Nanog, Human Polyclonal
- Known as:
- Nanog, Human Polyclonal
- Catalog number:
- PC-102
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Kamiya
- Gene target:
- Nanog Human Polyclonal
Related genes to: Nanog, Human Polyclonal
- 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: Nanog, Human Polyclonal
Related articles to: Nanog, Human Polyclonal
- Ovarian cancer remains difficult to treat due to the persistence of chemoresistant cancer stem-like cells (CSCs), which are major drivers of tumor relapse. Herein, we engineered a hyaluronic acid-functionalized nanoplatform (HS-Cu@DOX) via the assembly of a shikonin-copper (SKN-Cu) coordination complex with hyaluronic acid, followed by electrostatic loading of doxorubicin (DOX), enabling tumor-targeted co-delivery of both therapeutic agents. This nanoplatform disrupts intracellular redox homeostasis to induce cuproptosis while concurrently suppressing CSC stemness through downregulation of key pluripotency-associated transcription factors (e.g., SOX2, OCT4, and NANOG). By depleting intracellular glutathione (GSH) and impairing antioxidant defenses, HS-Cu@DOX disrupts the oxidative stress resilience of CSCs, thereby restoring their sensitivity to DOX-induced apoptosis. Consequently, this strategy enhances DOX-mediated cytotoxicity and reduces systemic toxicity while maintaining potent antitumor efficacy. Collectively, our findings demonstrate that combining cuproptosis induction with CSC stemness suppression represents a promising strategy for overcoming chemoresistance, highlighting HS-Cu@DOX as a potential therapeutic candidate for recurrent ovarian cancer. - Source: PubMed
Publication date: 2026/07/09
Liu ShanshanHuang YichunYan FanchenTian HailongLi BowenZhang YayingZhu HuiliTong WeihuaHuang Canhua - Fc gamma receptor IIIA (FCGR3A) encodes CD16a, a key mediator of antibody-dependent cellular cytotoxicity (ADCC) that regulates innate and adaptive immunity, especially in natural killer (NK) cells and monocytes. We generated an FCGR3A-EGFP knock-in human embryonic stem cell (hESC) line via CRISPR/Casn9n. The cell line showed a normal karyotype, maintained expression ofthe pluripotency markers OCT4, SOX2, and NANOG, and retained trilineage differentiation potential. This reporter line enables real-time tracking of FCGR3A expression during immune cell differentiation, serving as a useful tool for studying FCGR3A immune cell development and related immune mechanisms. - Source: PubMed
Publication date: 2026/07/15
Dong QifeiLuo ShahangSun JiaqiLiu Huisheng - Baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5) (survivin) is known to play an important role in cell survival and tumor progression; however, its involvement in cancer stem cell (CSC) properties and epithelial-mesenchymal transition (EMT) in breast cancer remain unclear. In this study, we investigated the role of BIRC5 in regulating CSC-like characteristics and EMT in human breast cancer cells. Analysis of public datasets revealed that BIRC5 expression is significantly elevated in breast cancer tissues and is associated with poor patient prognosis. Treatment with CSC-inducing conditioned medium (CSC-CM) increased the expression of CSC markers, including CD44, ALDH1A1, and ALDH1A3. Silencing of BIRC5 using siRNA reduced the expression of CSC-associated markers as well as pluripotency-related transcription factors (Sox2, Oct4, and Nanog). In addition, BIRC5 knockdown significantly decreased sphere-forming ability, indicating reduced self-renewal capacity. Furthermore, suppression of BIRC5 altered EMT-related protein expression, as evidenced by increased E-cadherin and decreased N-cadherin, Vimentin, and EMT-associated transcription factors (Snail, Slug, Twist, and Zeb1). In addition, BIRC5 knockdown also significantly reduced cell migration and invasion. These results suggest that BIRC5 is involved in the regulation of CSC properties and EMT in breast cancer cells and may contribute to tumor progression. - Source: PubMed
