Ask about this productRelated genes to: Nanog antibody
- 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 antibody
Related articles to: Nanog antibody
- Regulation of all- retinoic acid (ATRA) signaling is crucial to early embryonic development. Embryonic stem (ES) cell-derived gastruloids mimic normal development in response to the Wnt/β-catenin agonist CHIR9901, and this study has examined the importance of the activities of RAR (retinoic acid receptor) α and γ to gastruloid development. Expression of retinoic acid receptor (RAR)γ within developing gastruloids was spatially restricted to primitive cells that co-expressed ES cell and early progenitor cell markers, i.e., Nanog, Sox2, and Oct4. In contrast, RARα expression was ubiquitous. mRNAs for the key enzymes involved in ATRA synthesis (Aldh1a2) and degradation (Cyp26a1) were not seen in cells that expressed RARγ. Treatment of ES cell-derived gastruloids with physiologically relevant (10 nm) levels of ATRA or with a highly selective RARγ agonist blocked normal developmental processes, preventing symmetry-breaking and axial elongation. This was not seen following treatments with an RARα agonist, where there was a tendency for enhanced axial elongation. Brachyury (TBXT) immuno-positive cells localized in the posterior end of elongated gastruloids in control- and RARα agonist-treated cultures, with Sox2 immuno-positive cells seen more widely, whilst both TBXT and Sox2 immuno-positive cells were randomly distributed throughout ATRA- and RARγ agonist-treated gastruloids. Concurrent treatment of gastruloids with 10 nm ATRA and 100 nm of an RARγ antagonist partially abrogated the ATRA-mediated block to axial elongation. Conversely, 10 nm RARγ antagonist treatments were associated with the formation of multi-axis gastruloid elongations, with comparatively little effect seen after treatments with an RARα antagonist. These findings reveal that RARγ plays a crucial role in the development of embryonic tissues. - Source: PubMed
Publication date: 2026/04/29
Olanipekun Jide TEdginton-White BenjaminMcQueen CaitlinBrown GeoffreyJohnson William E B - Chronic hepatitis B virus (HBV) infection is a leading cause of hepatocellular carcinoma (HCC). This review elucidates the molecular pathways by which HBV promotes the expression of the stemness transcription factors OCT4, Sox2, and NANOG. Through a comprehensive literature review, we found that HBV enhances their expression via multiple mechanisms. These include HBxAg-induced chromatin remodeling, activation of histone demethylase KDM5B, and integration of the truncated HBx-ΔC protein into the host genome. Furthermore, chronic inflammation driven by persistent HBV infection acts as a key driver for their overexpression. This dysregulation is strongly associated with increased tumor proliferation, metastasis, and poor prognosis in HBV-infected HCC patients. Consequently, OCT4, Sox2, and NANOG emerge as promising biomarkers for early detection and prognosis, as well as potential therapeutic targets. Modulating their activity could offer novel strategies for targeted treatment. In conclusion, HBV-induced alterations in these transcription factors represent critical oncogenic mechanisms in HCC. Further research is essential to develop novel therapeutic approaches that regulate their activity, ultimately improving clinical outcomes for patients. - Source: PubMed
Publication date: 2026/05/01
Razaghi NeginKariminik AshrafRanjbar MehdiBahaaldin-Beygi Morteza - Triple-negative breast cancer (TNBC) is defined by the absence of estrogen, progesterone, and HER2 receptor expression. A critical challenge in managing TNBC is its high concentration of cancer stem cells (CSCs), which drives chemotherapy resistance and correlates with poor patient survival. In normal physiology, stem cell pluripotency and differentiation are governed by core transcription factors (such as Oct4, Sox2, Nanog, Klf4, and c-Myc) alongside key signaling networks, including the Notch, Wnt/β-catenin, and Sonic Hedgehog (Shh) pathways. During carcinogenesis, aberrant activation of these regulators in TNBC not only promotes the self-renewal of tumor cells but also actively facilitates immune evasion. Specifically, overexpressed pluripotency transcription factors enable cancer cells to downregulate antigen presentation molecules (e.g., MHC class I) and secrete immunomodulatory cytokines. Concurrently, dysregulated signaling, such as the Wnt/β-catenin pathway, inhibits dendritic cell maturation and recruits Myeloid-Derived Suppressor Cells (MDSCs) and regulatory T cells (Tregs) into the tumor microenvironment, thereby blunting the anti-tumor T cell response. This review examines the role of key pluripotency regulators in TNBC-mediated immune evasion, highlighting emerging immunotherapeutic strategies targeting these networks and summarizing current clinical research. - Source: PubMed
Publication date: 2026/04/23
López-Santana CarolinaMendez-Rivera FabioBernal-Estévez David A - POU5F1 (OCT4), a core regulator of pluripotency, plays an important role in tumor stemness and immune microenvironment remodeling, yet its systematic function and mechanisms in lung adenocarcinoma (LUAD) remain incompletely elucidated. - Source: PubMed
Publication date: 2026/05/06
Yu BingbingZhang MeiliZhu HaiyongWu ZhuGao HongBai Yang - Multiple myeloma (MM) is a hematologic malignancy associated with a poor prognosis. MM-derived mesenchymal stromal cells (MM-MSCs) contribute to disease progression by creating a supportive stromal microenvironment for malignant cells. Elucidating transcriptomic alterations in MSCs may therefore facilitate the development of novel therapeutic strategies for treatment-resistant MM. - Source: PubMed
Publication date: 2026/05/07
Soleymani FatemehKavousi SaeidehKhodakarim NastaranAhmadvand Mohammad