Project description:We identified potential TCF4 targeted genes by performing CHIP-Seq using TCF4 antibody in ABC like DLBCL cell lines. We have identified strong binding of TCF4 to enhancer elements of B-cell receptor signaling components which drives B-cell receptor signaling.
Project description:genome-wide ChIP-on-chip against TCF4 in LS174T cells, performed on NimbleGen Systems, Inc. human genome-wide 38-chip, hg17 array set followed by verification using biological replicates on a dedicated design.
Project description:We identified potential TCF4 targeted genes by performing CHIP-Seq using TCF4 antibody in ABC like DLBCL cell lines. We have identified strong binding of TCF4 to enhancer elements of B-cell receptor signaling components which drives B-cell receptor signaling.
2019-04-18 | GSE119475 | GEO
Project description:Wnt signaling and Cal27 sphere cells
Project description:In order to study the molecular mechanisms involving TCF4 in keratinocytes under different inflammatory responses, control and TCF4 knock down keratinocytes were stimulated with inflammatory cytokines and conducted RNA-seq to profile the gene expression.
Project description:Mutations of TCF4, which encodes a basic helix-loop-helix transcription factor, cause Pitt-Hopkins syndrome (PTHS) via multiple genetic mechanisms. TCF4 is a complex locus expressing multiple transcripts by alternative splicing and use of multiple promoters. We report a three-generation family segregating mild intellectual disability with an apparently balanced chromosomal translocation t(14;18)(q23.3;q21.2) that we characterized as a complex unbalanced karyotype 46,XY,der(14)del(14)(q23.3q23.3)t(14;18)(q23.3;q21.2)del(18)(q21.2q21.2) del(18)(q21.2q21.2)inv(18)(q21.2q21.2),der(18)t(14 ;18)(q23.3;q21.2) disrupting TCF4. Using whole genome sequencing, transcriptome sequencing, qRT-PCR and nCounter analysis, we characterized the breakpoint junctions from derivative chromosomes and gene expression at the TCF4 locus. Our analyses revealed that family members segregating mild intellectual disability with the complex chromosome aberration had normal expression of genes along chromosomes 14 or 18 and no marked changes in expression of genes other than TCF4. Affected individuals had 12-33 fold higher mRNA levels of TCF4 than did unaffected controls or individuals with PTHS. Increased levels of TCF4 transcript variants originating distal to the translocation breakpoint, not the fusion transcript generated by the derivative chromosome, contributed to this increased. Although validation in additional patients is required, our findings suggest that the dysmorphic features and severe intellectual disability characteristic of PTHS is partially rescued by overexpression of short TCF4 transcripts encoding a nuclear localization signal, a transcription activation domain, and the basic helix-loop-helix domain. Examination of TCF4 Isoform expression comparison between mutant and control skin fibroblast tissues
Project description:To identify the genes directly regulated by H3K9la on a genome-wide scale, we performed CUT&Tag assays using a H3K9la specific antibody in CAL27 and HN30 with or without the lactic acid treatment, and performed CUT&Tag assays using a H3K9la specific antibody in HN30 under hypoxia condition.
Project description:Haplo-insufficiency of TCF4 induced by mutations or microdeletion of TCF4 gene causes Pitt-Hopkins Diseases. Recent gene association studies revealed that mutations of TCF4 is significantly associated with schizophrenia. But the role of TCF4 in developing neocortex is not known. The goal of this study is to identify TCF4 itranscriptional regulatory pathways in developing neocortex by analyzing transcriptomes of dorsal telencephalons of TCF4knockout, TCF4Heterozygote and WT littermates and comparing differential expressed genes between these genotypes.
