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Leukemia inhibitory factor (LIF) regulates mouse embryonic stem cell (mESC) pluripotency through STAT3 activation, but the downstream signaling remains largely unelucidated. Using cDNA microarrays, we verified B cell leukemia/lymphoma 3 ( Bcl3 ) as the most significantly downregulated factor following LIF withdrawal in mESCs.  Bcl3  knockdown altered mESC morphology, reduced expression of pluripotency genes including  Oct4 ,  Sox2 , and  Nanog , and downregulated DNA binding of acetylated histone 3 and RNA polymerase II on the  Oct4  promoter. Conversely, Bcl3 overexpression partially prevented cell differentiation and promoted  Oct4  and  Nanog  promoter activities. Furthermore, coimmunoprecipitation and chromatin immunoprecipitation experiments demonstrated that Bcl3 regulation of mESC pluripotency may be through its association with Oct4 and β‐catenin and its promoter binding capability. These results establish that Bcl3 positively regulates pluripotency genes and thus shed light on the mechanism of Bcl3 as a downstream molecule of LIF/STAT3 signaling in pluripotency maintenance. S tem  C ells   2015;33:3468–3480

Bcl3 Bridges LIF‐STAT3 to Oct4 Signaling in the Maintenance of Naïve Pluripotency