Nanog Blocking Peptide
- Known as:
- Nanog Blocking Peptide
- Catalog number:
- BP300-397
- Product Quantity:
- 50 ug
- Category:
- Peptides
- Supplier:
- Beth
- Gene target:
- Nanog Blocking Peptide
Related genes to: Nanog Blocking Peptide
- 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 Blocking Peptide
Related articles to: Nanog Blocking Peptide
- 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 - 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
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