Project description:NFIB is a transcription factor that can both positively and negatively regulate gene transcription. We have identified NFIB as an arginine methylation substrate of CARM1. To elucidate how CARM1 could regulate NFIB target genes by methylating NFIB, we performed this ChIP-seq to firstly identify NFIB direct binding gengs.
Project description:This project identified NFI family members as CARM1 substrates. NFIB was previously reported to play a critical role in the development of small cell lung cancer. We provided evidence that the arginine methylation of NFIB is required for its oncogenic function in small cell lung cancer.
Project description:To identify direct NFIB target genes in HFSCs, we performed chromatin immunoprecipitation and deep sequencing (ChIP-seq) analysis using FACS-isolated HFSCs. Two independent NFIB ChIP-seq experiments were conducted.
Project description:We identified NFIB as a CARM1 substrate and showed that this transcription factor utilizes CARM1 as a coactivator. Importantly, NFIB harbors both oncogenic and metastatic activities, and is often overexpressed in small cell lung cancer (SCLC). Using a SCLC mouse model, we show that both CARM1 and the CARM1 methylation site on NFIB are critical for the rapid onset of SCLC. By performing the high-throughput sequecing analysis, we found that CARM1-null and NFIB-R388K mutant mouse SCLC tumors share the ability to regulate chromatin accessbility and have similar gene expression pattern.
Project description:To identify direct NFIB target genes in HFSCs, we performed chromatin immunoprecipitation and deep sequencing (ChIP-seq) analysis using FACS-isolated HFSCs.