c_Myc
- Known as:
- c_Myc
- Catalog number:
- ANT-211
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- 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
- - Source: PubMed
Publication date: 2026/04/20
He Tian-LinZhang Yi-JieJiang HuiLi Xiao-HuiZhu HaiZheng Kai-Lian - Cutaneous T-cell lymphoma (CTCL) represents a heterogeneous group of non-Hodgkin lymphomas with limited curative treatment options. The pronounced male predominance in CTCL incidence suggests hormonal influences in disease pathogenesis, prompting investigation into estrogen receptor signaling pathways as therapeutic targets. Building upon previous evidence of tumor-suppressive roles of estrogen signaling via estrogen receptor β, we investigated the therapeutic potential of targeting the G-protein-coupled estrogen receptor (GPER) in CTCL models. We evaluated the antitumor effects of G-1, a selective GPER agonist, in CTCL cell lines and primary patient-derived malignant T cells using in vitro and in vivo approaches. G-1 demonstrated robust dose-dependent cytotoxic effects against CTCL cells, with notable selectivity, as healthy CD4 T lymphocytes were largely unaffected. Mechanistically, G-1 induced G/M arrest and apoptosis, involving activation of DNA damage responses and extrinsic apoptotic signaling, along with suppression of proliferative and survival pathways, including c-Myc and NF-κB. In vivo validation using a MyLa xenograft model demonstrated significant tumor growth inhibition following G-1 treatment without toxicity. These findings position GPER as a promising therapeutic target in CTCL, and support further development of GPER-targeted strategies for treating CTCL. - Source: PubMed
Publication date: 2026/03/02
Özistanbullu DenizBahrami KarolaDoll MonikaReichenbach GabiPöschl Martina SarahWilhelm RaphaelZöller NadjaKönig AnkeSpahn PascalJäger ManuelQuist Sven RScheller TheresiaWinkler LarsNicolay Jan PSchilling BastianKaufmann RolandMeissner MarkusKleemann JohannesKippenberger Stefan - The present study investigates the therapeutic potential of L-sodium lactate in a dextran sodium sulfate (DSS)-induced colitis C57BL/6J mice model. Treatment with L-sodium lactate significantly mitigated disease severity, as evidenced by reduced colon shortening ( < 0.05) and elevated levels of the anti-inflammatory cytokine IL-10 ( < 0.05). Tandem mass tag (TMT)-based proteomic profiling revealed dual mechanisms, involving the up-regulation of cell cycle- and proliferation-associated proteins (PCNA, SMC, eEF2K) and the down-regulation of immune-related proteins (immunoglobulin variants, Granzyme A). , 10 μM L-sodium lactate has been demonstrated to promote the proliferation and migration of colorectal cancer cells (MC38/HCT116) ( < 0.05), accompanied by increased expression of c-Myc and PCNA. Collectively, these findings suggest that L-sodium lactate may enhance mucosal repair while suppressing histopathological injury in colitis, although further studies are needed to confirm these mechanisms. - Source: PubMed
Publication date: 2026/03/15
Huang PanShao Kang-PingWang Si-YuShao Gen-BaoHu Jian-PengZhou Zheng-Rong - The effects of natural compounds in cancer chemoprevention are being extensively studied. This study assesses the cytotoxic, apoptotic and autophagic effects of cirsimaritin and humulene in hepatoma cells. Antioxidant activity in normal kidney epithelial cell line (VERO) and cytotoxicity tests in HepG2 cells were investigated. Their effects on P53, c-myclocus , apoptotic, and autophagic proteins in HepG2 cells along with flow cytometric analysis of cell cycle and apoptosis were determined. Molecular docking to some proteins was studied. The in vitro results indicated an enhanced antioxidant activity in VERO cells by cirsimaritin and humulene, with low cytotoxic effects in HepG2 cells (half maximal inhibitory concentrations (IC) were 363 and 378 µg/ml respectively) and no cytotoxicity in normal cells at high concentration. They reduced expression and induced P53 activity, G1-cell cycle arrest, and proapoptotic and autophagic cascades in HepG2 cells. Flow cytometric analysis of cell cycle and apoptotic cells and the in silico study confirmed the biochemical results of cirsimaritin against P53, proapoptotic, and autophagic proteins. Collectively, cirsimaritin could markedly inhibit HepG2 cell progression through induction of P53, apoptotic, and autophagic cascades in tested hepatocellular carcinoma cells over humulene's effects. Its protective antioxidant effects in normal cells and anticancer effect make it a promising candidate for preventing the progression of HCC. - Source: PubMed
Publication date: 2026/04/15
Ismail Abo-Elfadl Huda MMegahd Huda ESharaky MarwaAlshazly OmarMohamed Mamdouh F AEl-Rhman Amira Abd - Pancreatic ductal adenocarcinoma shows early dissemination, stromal remodeling, and therapy resistance, but how tumor programs co-evolve with immune and stromal changes across stages remains unclear. We built a stage-resolved transcriptomic atlas using bulk RNA sequencing of FFPE samples from 443 untreated tumors spanning resectable, locally advanced, primary metastatic, and liver metastatic disease. Integrative modeling identified ten transcriptional programs with monotonic dynamics during progression. Early stages were enriched for epithelial differentiation and immune-stimulatory signals. Advanced stages showed increased cytoskeletal remodeling, vesicular trafficking, oxidative stress responses, and mitochondrial metabolism. Pathway analysis revealed enhanced PI3K-AKT-mTOR signaling and MYC target engagement in metastatic disease. Immune deconvolution showed loss of CD8 T cells, dendritic cells, and M1 macrophages. Compact gene signatures stratified stage and survival and generalized to TCGA and ICGC cohorts. Functional assays confirmed greater invasiveness, altered redox balance, and mitochondrial dependence in advanced disease, suggesting stage-associated metabolic vulnerabilities. - Source: PubMed
Publication date: 2026/02/27
Chuluyan EduardoChanez BriceMeilerman AnaliaRemolins CarlaPaes de Lima AndreaMatamoros KevinIncardona ClaudioGuerrieri DiegoKohan GustavoGottardo FlorenciaLedesma MartinGarona JuanDavio CarlosYaneff AgustinSahores AnaGrasso DanielGarcia Maria NoePapademetrio DanielaPasqualini Maria EugeniaSarotto LuisLezcano Felix GabrielGarnier JonathanPasqua AnaliaMazza OscarHammel PascalFraunhoffer NicolasDusetti NelsonIovanna Juan