Publication date: 2026/06/30
Jang Jin YoungKim Rae-Kwon - The derivation of authentic embryonic stem cells (ESCs) across mammalian species remains a major challenge. Here, we report the development of a defined, serum-free culture system, termed 6iL/E4, that enables the derivation and long-term self-renewal of ESCs across diverse mammalian species. Through systematic dissection of signaling pathways, we identified conserved regulatory modules involving GSK3α, WNT, STAT3, PDGFR, and MEK/ERK signaling. The optimized 6iL/E4 conditions support stable derivation and expansion of ESCs from mouse, rat, rabbit, and bovine embryos. For rabbit, ESC derivation required supplementation with the LATS inhibitor TDI-011536 (TDI), and 6iL/TDI-cultured rabbit ESCs exhibited chimera-forming capability. In bovine ESCs, inducible expression of Klf2 and Nanog reinforced pluripotency and promoted in vivo chimeric contribution. Importantly, we demonstrated that 6iL robustly establishes and maintains human pluripotent stem cells in a naïve-like state. These findings reveal conserved principles underlying ESC self-renewal across divergent mammalian species and provide a universal platform for cross-species stem cell research, disease modeling, and biotechnological applications. - Source: PubMed
Publication date: 2026/07/13
Wang DuoMing HaoYang DongshanCui XiangFreeman ZacharyTsai Li-KuangWei ZhuyingLiu LiuScatolin Giovanna NascimentoBennett BrianWang XiukunYau KimberlyTao LitaoTong XinyiWang ShulingShi Kai-XuanEvseenko DenisVan Handel BenGuo LonghuaDai XiaotingXiong YoucaiZhang BingjingWang YinjuanIyyappan RajanOjeda-Rojas Oscar AlejandroHu GuangMcGinnis LyndaPaulson RichardMckim DanielKong XiangboXia XiaofengZhang JifengChen Y EugeneJiang ZongliangXu JieYing Qi-Long - Astrocytes play a significant role in neuroprotection by internalizing neurodegenerative aggregates and facilitating their degradation. Recent studies indicate that α-Synuclein (α-SYN) protofibrils promote the transfer of pathogenic aggregates and dysfunctional mitochondria between astroglia via tunneling nanotubes (TNTs), which enhances cell survival and resistance to apoptosis. However, the underlying mechanism of TNT-driven apoptosis resistance remains unclear. We find that α-SYN protofibrils induce aberrant mitochondria with decreased membrane potential (Ψm) and promote dynamic actin remodeling by relocating phosphorylated focal adhesion kinase (pFAK) to the nucleus, which triggers TNT formation in human astrocytoma cell lines and primary murine astrocytes. The important novel finding of this study is that pFAK in the nucleus co-localizes with Nanog, a crucial transcription factor for preserving stemness, and the interaction between pFAK and Nanog is critical for promoting p53 degradation via Mdm2-mediated ubiquitination and upregulating autophagy, thereby supporting the survival of astroglia exposed to toxic α-SYN protofibrils. ROCK inhibitor y-27632 also drives TNT-formation via pFAK translocation to the nucleus, colocalizes with Nanog, and enhances stemness-related gene expression. Inhibiting TNT with the actin depolymerizing agent cytochalasin-D prevents pFAK co-localization with Nanog in the nucleus and fails to protect cells from α-SYN-induced apoptosis. Nanog knockdown does not degrade p53 and hinders cell rescue from apoptosis. Furthermore, these transient TNTs transfer mitochondria to adjacent cells, potentially helping maintain metabolic stability. This study reveals that the TNT formation pathway promotes pFAK-Nanog interaction in the nucleus, leading to p53 degradation, which protects astroglia against α-SYN proteotoxicity and prevents apoptosis. - Source: PubMed
Publication date: 2026/07/05
Kashyap RachanaAnirudh Sreenivas B KVarshith M RMundada Rajashri RameshwarSreedevi PJain ShreshtaKambaru ArchanalakshmiDastidar Somasish GhoshPadavattan SivaramanRao Vinay KumarManjithaya RaviNeuzil JiriNath Sangeeta