Human Nanog Differentiation Reporter (pRedZeo, pre-packaged)
- Known as:
- Human Nanog Differentiation Reporter (pRedZeo, pre-packaged)
- Catalog number:
- sr10042va-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Human Nanog Differentiation Reporter (pRedZeo pre-packaged)
Related genes to: Human Nanog Differentiation Reporter (pRedZeo, 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 (pRedZeo, pre-packaged)
Related articles to: Human Nanog Differentiation Reporter (pRedZeo, pre-packaged)
- Proteins and nucleic acids form non-Newtonian liquids with complex rheological properties that contribute to their function in vivo. Here, we investigate the rheology of the transcription factor NANOG, a key protein to maintain embryonic stem cell pluripotency. We find that, at high concentrations, NANOG forms macroscopic aging gels that are dependent on its intrinsically disordered domain. By combining molecular dynamics simulations, mass photometry, and cryo-EM, we also discover that-in contrast to unbounded condensates formed by other intrinsically disordered proteins-NANOG forms self-limiting micelles with exposed DNA-binding domains. We show that these micelles can stabilize DNA entanglements and, in turn, modulate DNA dynamics. Based on our findings, we conjecture that NANOG may contribute to regulate gene expression by creating local gel-like environments that restrict genome dynamics and that its aging may ingrain mechanical memory in gene regulatory networks. - Source: PubMed
Hong-Minh AmandineFosado Yair Augusto GutiérrezGuild AbbieMullin NicholasSpagnolo LauraChambers IanMichieletto Davide - Although phosphorodiamidate morpholino oligomers (PMOs) are potent and stable antisense agents, their neutral backbone limits cellular uptake and biodistribution, requiring specialized delivery strategies to improve therapeutic efficacy. Chimeric guanidinium-linked morpholino oligomers (GMOs) with PMOs are designed to enhance cellular delivery yet compromise hybridization with the target sequence due to backbone rigidity. To address this, we designed flexible GMO-PMO chimeras by incorporating sarcosine, β-alanine, and ethanamine as internucleotide spacers in the oligonucleotide. Thermal melting studies on a 19-mer polythymidine (polyT) sequence demonstrate that these flexible GMO-PMOs partially restore duplex stability in a modification-dependent manner. This structural restoration is also observed in biologically relevant mixed GMO-PMO sequences targeting a gene linked to stemness and cancer biology, while retaining their B-type global geometry as confirmed by circular dichroism analysis. The optimized ethanamine-modified chimera elicited strong, dose-dependent silencing, with up to 95% repression in MCF7 and ∼73% in HCT116 cells at 1 μM after 48 h. Importantly, both rigid and flexible GMO-PMOs exhibit similar lysosomal sequestration, varying in a cell-line-dependent manner. Collectively, flexible GMO-PMO chimeras mitigate the long-standing trade-off between carrier-free PMO delivery and duplex stability, establishing a robust platform for antisense gene silencing and potential therapeutic applications. - Source: PubMed
Publication date: 2026/07/21
Qasim MohammedNaaz SharmeenPratihar SubhamoySharma Swrajit NathSinha Surajit - To investigate the molecular mechanism of long intergenic non-protein coding RNA, regulator of reprogramming (Linc-ROR) in regulating the stemness of cancer stem cells in hypoxic microenvironment. A2780 cells were induced into ovarian cancer stem-like cells (OCS-LC) by sphere formation assay and identified by differentiation assay and flow cytometry analysis. Knockdown or overexpression of Linc-ROR, microRNA (miR)-181c-5p, and simultaneous knockdown or simultaneous overexpression of Linc-ROR and miR-181c-5p were constructed in OCS-LC cell lines. The mRNA levels were detected by quantitative reverse transcription PCR (RT-qPCR). Western blot was used to detect the stemness related octamer-binding transcription factor 4 (Oct-4) and Nanog homeobox transcription factor (Nanog). The protein expression levels of E-cadherin, Vimentin related to epithelial-mesenchymal transition (EMT) and hypoxia inducible factor-1α (HIF-1α) were also detected. Cell counting kit-8 (CCK-8), colony formation assay and transwell chamber assay were used to detect the effects of different factors on cell proliferation, invasion and other malignant