Human Nanog Differentiation Reporter (pGreenZeo, plasmid)
- Known as:
- Human Nanog Differentiation Reporter (pGreenZeo, plasmid)
- Catalog number:
- SR10030PA-1
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- SBI
- Gene target:
- Human Nanog Differentiation Reporter (pGreenZeo plasmid)
Related genes to: Human Nanog Differentiation Reporter (pGreenZeo, plasmid)
- 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, plasmid)
Related articles to: Human Nanog Differentiation Reporter (pGreenZeo, plasmid)
- - Source: PubMed
Publication date: 2026/08/14
Chen Chia-LinUthaya Kumar Dinesh BabuPunj VasuXu JunSher LindaTahara Stanley MHess SonjaMachida Keigo - Vital pulp therapy (VPT) aims to preserve pulp vitality and stimulate regeneration of the dentin-pulp complex. Dental pulp stem cells (DPSCs) are clonogenic mesenchymal stem cells with high self-renewal and multipotent differentiation capacity. Bioactive cements such as mineral trioxide aggregate (MTA) and calcium-enriched mixture (CEM) are widely used as pulp-capping agents due to their biocompatibility. Platelet-rich fibrin (PRF), an autologous fibrin matrix rich in cytokines and growth factors, has been used to support tissue healing and regeneration. - Source: PubMed
Publication date: 2026/08/03
Pourmohammadi-Nejad FatemehIrannezhad AliAbazarpour RaminAbedi PouyaYousefi-Ahmadipour Aliakbar - Pancreatic stellate cells (PSCs) play a central role in pancreatic physiology and disease, and the transition between their quiescent and activated states influences processes such as fibrosis and regeneration. However, the stem cell-like properties of PSCs remain unclear. This study aims to clarify the stem cell characteristics of PSCs and establish a method to maintain their quiescent state, thereby providing a new perspective on pancreatic regeneration. - Source: PubMed
Publication date: 2026/07/30
Cai ZhenShengNi ChengmingWang QianQianWang XiaohangWang HuanChen YangGuo YanLin HaoSun BoQiu ShanhuSun Zilin - Mitochondria have emerged as key regulators of breast cancer stem cell (CSC) biology. Mitochondrial metabolic pathways, including oxidative phosphorylation (OXPHOS) and mitochondrial biogenesis, are frequently altered during tumorigenesis, highlighting their role in breast cancer pathogenesis. Since breast CSCs are highly dependent on mitochondrial metabolism, targeting mitochondrial DNA (mtDNA) replication may represent a strategy to impair CSC maintenance. Mitochondrial DNA polymerase-γ (POLG), composed of a catalytic subunit encoded by POLG1 and an accessory subunit encoded by POLG2, is essential for mtDNA replication and repair. In this pilot study, we investigated whether targeting POLG could modulate breast CSC activity. Genetic knockdown of POLG1 and POLG2 in MCF-7 cells resulted in mtDNA depletion, reduced mitochondrial protein expression, impaired energy production, and loss of stemness-related features. To pharmacologically target POLG, we tested Alovudine, a nucleoside reverse transcriptase inhibitor known to act as an off-target POLG inhibitor. In MCF-7 cells, Alovudine reduced clonogenic potential, decreased mitochondrial DNA-encoded protein levels, and lowered oxygen consumption. To further validate these findings, we employed the independent POLG inhibitor Zalcitabine (ddC) in additional breast cancer models. ddC impaired mitochondrial respiration, reduced mammosphere formation, and modulated SOX2 and NANOG expression. Preliminary Kaplan-Meier analyses in a cohort of 458 breast cancer patients showed that high POLG1 expression correlates with worse clinical outcomes, including relapse-free and overall survival. Taken together, these findings suggest that POLG supports mitochondrial function and CSC maintenance, highlighting its potential as a therapeutic target and prognostic biomarker in breast cancer. - Source: PubMed
Publication date: 2026/08/08
Chinigò ChiaraSugden Conor JFiorillo MarcoCappello Anna RitaSotgia FedericaLisanti Michael P - Non-small cell lung cancer (NSCLC) progression is strongly influenced by tumor-associated macrophages (TAMs), which frequently acquire an M2-like phenotype that promotes proliferation, epithelial-mesenchymal transition (EMT), angiogenesis, stemness, and therapy resistance. Previous studies from our group established the direct cytostatic and macrophage-polarizing effects of the synthetic coumarin derivative 4-fluorophenylacetamide-acetyl coumarin (4-FPAC), including ROS-mediated apoptosis, G0/G1 cell-cycle arrest, suppression of EMT-associated signaling in A549 cells, and promotion of M1-like macrophage polarization. In the present study, we investigated whether 4-FPAC-modulated TAM-derived conditioned media could suppress tumor-promoting behavior in A549 NSCLC cells. THP-1 monocytes were differentiated into macrophages and polarized using A549-conditioned medium to generate TAM-like macrophages. These TAMs were subsequently treated with 4-FPAC, and conditioned media from control or treated TAMs were applied to A549 cells to evaluate macrophage-associated anti-tumor effects. MTT analysis further showed that direct exposure of A549 cells to 4-FPAC under TAM-CM-supported conditions reduced cell viability in a dose-dependent manner. Functional assays demonstrated that conditioned media derived from 4-FPAC-treated TAMs significantly reduced A549 proliferation, inhibited migration and invasion, and impaired angiogenic responses in a chick chorioallantoic membrane model. Flow cytometry revealed G0/G1 cell-cycle arrest and reduced NANOG-positive stem-like cells, while DNA fragmentation and TUNEL assays confirmed enhanced apoptosis. Mechanistically, qRT-PCR and immunoblotting demonstrated EMT reversal, suppression of AKT signaling, VEGFα, IL8, OCT3/4, and NANOG, and upregulation of p21, p53, and caspase-3/cleaved caspase-3. Collectively, these findings demonstrate that 4-FPAC directly suppresses A549 viability under TAM-CM-supported conditions and modulates TAM-derived conditioned-media activity, highlighting its potential to target both tumor cells and tumor-macrophage interactions within the NSCLC microenvironment. - Source: PubMed
Singh AnjaliDanes DhanushBalakrishnan Suresh