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MYLIP — NANOG

Text-mined interactions from Literome

Bourguignon et al., Oncogene 2012 (Carcinoma, Squamous Cell...) : Further analyses reveal that miR-21 is controlled by an upstream promoter containing Stat-3 binding site ( s ), while chromatin immunoprecipitation assays demonstrate that stimulation of miR-21 expression by HA/CD44 signaling is Nanog/Stat-3 dependent in HNSCC cells
Wong et al., PloS one 2012 : We then determined that miR-125b overexpression inhibits the expression of Nanog and Oct4 and promotes the onset of Brachyury expression, suggesting that miR-125b controls the early events of human CM differentiation by inhibiting hESC pluripotency and promoting mesodermal differentiation
Bourguignon et al., J Biol Chem 2012 (Carcinoma, Squamous Cell...) : Hyaluronan-CD44v3 interaction with Oct4-Sox2-Nanog promotes miR-302 expression leading to self-renewal, clonal formation, and cisplatin resistance in cancer stem cells from head and neck squamous cell carcinoma ... Further analysis reveals that microRNA-302 (miR-302) is controlled by an upstream promoter containing Oct4-Sox2-Nanog binding sites, whereas chromatin immunoprecipitation ( ChIP ) assays demonstrate that stimulation of miR-302 expression by HA-CD44 is Oct4-Sox2-Nanog dependent in HNSCC-specific CSCs
Xu et al., J Biol Chem 2012 (Ovarian Neoplasms) : MicroRNA miR-214 regulates ovarian cancer cell stemness by targeting p53/Nanog ... Furthermore, we found that p53 is directly repressed by miR-214 and that miR-214 regulates Nanog through p53
Mintz et al., Molecular therapy. Nucleic acids 2012 : We demonstrate that inhibiting miR-181a* upregulates the Nanog expression level, in addition to an increase in alkaline phosphatase activity
Goossens et al., Stem Cells Dev 2013 : By interfering with the FGF signaling pathway, we found functional evidence that miR-218 , mainly expressed in the inner cell mass, regulates the NANOG expression in the bovine blastocyst in response to FGF signaling
Niu et al., Int J Oncol 2013 (Brain Neoplasms...) : In our study, overexpression of miR-134 in U87 glioblastoma cells resulted in significant downregulation of Nanog mRNA levels as well as protein levels