Gene interactions and pathways from curated databases and text-mining

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MYLIP — POU5F1

Text-mined interactions from Literome

Lee et al., Biochem Biophys Res Commun 2008 : Here, we show that miR-302b indirectly regulates expression of the pluripotent stem cell marker Oct4 , and it directly regulates expression of Cyclin D2 protein, a developmental regulator during gastrulation
Rosa et al., EMBO J 2011 : In the undifferentiated state, both OCT4 and the OCT4 induced miR-302 directly repress NR2F2 at the transcriptional and post-transcriptional level, respectively
Wu et al., Cancer 2011 (Adenocarcinoma...) : Up-regulating miR-145 reduced the expression of OCT4 and induced the differentiation of Ishikawa cells to closely resemble normal endometrial epithelium both in vitro and in vivo
Yang et al., Biomaterials 2012 (Cell Transformation, Neoplastic...) : We demonstrated that miR145 negatively regulates GBM tumorigenesis by targeting Oct4 and Sox2 in GBM-CD133 ( + )
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
Campayo et al., Eur Respir J 2013 : miR-145 regulates SOX2 and OCT4 translation and p53 regulates miR-145 expression
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
Hu et al., PloS one 2012 (Breast Neoplasms...) : Mechanistic studies showed that miR-145 mimics inhibited Oct4 expression and miR-145 inhibitor enhanced it ... Over-expression of Oct4 reversed miR-145 regulated expression of EMT markers, suggesting that Oct4 mediated the inhibitory effects of miR-145
Wang et al., Cell death & disease 2013 : OCT4 induces upregulation of miR-125b through directly binding to the promoter of miR-125b-1 confirmed by chromatin immunoprecipitation analysis ... These findings suggest an undescribed regulatory pathway in cervical cancer, by which OCT4 directly induces expression of miR-125b , which inhibits its direct target BAK1, leading to suppression of cervical cancer cell apoptosis