Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Known as:
- Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Catalog number:
- sr10030va-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Human Nanog Differentiation Reporter (pGreenZeo pre-packaged)
Related genes to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Gene:
- NANOG NIH gene
- Name:
- Nanog homeobox
- Previous symbol:
- -
- Synonyms:
- FLJ12581, FLJ40451
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-10
- Date modifiied:
- 2014-11-19
Related products to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
Related articles to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- β-elemene (ELE), a natural sesquiterpene with antitumor properties, exerts immunomodulatory effects on osteosarcoma (OS), but its impact on the tumor microenvironment and cancer stemness remains unclear. This study investigated how ELE reprograms tumor-associated macrophages (TAMs) to suppress OS progression. - Source: PubMed
Publication date: 2026/09/12
Zhang ShaochunLiu TingKe Jing - Cancer stem cells (CSCs) drive tumor initiation, metastasis, and therapy resistance, yet their remarkable persistence remains poorly understood. While CSCs share stemness attributes with embryonic stem cells (ESCs), including self-renewal, transcriptional plasticity, and permissive chromatin, they exhibit a fundamentally divergent regulatory logic that prioritizes survival over developmental fidelity. ESCs maintain globally open chromatin that supports transcriptional hyperactivity but predisposes them to apoptosis under genotoxic stress, whereas CSCs maintain dynamically inducible, permissive chromatin at survival loci while repressing differentiation programs, enabling adaptive stress responses. We advance the hypothesis that CSC persistence emerges not from any single factor, but from the integrative rewiring of signaling cascades (Wnt/β-catenin, Notch, Hedgehog, PI3K/AKT/mTOR), stress-responsive transcription factors (HIFs, NF-κB, STAT3), and core pluripotency networks (OCT4, SOX2, NANOG) within a survival-centric context, reinforced by dynamic chromatin remodeling, inducible super-enhancer landscapes, and microenvironmental cues (hypoxia, inflammation, matrix stiffness). Within this framework, the E2F family serves as a key contextual integrator: in ESCs, constitutive E2F activity triggers p53-mediated apoptosis upon DNA damage, preserving genomic integrity; in CSCs, deregulated E2F activity redirects transcription toward DNA repair, antioxidant defenses, and anti-apoptotic programs. This functional divergence underscores that phenotypic outcome is determined by the broader cellular and epigenetic landscape rather than any single factor. We conclude that CSC persistence is an emergent property of this integrated, survival-centric program, fundamentally distinct from the developmental imperative of ESCs. Effective therapeutic strategies must therefore move beyond targeting individual pathways to dismantle the interconnected regulatory networks that define the CSC survival context, offering a more robust approach to overcome therapy resistance and prevent tumor relapse. - Source: PubMed
Publication date: 2026/09/11
Ahmadi YasinFar Babak ElyasiAbolhasani Sakhavat - Originating from notochord remains, chordoma is a rare, chronic, low-grade axial skeletal cancer that is characterized by metastasis and adjacent tissue invasion, as well as a high risk of treatment resistance. Surgical intervention is the most common method used for treatment followed by radiotherapy to avoid the relapse of the tumor. Targeting the proteins involved in tumor-associated pathways is crucial since alternative drugs are required for the cure. The nuclear receptor REV-ERBα, a member of the circadian rhythm family, has elevated expression levels, which function as a tumor suppressor. SR9009 is a pyrrole-derived specific agonist that target REV-ERBα negatively regulates autophagy in cancer and induce apoptosis in a caspase-dependent manner and shown antitumor activity in several cancer models. Chordoma cells were treated with SR9009, and functional assays including colony formation, viability, and migration were tested. In addition, molecular docking analyses were performed to predict the interaction of SR9009 with proteins involved in migration, colony formation, proliferation were targeted. SR9009 reduced viability of chordoma cells in a concentration-dependent manner while sparing HNPCs, and 30 µM was selected as an effective concentration for subsequent experiments. At this concentration, SR9009 markedly inhibited chordoma cell migration and strongly suppressed colony formation in both CH22 and MUG-Chor1 cells. Molecular docking predicted high-affinity binding of SR9009 to PI3K, Akt1, Wnt3, β-catenin, and Nanog, suggesting potential interference with signaling networks implicated in chordoma cell proliferation and survival. Our findings indicate that SR9009 exerts robust anti-cancer effects in chordoma cell lines and highlight SR9009 as a promising candidate for further preclinical evaluation in chordoma. The involvement of circadian clock-related and associated signaling pathways in these effects remains putative and warrants mechanistic validation in future studies. - Source: PubMed
Publication date: 2026/09/11
Görkay Ahmet HakanFettah Muhammed ÜmeyrÇataltepe Sude NazTüten Çağla NurBilen YaseminDurak EnesAyaz FurkanAydemir Esra - - Source: PubMed
Publication date: 2026/09/07
Chen Chia-LinUthaya Kumar Dinesh BabuPunj VasuXu JunSher LindaTahara Stanley MHess SonjaMachida Keigo - For the first time, this study aimed to investigate the potential protective effects of L-carnitine and moderate-intensity exercise training (MIET), both individually and in combination, against varicocele (VCL)-induced impairment of spermatogonial stem cell (SSC) self-renewal. - Source: PubMed
Publication date: 2026/08/08
Ibrahim Abdulameer Al-Khuzaie ZainabTolouei Azar JavadNasr-Esfahani Mohammad HosseinRazi Mazdak