunnyZai ZhuoyanObernberger Victoria AWeerawardhene KavinuTourdot Taylor KPetta SophieConyers Madison JCapitini Christian MRui Lixin - Keloids represent a pathological fibroproliferative disorder with high recurrence rates and limited therapeutic options. This study integrates multi-dataset transcriptomics (GSE158395, GSE188952, GSE92566, GSE173900) and machine learning algorithms (XGBoost, Random Forest, LASSO) to systematically investigate the role of lactylation modification in keloid pathogenesis. We identified 26 lactylation-related differentially expressed genes (15 upregulated, 11 downregulated) enriched in oxidative stress, immune response, and extracellular matrix pathways. Machine learning convergence revealed five lactylation hub genes (PRDX1, CSRP1, IFI16, CALD1, VIM), with PRDX1 exhibiting the highest diagnostic efficacy (AUC = 0.85). Immune infiltration analysis demonstrated significant correlations between hub genes and dysregulated immune cells. Experimental validation confirmed reduced PRDX1 expression in keloid tissues; its knockdown in fibroblasts elevated ROS levels and enhanced proliferation and migration. Regulatory network analysis predicted shared transcription factors (KLF12, NFKB1, MYC) governing hub genes, while drug screening prioritized three clinically actionable compounds (acetaminophen, valproic acid, vorinostat) targeting PRDX1. These findings establish lactylation as a critical regulator of keloid pathogenesis and identify PRDX1 as a promising therapeutic target. - Source: PubMed
Publication date: 2026/04/17
He RuizheSun MengzheLiu TiantianPeng YinboPeng LinboFang Yong - The N-6-methyladenosine (m6A) modification of mRNA regulates transcript abundance in endocrine therapy (ET)-resistant breast cancer (BCa) cells. We reported that m6A reader HNRNPA2B1 decreased miR-145p and miR-424-5p targeting PSAT1 and miR-34b-5p and miR-876-5p targeting PHGDH, thus stimulating the serine synthesis pathway (SSP) in ET-resistant BCa cells. Here we examined m6A regulation of PSAT1 and PHGDH. We report that siMETTL3 increased miR-145-5p, reducing PSAT1, and miR-34b-5p and miR-876-5p, reducing PHGDH, without affecting HNRNPA2B1 or NFkB and decreasing MYC, known to stimulate PSAT1 and PHGDH transcription. In contrast, the METTL3 inhibitor STM2457 increased METTL3, MYC, HNRNPA2B1, NFkB, PSAT1, PHGDH, and serine synthesis, and decreased the miRNAs. These data suggest that reducing METTL3 protein and inhibition of its catalytic activity have different effects on these targets. Selected results were verified in ET-resistant T47D and ZR-75-1 BCa cells. METTL3's stimulation of translation may play a role in these differences. Indeed, siMETTL3 had no effect on MYC, PHGDH, or PSAT1 pre-mRNA whereas STM2457 increased these pre-mRNAs. Overall, our data support a model for m6A regulation of PHGDH and PSAT1 indirectly through miRNAs that target PHGDH and PSAT1. - Source: PubMed
Publication date: 2026/04/15
Piell Kellianne MVallarta AnnaWilt Ali EAvila-Valdes Bailey LSumlut Mary HGoli NavyaPetri Belinda JHe LiqingZhang XiangClem Brian FKlinge Carolyn M - How CoREST-linked chromatin activities are regulated at promoters independently of canonical REST repression remains unclear. Here, we identify the zinc-finger proteins rearranged L-myc fusion (RLF) and ZFP292 as redundant promoter-associated factors that stabilize CoREST-linked LSD1 engagement within RCOR2-containing CoREST assemblies at active and bivalent promoters in embryonic stem cells. Loss of RLF/ZFP292 reduces ZMYM3 occupancy while diminishing LSD1 enrichment at target promoters, whereas RCOR2 and HDAC1 occupancy remain largely unchanged, consistent with a role in stabilizing enzymatic engagement rather than in complex recruitment. Loss of RLF/ZFP292 increases promoter-associated active chromatin features at both promoter classes, but transcriptional upregulation is most evident at genes with bivalent promoters. At a subset of active promoters, selective loss of ZMYM3 coincides with reduced transcription despite retained RCOR2-HDAC1-LSD1 signals. Together, these findings reveal a REST-independent mechanism in which RLF/ZFP292 modulate the functional output of promoter-associated CoREST assemblies to maintain transcriptional balance in pluripotent cells. - Source: PubMed
Publication date: 2026/04/16
Ito TakamasaYoshino MasahitoIsobe Shin-YaObuse Chikashi - Invasive lobular carcinoma (ILC) is the second most common subtype of breast cancer after invasive breast cancer of no special type (IBC-NST). This retrospective analysis of the MINDACT trial investigated transcriptomic differences between estrogen receptor-positive/HER2-negative (ER+/HER2-) ILC versus ER+/HER2- IBC-NST, classic and non-classic ER+/HER2- ILC, and, recurring and non-recurring ER+/HER2- ILC in patients with a low genomic risk and either a low (cL/gL) or high clinical risk (cH/gL). - Source: PubMed
Publication date: 2026/04/17
Desmedt ChristineNguyen Ha-LinhRichard FrançoisLinn SabineMetzger Fihlo OttoPoncet CoralieWesseling JelleAalders KimDelorenzi MauroDelaloge SuzettePierga Jean-YvesBrain EtienneVrijaldenhoven SuzanVan Baelen KarenMaetens MarionRutgers EmielPiccart Martinevan 't Veer LauraViale GiuseppeCardoso Fatima