Fig. 5
From: The p52 isoform of SHC1 is a key driver of breast cancer initiation
RNAseq analysis reveals enriched genes dis-regulated by loss of p52SHC. a Histogram comparing log2 fold change in transcript expression in p52SHC-KO tumors compared to WT (X-axis) with fold change in transcript expression in p66SHC-KO tumors (Y-axis). Green dots symbolize genes that are differentially expressed in only one knockout group. Blue dots symbolize genes that are differentially expressed in p52SHC-KO and p66SHC-KO tumors in the opposite directions. Red dots symbolize differentially expressed genes p52SHC-KO and p66SHC-KO tumors in the same direction. b Bar graph indicating the top 20 enriched pathways with Z-score greater than ± 2 in p52SHC-KO tumors, ranked by Z-score. c–e Heat map of ESR1 (c) and RICTOR (d) pathway targets identified by RNAseq analysis of wild-type, p52SHC-KO, and p66SHC-KO DMBA-induced tumors