Transcript expression level in control and Setd1a-knockdown mouse explant retina
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA646500 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Knockdown of Kmt2f in a embryonic mouse retina caused increased apoptosis and decreased proliferation. To investigate downstream molecular mechanisms of Kmt2f in retina, RNA-sequencing was performed with control or shKmt2f-expressing retina. Mouse retinas at embryonic dat 17 were electroporated with plasmids and cultured for 2 days. EGFP-expressing cells were purified by a cell sorter, and RNA-seq was carried out.
2021-05-19 | GSE154498 | GEO
Project description:Investigation of gene expression level changes in the SETD1A depleted cancer cells (shSETD1A), compared to the GFP depleted cancer cells (shGFP) as control. This analysis was performed to gain an understanding of the transcriptional changes induced by chromation modifications through H3K4 methyltransferase SETD1A. Key Word: SETD1A, Epigenetics
2017-07-18 | GSE71498 | GEO
Project description:Mapping physical interactions of SETD1A COMPOASS in HEK293T cells using endogenous immunoprecipitation followed by label-free quantitative proteomics. We found a novel protein interacts with SETD1A, which is RAD18 (DNA damage repair protein).
2019-06-13 | PXD012549 | Pride
Project description:RNA-Seq: assessment of transcript level analysis tools
| PRJNA302625 | ENA
Project description:SETD1A, a histone methyltransferase, is a key schizophrenia susceptibility gene. Mutant mice carrying a heterozygous loss-of-function mutation of the orthologous gene exhibit alterations in axonal branching and cortical synaptic dynamics, accompanied by specific deficits in working memory that recapitulates SCZ-related alterations. We show that Setd1a targets mostly enhancers and reveal a striking overlap between Setd1a and Mef2 chromatin targets. Setd1a targets are highly expressed in pyramidal neurons and enriched for genes with postnatally-biased expression involved in synaptic structure and function. Notably, evolutionary conserved Setd1a binding sites and target genes are strongly associated with neuropsychiatric genetic risk burden. Reinstating Setd1a expression in adulthood rescues working memory deficits. We identify LSD1 as a major demethylase counteracting the effects of Setd1a methyl transferase activity and show that LSD1 antagonism in adult Setd1a-deficient mice results in a full rescue of the behavioral abnormalities and axonal branching deficits. Our findings advance our understanding of how SETD1A mutations predispose to SCZ and point to therapeutic interventions.
2019-10-09 | GSE123652 | GEO
Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics revealed an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disturbs a non-enzymatic SETD1A domain-dependent cyclin K function, increases the mono-Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.
2022-12-09 | GSE189893 | GEO
Project description:Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics revealed an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disturbs a non-enzymatic SETD1A domain-dependent cyclin K function, increases the mono-Ser5P RNA polymerase II (RNAP2) at TSS, and induces the promoter-proximal pausing of RNAP2 in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAP2 pausing and its function in cancer.
2022-12-09 | GSE190994 | GEO
Project description:Nuclear interaction studies by ChIP coupled with mass spectrometry identified the COMPASS/SETD1A complex as interaction partner of the glucocorticoid receptor (GR) in murine bone marrow-derived macrophages (BMDMs). Here, we profiled the occupancy of SETD1A and CXXC1, two subunits of the COMPASS/SETD1A complex in murine macrophages after LPS and Dex+LPS stimulation. We show, that GR recuits SETD1A and CXXC1 to GR enhancer and that SETD1A recruitment does correlate with changes in H3K4methylation at some of those enhancers.
2020-12-31 | GSE136070 | GEO
Project description:SETD1A is a histone H3K4 methyltransferase and function as a coactivator for nuclear receptors (NRs) and other transcription factors. We performed genome-wide gene expression analysis in non-specific siRNA transfected or SETD1A knockdown MCF-7 cells to investigate global gene expression changes induced by SETD1A knockdown.
2018-10-24 | GSE101860 | GEO
Project description:The H3K4 methyltransferase SETD1A plays a crucial role in leukemia cell survival through its non-catalytic FLOS domain mediated recruitment of cyclin K and regulation of DNA damage response genes. In this study, we identify a functional nuclear localization signal and interaction partners for the FLOS domain. Our proteomics analysis against FLOS domain-binding partners reveals that the SETD1A FLOS domain binds mitosis-associated proteins BuGZ/BUB3. Targeted inhibition of both cyclin K and BuGZ/BUB3 binding motifs on SETD1A shows synergistic anti-leukemic effects. BuGZ/BUB3 localize to SETD1A-positive promoter-TSS regions and SETD1A-negative H3K4me1-positive enhancer regions adjacent to SETD1A-target genes. The GLEBS motif and intrinsically disordered region of BuGZ are required for both SETD1A binding and the leukemia cell proliferation. Despite the role of BuGZ/BUB3 at mitotic phase, the cell-cycle specific SETD1A restoration study indicates the roles of SETD1A at G1/S phase of cell cycle. Discovery of this complex indicates the indispensable role of the SETD1A-BuGZ axis in cancer.
2023-07-29 | GSE159145 | GEO