E-mail address: haifeng.yang@jefferson.edu (H. Yang).

The data presented in this article are companion materials to our manuscript titled "BAP1 maintains HIF-dependent in-terferon beta induction to suppress tumor growth in clear cell renal cell carcinoma" (Langbein et al., 2022), where we investigated the downstream effects of BAP1 (BRCA1-associated protein 1) expression in clear cell renal cell carci-noma (ccRCC) cell lines and mouse xenograft models. In the manuscript, we showed that BAP1 upregulates STING (stim-ulator of interferon genes) expression and activity in ccRCC cells, leading to IFN-beta transcription and activation of inter-feron stimulated gene factor 3 (ISGF3), the transcription fac-tor that mediates the effects of type I interferons (IFNs). Here, we suppressed additional components of the type I IFN pathway, including IRF9 (a component of ISGF3), IFNAR1 (the type I IFN receptor), and STING (a stimulator of IFN pro-duction) by shRNA to investigate their involvement in BAP1-mediated upregulation of ISGF3 activity. We also inhibited extracellular IFN-beta via neutralizing antibody treatment in BAP1-expressing cells to ascertain the role of the secreted cy-tokine in this pathway. ISGF3 activity was assessed by west-ern blot analysis and qPCR measurement of its transcriptional targets. To examine the relevance of our observations in an-