Project description:To understand the role of LSD1 in B cell differentiation, mice with B cell conditional deletion of LSD1 were intravenously inoculated with LPS. After 3 days, B220+GL7-CD138- naïve B cells and CD138+ plasmablasts were FACS-sorted from the spleens and RNA-seq was performed to identify LSD1-target regulated genes.
Project description:To understand the role of LSD1 in marginal zone B cell development, CD93+ transitional B cells were enriched from the spleens of mice with B cell conditional deletion of LSD1, the cells were cultured for 3 days in the presence of OP9-DL1 cells and BAFF, and day 0 B220+CD93+ transitional B cells and day 3 B220+CD21+CD1d+ ex vivo-derived marginal zone B cells were FACS-sorted and RNA-seq was performed to identify LSD1-target regulated genes.
Project description:To understand the role of LSD1 in B cell differentiation, mice with B cell conditional deletion of LSD1 were intravenously inoculated with LPS. After 3 days, B220+GL7-CD138- naïve B cells and CD138+ plasmablasts were FACS-sorted from the spleens and RNA-seq was performed to identify LSD1-target regulated chromatin.
Project description:To study the plasmablast response to influenza vaccines We want to test and see that LAIV, TIV and ID TIV induced different plasmablast response We take peripheral plasmablast and test its response to influenza vaccines at day 7 after vaccination. This array data set is for day 0 (before vaccines)
Project description:Transcriptome analysis of LSD1-depleted HepG2 cells revealed that LSD1 regulates the expression of glycolytic and mitochondrial metabolism genes. We found that LSD1 is an important regulator of glycolysis and mitochondrial respiration in hepatoma. We depleted LSD1 in HepG2 human hepatoma cells using two different siRNAs, and then carried out an expression microarray experiment.
Project description:During brain development, histone-modifying enzymes play an important role by orchestrating transcriptional programs that regulate neuronal maturation. Lysine-Specific Demethylase 1 (LSD1, also named as KDM1A) functions as a transcriptional repressor by removing methyl groups at lysine 4 of histone H3 (H3K4). In neurons, alternative splicing can include an additional exon (exon E8a) within LSD1 transcripts, generating a LSD1+8a neuro-specific isoform. We here report that LSD1+8a isoform does not have the intrinsic ability to demethylate H3K4. LSD1+8a functions as a co-activator on its target genes by removing H3K9 repressive histone marks. We identify the supervillin protein (SVIL) as a LSD1+8a interacting partner and demonstrate that SVIL protein regulates neuronal maturation by controlling LSD1+8a mediated H3K9 demethylation. Thus, our results show that alternative splicing provides a genius mechanism by which LSD1 isoforms can acquire a dual specificity (H3K9 vs H3K4) and therefore differentially control specific gene expression patterns during brain development. In order to find some LSD1+8a regulated genes at differentiated SH-SY5Y cell lines, we infected SH-SY5Y with control or LSD1+8a shRNA, then induced differentiation with RA and BDNF, (Retinoic acid (RA) (Sigma) was added at a final concentration of 10 μM the next day after plating. After 4 days, the cells were washed three times with PBS and incubated with 50 ng/mL of Brain Derived Neural Factor (BDNF) (Millipore) in serum-free medium for 3 days), we extracted RNA from BDNF induced SH-SY5Y cells for expression analysis.Duplicates were included for Affymetrix Human transcriptome version 2 array.