7 research outputs found
Supplementary Table S2 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
List of HDACi regulated pathways</p
Supplementary Table S3 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
List of HDACi altered GATA-3 target genes</p
Supplementary Figure S3 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
ChlP-seq occupancy binding peaks at GATA-3 target genes in vehicle/HDACi treated H9 cells</p
Supplementary Figure S2 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
HDACi alters GATA-3 target genes expression in independent datasets</p
Supplementary Figure S1 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
BHLHE40 and KLF6 are transcriptionally activated by GATA-3, and their expression impaired upon HDAC inhibition</p
Supplementary Table S1 from GATA-3–dependent Gene Transcription is Impaired upon HDAC Inhibition
Primers used in qRT-PCR.</p
GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms
Neoplasms originating from thymic T-cell progenitors and post-thymic mature T-cell subsets account for a minority of lymphoproliferative neoplasms. These T-cell derived neoplasms, while molecularly and genetically heterogeneous, exploit transcription factors and signaling pathways that are critically important in normal T-cell biology, including those implicated in antigen-, costimulatory-, and cytokine-receptor signaling. The transcription factor GATA-3 regulates the growth and proliferation of both immature and mature T cells and has recently been implicated in T-cell neoplasms, including the most common mature T-cell lymphoma observed in much of the Western world. Here we show that GATA-3 is a proto-oncogene across the spectrum of T-cell neoplasms, including those derived from T-cell progenitors and their mature progeny, and further define the transcriptional programs that are GATA-3 dependent, which include therapeutically targetable gene products. The discovery that p300-dependent acetylation regulates GATA-3 mediated transcription by attenuating DNA binding has novel therapeutic implications. As most patients afflicted with GATA-3 driven T-cell neoplasms will succumb to their disease within a few years of diagnosis, these findings suggest opportunities to improve outcomes for these patients