Nanog Recombinant Protein
- Known as:
- Nanog Recombinant Protein
- Catalog number:
- 40-121
- Product Quantity:
- 0.005 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Nanog Recombinant Protein
Related genes to: Nanog Recombinant Protein
- 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 Recombinant Protein
Related articles to: Nanog Recombinant Protein
- Small intestinal adenocarcinoma (SIAC) is a rare malignancy with a rising incidence and poor prognosis. Although exportin-7 (XPO7) is typically characterized as a tumor suppressor, recent evidence suggests context-dependent oncogenic functions, yet its role in SIAC remains unexplored. This study evaluated the clinicopathological significance of XPO7 expression and its association with status, autophagy, and cancer stemness in 191 surgically resected primary SIAC cases using immunohistochemistry and automated digital quantification. XPO7 was significantly upregulated in SIAC compared to normal mucosa ( < 0.001). High XPO7 expression, observed in 27.2% of cases, correlated with higher histological grade ( = 0.023) and was identified as an independent predictor of poor overall survival (hazard ratio = 1.703; = 0.008). Subgroup analysis revealed that high XPO7 levels were associated with significantly shorter median overall survival specifically in cases featuring lymphovascular invasion, nodal metastasis, and mutations. Furthermore, XPO7 expression demonstrated a significant positive correlation with autophagy markers (LC3B and p62) but not with stemness markers (Sox2, Oct4, and Nanog). In conclusion, XPO7 serves as a significant independent prognostic biomarker for SIAC, and its correlation with autophagy markers in aggressive subgroups highlights its potential as a promising therapeutic target. - Source: PubMed
Publication date: 2026/07/19
Kim Jeong WonYlaya KrisChung Eun JooJun Sun-YoungHong Seung-MoChung Joon-Yong - Extracellular vesicles (EVs) participate in tumor progression and immune regulation through the transfer of bioactive molecules. Although tumor-derived EVs are generally considered to promote metastasis, accumulating evidence suggests that their functions vary according to the biological characteristics of their cells of origin. This study investigated the mechanisms underlying the anti-metastatic effects of EVs derived from -overexpressing melanoma cells (F10-EVs). - Source: PubMed
Publication date: 2026/07/08
Nakano MisatoTamura AsukaYorikawa SoraMatsuki NahokoIto RunaMatsuoka HideakiSaito Mikako - Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, leading to multi-organ dysfunction. Toll-like receptor signaling via MYD88- and TRIF-dependent pathways plays a central role in this process; however, its temporal and tissue-specific dynamics remain incompletely understood. The aim of this study was to investigate time-dependent transcriptional changes in MYD88- and TRIF-dependent signaling pathways across multiple organs in a murine model of sepsis. mRNA expression of MYD88, IRAK1, IRAK4, NF-kB, CCL4, CCL20, CCR2, IFN-β, IFN-γ, TNF-α, IL-1β, IL-2, IL-4, IL-8, IL-10, IL-18, Klotho, KLF4, HOXA5, NANOG and HIF1α was quantified using qRT-PCR in intestinal, kidney, liver and lung tissues at 24, 48, and 72 h following cecal ligation and puncture-induced sepsis in male C57BL/6J mice. Significant upregulation of innate immune signaling molecules, cytokines, chemokines, and interferon-related genes was observed in all tissues compared with controls. Genes associated with hypoxia and cellular regulation were also increased. These responses were tissue-specific and progressively intensified over time. Sepsis represents a dynamic, time-dependent, and tissue-specific process characterized by sustained activation of immune and hypoxic pathways, providing potential targets for time-stratified therapeutic strategies. - Source: PubMed
Publication date: 2026/06/26
Erodotou MariaKapelouzou AlkistisMylonas Konstantinos SSoukouli IoannaBoletis John NTsourouflis GerasimosLiakakos TheodoreSchizas Dimitrios - Diabetes mellitus impairs bone metabolism through chronic hyperglycemia, oxidative stress, and inflammation, leading to reduced osteoblast activity and downregulation of key pluripotency genes such as Octamer-binding transcription factor 4 (OCT4), Nanog homeobox (NANOG), SRY-box transcription factor 2 (SOX2), and Reduced expression protein 1 (REX1).The present study investigated whether the timing of aerobic exercise (morning vs. evening) influences the expression of pluripotency genes in the bone tissue of diabetic mice. - Source: PubMed
Publication date: 2026/07/27
Janbozorgi MaryamTaheri AsmaHosseinzadeh MasoumehGhafaripur Sahar - Understanding how pluripotency regulatory networks evolve across mammals remains a central question in developmental and stem cell biology. While rodent models have defined the canonical core circuitry of pluripotency, the extent to which these regulatory hierarchies are conserved in large mammals is unclear. Here, we provide evidence that contributes to the species-specific regulatory network as a modulator that sustains pluripotency and preserves functional differentiation capacity in porcine embryo-derived stem cells. Comparative sequence analysis revealed strong conservation of the HMG domain across mammals, yet promoter divergence suggested lineage-specific regulatory evolution. Transcriptomic profiling demonstrated that, unlike in mice, is robustly upregulated from the 2-cell stage and remains highly expressed in the porcine epiblast, coinciding with key windows of pluripotency establishment. In porcine embryo-derived stem cells, stable knockdown resulted in reduced colony integrity, diminished alkaline phosphatase activity, impaired proliferation, and downregulation of core pluripotency genes, including and . Furthermore, loss of disrupts embryoid body formation and abolishes teratoma-forming capacity in vivo. This deficit likely reflects impaired pluripotency, but may also be attributed to compromised cell survival or proliferative fitness following transplantation. Notably, comparable perturbations in mouse models do not produce equivalent phenotypes, underscoring a lineage-dependent functional divergence. Together, our findings suggest that contributes to the support of the porcine pluripotency network, and hint at evolutionary plasticity in the hierarchical architecture of mammalian pluripotency. These findings move beyond the rodent-centric paradigm and offer a refined perspective on the evolutionary plasticity of pluripotency networks, highlighting as a pivotal lineage-specialized node governing naive pluripotency in large mammals. Notably, these inferences are based on functional perturbation using a single validated miRNAi construct; definitive confirmation of -specific causality will require future orthogonal validation via independent knockdown sequences, CRISPR interference, or RNAi-resistant rescue experiments. - Source: PubMed
Publication date: 2026/07/17
Jian ChengheLv YanjiaoXu MiaoWang HongxingDu HanWang YiyangSu MuhanSong JunYan TingshengLiu Zhonghua