biological behaviors. A subcutaneous xenograft model was constructed to explore the effect of Linc-ROR on the tumorigenicity of OCS-LC in vivo. A2780 cells were successfully induced into OCS-LC. Flow cytometry analysis showed that the positive expression rate of CD on the surface of OCS-LC was significantly higher than that of A2780 cells (<0.05). The results of dual luciferase reporter assay showed that there was a targeted binding site between Linc-ROR and miR-181c-5p. Under hypoxic condition, overexpression of Linc-ROR or knockdown of miR-181c-5p increased OCS-LC spheroid formation rate, shortened spheroid formation cycle, longer maximum spheroid diameter, and increased relative expression of Oct-4, Nanog, HIF-1α and Vimentin proteins compared with control group; the relative expression of E-cadherin protein was decreased, and the proliferation, invasion and metastasis ability of OCS-LC were enhanced (all <0.05). However, knockdown of Linc-ROR or overexpression of miR-181c-5p showed opposite experimental results (all <0.05). Simultaneous knocking down of Linc-ROR and miR-181c-5p or simultaneous overexpressing of Linc-ROR and miR-181c-5p could reverse the above biological effects of knocking down or overexpressing Linc-ROR. The results of animal experiments showed that overexpression of Linc-ROR enhanced the tumorigenic ability of OCS-LC in vivo. At the same time, the expression levels of Nanog, Oct-4, HIF-1α and Vimentin were increased, and the expression level of E-cadherin was decreased in transplanted tumor tissues (all <0.05). Knockdown of Linc-ROR showed the opposite results (all <0.05). Under hypoxia, Linc-ROR negatively regulates the expression of miR-181c-5p and upregulates the expression of HIF-1α to promote the stemness of OCS-LC and activate EMT, which may be one of the important mechanisms of Linc-ROR promoting the proliferation, invasion and metastasis of tumor cells. - Source: PubMed
Cheng L HWen X LXia Y FYu XSun XTian CLou Y H - Alzheimer's disease (AD) is a neurodegenerative condition caused by amyloid β (Aβ42) accumulation, neuroinflammation, oxidative stress and cholinergic dysfunction, resulting in neuronal death and cognitive decline. Excessive Aβ42 accumulation disrupts redox equilibrium, increases reactive oxygen species (ROS), and activates inflammatory and apoptotic pathways. Natural bioactive compounds with immunomodulatory and antioxidant properties are increasingly being explored as possible multi-target therapies. Alkylglycerol (AKG), a lipid-derived immunomodulator, and fucoidan, a sulfated polysaccharide found in brown algae, have both shown neuroprotective properties. This study examines the effectiveness of Fucoidan and AKG in preventing Aβ42-induced diseases in a Drosophila melanogaster model, both individually and in combination. - Source: PubMed
Publication date: 2026/07/20
Kale DeepikaDcunha Blairil VishmaLakshmi SreejaRaghu Shamprasad VarijaElumalai Preetham - Specificity protein 1 (SP1) is the most active member of the specificity protein and Krüppel-like factor (Sp/KLF) family and is widely expressed across all mammalian cell types. However, more detailed studies on the role of SP1 in preimplantation embryonic development are needed. Here, we analyzed the role of SP1 in the development of preimplantation mouse embryos through supplementation with a small molecular inhibitor (plicamycin) and microinjection of Sp1 siRNA. We found that SP1 was indispensable for zygotic genome activation (ZGA) and the morula-to-blastocyst transition. Plicamycin supplementation arrested embryo development at the 2-cell stage and resulted in aberrant RNA polymerase II preconfiguration. Sp1 expression knockdown by Sp1 siRNA microinjection caused most embryos to arrest at the morula stage, and the expression of NANOG, POU5F1 and CDX2 significantly decreased. Both plicamycin supplementation and Sp1 siRNA microinjection decreased embryonic H3K4me3 levels and increased H3K9me3 levels. Moreover, when Sp1 was overexpressed, the embryos were arrested at the 2-cell stage, the H3K4me3 level increased, and the H3K9me3 level decreased. In conclusion, our findings demonstrate that SP1 is crucial for mouse preimplantation embryonic development through the regulation of gene expression and histone modifications. - Source: PubMed
Publication date: 2026/07/20
Di AiRong HuangFang WangZhi CuiXinglan AnLi ZiyiHaibo ZhuZhang Sheng