Human Nanog Differentiation Reporter (pRedTK, pre_packaged)
- Known as:
- Human Nanog Differentiation Reporter (pRedTK, pre_packaged)
- Catalog number:
- SR10055VA-1
- Product Quantity:
- >2 x 10^6 IFUs
- Category:
- -
- Supplier:
- SBI
- Gene target:
- Human Nanog Differentiation Reporter (pRedTK pre_packaged)
Related genes to: Human Nanog Differentiation Reporter (pRedTK, 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 (pRedTK, pre_packaged)
Related articles to: Human Nanog Differentiation Reporter (pRedTK, pre_packaged)
- 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 - The proteasome is a critical cellular degradative machinery impaired in late-stage Alzheimer's disease (AD). However, the status and activity of the proteasome in early-stage sporadic AD (sAD) is unknown. - Source: PubMed
Publication date: 2026/06/28
Aladeokin Aderemi CalebJeltsch MichaelDavtyan HaykBlurton-Jones MathewKoistinaho Jari - This study reports the generation and comprehensive characterization of the LATS1/2 knockdown (KD) induced pluripotent stem cell (iPSC) line, MUSIi012-A-9. Created via CRISPR/Cas9-mediated modification of the LATS2 gene in a parental LATS1-KD line, this resource serves as a crucial human model to investigate the roles of LATS1/2 kinases, key regulators of the Hippo signaling pathway. Comprehensive validation confirmed normal iPSC morphology, pluripotency marker expression (OCT3/4, NANOG, SOX2), genetic stability (46,XX karyotype), and robust multilineage differentiation potential. This well-characterized iPSC line is a vital tool for advancing research into Hippo pathway regulation, lineage specification, and cell fate determination in development and disease. - Source: PubMed
Publication date: 2026/06/29
Lorthongpanich ChanchaoSrisook PimonwanJiamvoraphong NittayaKlaihmon PhatchanatKumsui SirilukLaowtammathron ChutiIssaragrisil Surapol - Human multilineage-differentiating stress-enduring (MUSE) cells represent a promising cell population for tissue engineering and translational medicine owing to their intrinsic pluripotency and stress resistance. MUSE cells express pluripotency markers such as SSEA-3, Nanog, Sox2, and Oct3/4, while maintaining their immunomodulatory capabilities. This systematic review (PROSPERO CRD42024532621) analyzed studies on human MUSE cell isolation, characterization, and translational potential through searches of the PubMed, Scopus, and Web of Science databases in April 2024. The TIDieR and SYRCLE checklists were used to assess the risk of bias. Our findings identified 34 studies that followed the PRISMA guidelines for assessing different tissue sources, isolation techniques, and characterization methods. MUSE cells are primarily obtained from bone marrow mesenchymal stem cells, and fluorescence-activated cell sorting is the predominant isolation method. Characterization was mainly performed using SSEA-3 immunodetection (positivity ranged from <1% to 6.30%) and was linked to the expression of pluripotency and mesenchymal markers. These findings highlight the relevance of MUSE cells in regenerative medicine as a distinct pluripotent subpopulation within adult mesenchymal tissues. In addition, SSEA-3-based isolation approaches complemented by functional assays has emerged as a key methodological approach for the reliable identification and characterization of MUSE cells. However, isolation efficiency varies depending on the cell source and method. Standardized protocols are, therefore, needed to improve reproducibility and facilitate the translational development of MUSE cell-based regenerative therapies. - Source: PubMed
Garzón IngridMartín-Piedra Miguel ÁngelMartínez-Girón LuisAlaminos MiguelYoo James JAtala Anthony - Mesenchymal progenitor cells (MPCs) play a significant role in articular cartilage homeostasis and regeneration. Yet, the functional dynamics and molecular characteristics of MPCs may differ significantly across various pathological conditions. Hence, this study comprehensively investigates the biological and molecular characteristics of MPCs isolated from articular cartilage of patients with osteoarthritis (OA) and rheumatoid arthritis (RA), aiming to uncover disease-specific differences that could offer insights into targeted regenerative therapies. Using flow cytometry, gene expression analysis, and in vitro differentiation assays, we assessed the phenotype, growth potential, senescence, cytogenetic instability, and chondrogenic potential to delineate molecular pathways uniquely active in each disease context. Phenotypically, both OA and RA-MPCs retained markers of mesenchymal stem cells (MSCs), but OA-derived MPCs exhibited higher fold expression of progenitor markers (, , , and ), suggesting a more activated state. Functionally, OA-MPCs demonstrated increased growth kinetics (higher proliferation rate and decreased population doubling time) with a significant shift towards adipogenic lineages (increased fold expression of , , and ). However, there were no differences in the osteogenic and chondrogenic potential. Gene expression analysis revealed upregulation of genes involved in extracellular matrix production and cartilage development (, , , , , , , , and ) in 3D cultures compared with 2D or monolayer cultures. Collectively, these findings demonstrate that, while multipotent MPCs are present in both OA and RA articular cartilage, they can exhibit fundamentally altered biological behaviors and molecular signatures reflective of the local disease microenvironment. Understanding these differences is critical for optimizing cell-based therapeutic strategies tailored to each condition and may facilitate the development of novel interventions targeting endogenous progenitor cells for cartilage repair. - Source: PubMed
Publication date: 2026/06/10
Manjappa Akshay BairapuraNitilapura NarendraShetty SiddharthRao ShamaBabu SanthoshShetty JayaprakashaShetty ReshmaBasavarajappa Mohana Kumar