Project description:Profiling of promoter occupancy by SND1 coactivator in human hepatoma cells. Control and TNFα-treated HepG2 cells are immunoprecipitated with anti-SND1 antibody and input and immunoprecipitated material were hybridized in an Agilent human promoter microarray Two-condition experiment. Biological replicates: 3 control replicates, 3 TNFα-treated replicates. Input vs. Immunoprecipitated material
Project description:Using a transcriptome-wide profiling approach to map translation initiation start sites in human beta-cells under standard and inflammatory conditions, we identifies non-canonical start sites and translation initiation within lncRNA.
Project description:shRNA knockdown against SND1 in HepG2 cells followed by RNA-seq. (SND1 BGHLV14) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:Profiling of promoter occupancy by SND1 coactivator in human hepatoma cells. Control and TNFα-treated HepG2 cells are immunoprecipitated with anti-SND1 antibody and input and immunoprecipitated material were hybridized in an Agilent human promoter microarray
Project description:PyMT tumor cells with indicated status of Mtdh and Snd1 were treated with camptothecin (CPT) and the transcirptome profiles were determined and compared two sets of experiments: (1) vector control vs Snd1-KD under CPT treament (2) PyMT/Mtdh-KO cells reconstituted with either WT or Snd1-binding deficient mutant Mtdh (W391D) under CPT treatment
Project description:In this study, we provide a global overview of genome-wide OsHOX24 binding sites in rice under control and desiccation stress conditions in wild-type and OsHOx24 overexpressing rice plants (H49 line) via chromatin immunoprecipitation sequencing (ChIP-sequencing) approach. We identified numerous downstream targets of OsHOX24 under desiccation stress and control by analyzing the comprehensive binding site map of OsHOX24 at whole genome level in rice.
Project description:We have mapped m6A sites and endogenous SND1 binding sites in the viral and cellular transcriptome using TREx BCBL1-Rta cells. In addition, we have depleted SND1 in TREx BCBL1-Rta cells and BCBL1 cells and analyzed their RNA expression profile both during latency and lytic replication.
Project description:eCLIP experiment on HepG2 against SND1 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:eCLIP control experiment on HepG2 against SND1 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:The pancreatic β cell synthesizes, packages, and secretes insulin in response to glucose-stimulation to maintain blood glucose homeostasis. Under diabetic conditions, a subset of β cells fail and lose expression of key transcription factors (TFs) required for insulin secretion. Among these TFs is Pancreatic and duodenal homeobox 1 (Pdx1), which recruits a unique subset of transcriptional coregulators to modulate its activity. Here we describe a novel interacting partner of Pdx1, the Staphylococcal Nuclease and Tudor domain-containing protein (Snd1), which has been shown to facilitate protein-protein interactions and transcriptional control through diverse mechanisms in a variety of tissues. Pdx1:Snd1 interactions were confirmed in rodent β cell lines, mouse islets and human islets. Utilizing CRISPR-Cas9 gene editing technology, we deleted Snd1 from the mouse β cell lines, which revealed numerous differentially expressed genes linked to insulin secretion and cell proliferation, including limited expression of Glp1r. We observed Snd1 deficient β cell lines had reduced cell expansion rates, Glp1r protein levels and limited cAMP accumulation under stimulatory conditions, and further show that acute ablation of Snd1 impaired insulin secretion in rodent and human β cell lines. Lastly, we discovered that PDX1:SND1 interactions were profoundly reduced in human β cells from donors with type 2 diabetes (T2D). These observations suggest the Pdx1:Snd1 complex formation is critical for controlling a subset of genes important for β cell function and is targeted in diabetes pathogenesis
