RNA-seq data of PHF8 wild-type and PHF8 knockout TRAMP mouse
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE157621 | GEO | 2020/09/26
REPOSITORIES: GEO
Similar Datasets
Project description:RNA-seq analysis were applied to elucidate the transcriptional differences between 786-O cell lines transfected with control-sgRNA (Control) and PHF8-sgRNA (PHF8-KO). A total of 3575 differentially expressed genes (Fold Change > 2, or Fold Change＜0.5; FDR < 0.05) with 2097 down- and 1478 up-regulated genes were identified in PHF8-KO 786-O cells
2022-10-08 | GSE214183 | GEO
Project description:RNA-seq data of PHF8 wild-type and PHF8 knockout TRAMP mouse
| PRJNA662246 | ENA
Project description:We performed PHF8 ChIP-seq analysis of APOC2 overexpressed RKO cells and control cells to identify high-confident PHF8 regulated targets.
2021-05-07 | GSE114089 | GEO
Project description:PHF8 is a histone demethylase associated with X-linked mental retardation (XLMR). It has been described as a transcriptional coactivator involved in cell cycle progression, but its physiological role is still poorly understood. Here we show that PHF8 controls the expression of genes involved in cell adhesion and cytoskeleton organization such as RhoA, Rac1 and GSK3M-NM-2. A lack of PHF8 not only results in a cell cycle delay but also in a disorganized actin cytoskeleton and impaired cell adhesion. Our data demonstrate that PHF8 directly regulates the expression of these genes by demethylating H4K20me1 at promoters. Moreover, c-Myc transcription factor interacts with PHF8 and binds to the analyzed promoters, suggesting that c-Myc is involved on PHF8 recruitment to these promoters. Further analysis in the neuroblastoma cell line SH-SY5Y and in cortical neurons shows that depletion of PHF8 results in deficient neurite elongation. Overall, our results suggest that the mental retardation phenotype associated with loss of function of PHF8 could be due to abnormal neuronal connections as a result of alterations in cytoskeleton function. HeLa cells were transfected with either control or PHF8 siRNAs. Experiments were performed in biological triplicates. RNA were extracted and sujected to microarray analysis.
2012-07-31 | E-GEOD-38175 | biostudies-arrayexpress
Project description:TRAMP is a eukaryotic protein complex with RNA helicase and polyadenylase activity that marks and delivers a variety of RNA substrates to the nuclear exosome for degradation. Prior work has characterized binding of Trf4 and Air2 to the helicase core of Mtr4 and the regulation of both enzymatic activities in TRAMP. Air2 contains a conserved sequence that is predicted to bind the arch domain of Mtr4, though this interface is dispensable for TRAMP formation. To understand the interactions of the Saccharomyces cerevisiae TRAMP complex and its interactions with RNA, we have applied hydrogen-deuterium exchange mass spectrometry. We demonstrate that Air2 simultaneously binds the helicase core and the fist of Mtr4 in solution, constraining the arch to a conformation ready to bind RNA. We characterize the previously unknown interactions of Trf4 and Air2 with RNA and show how interactions with substrates are altered in TRAMP, supporting a mechanistic model for the enhancement of Mtr4 activity in TRAMP.
2024-12-11 | PXD053773 | Pride
Project description:Mutations in PHF8 are associated with X-linked mental retardationand cleft lip/cleft palate. PHF8 contains a plant homeodomain(PHD) in its N-terminus and is member of a family of JmjC-domaincontaining proteins. While PHDs can act as methyl lysine recognitionmotifs, JmjC-domains can catalyze lysine demethylation. Here,we show that PHF8 is a histone demethylase that removes repressivehistone H3 dimethyl lysine 9 marks. Our biochemical analysisrevealed specific association of the PHF8 PHD domain with histoneH3 trimethylated at lysine 4 (H3K4me3). Chromatin-immunoprecipitationfollowed by high throughput sequencing indicated that PHF8 isenriched at transcription start sites of many active or poisedgenes, mirroring the presence of RNA polymerase II (RNAPII)and of H3K4me3-bearing nucleosomes. We show that PHF8 can actas a transcriptional co-activator and its activation functionlargely depends on binding of the PHD to H3K4me3. Furthermore,we present evidence for direct interaction of PHF8 with theC-terminal domain of RNAPII. Importantly, a PHF8 disease mutantis defective in demethylation and in co-activation. This isthe first demonstration of a chromatin-modifying enzyme whichis globally recruited to promoters through its association withH3K4me3 and RNAPII. This SuperSeries is composed of the following subset Series: GSE20563: Knockdown of PHF8 in HeLa S3 cells GSE20725: ChIP-Seq of PHF8 and H3K4me3 Refer to individual Series
2010-04-26 | E-GEOD-20753 | biostudies-arrayexpress
Project description:PHF8 is an H3K9me2 demethylase, interacts with H3K4me3 and RNA Polymerase II, is enriched at thousands of transcription start sites and can act as a transcriptional co-activator. In the following experiment we wanted to analyze the impact of PHF8-knockdown on transcript levels in HeLa cells. Three independent replicate knockdown experiments with PHF8-shA and control NT-sh were performed (6 samples in total). The two samples of each replicate experiment were hybridized in two color dye swap experiments (6 arrays in total).
2010-05-07 | E-GEOD-20563 | biostudies-arrayexpress
Project description:In this dataset we show transcriptional profiles derived from adenocarcinoma or incipient neuroendocrine prostate cancer (NEPC) derived from TRAMP or SPARC-deficient TRAMP mice respectively. Genetic ablation of SPARC rendered prostate cancer cells to be prone to NEPC differentiation.
2024-07-01 | GSE242811 | GEO
Project description:PHF8 is an H3K9me2 demethylase, interacts with H3K4me3 and RNA Polymerase II, is enriched at thousands of transcription start sites and can act as a transcriptional co-activator. ChIP-seq of PHF8 in HeLa, 293T and Hs68 cells, and of H3K4me3 in Hs68 fibroblasts was performed. Normal IgG-IP or input DNA served as negative controls.
2010-04-27 | E-GEOD-20725 | biostudies-arrayexpress
Project description:PHF8 is a histone demethylase associated with X-linked mental retardation (XLMR). It has been described as a transcriptional coactivator involved in cell cycle progression, but its physiological role is still poorly understood. Here we show that PHF8 controls the expression of genes involved in cell adhesion and cytoskeleton organization such as RhoA, Rac1 and GSK3β. A lack of PHF8 not only results in a cell cycle delay but also in a disorganized actin cytoskeleton and impaired cell adhesion. Our data demonstrate that PHF8 directly regulates the expression of these genes by demethylating H4K20me1 at promoters. Moreover, c-Myc transcription factor interacts with PHF8 and binds to the analyzed promoters, suggesting that c-Myc is involved on PHF8 recruitment to these promoters. Further analysis in the neuroblastoma cell line SH-SY5Y and in cortical neurons shows that depletion of PHF8 results in deficient neurite elongation. Overall, our results suggest that the mental retardation phenotype associated with loss of function of PHF8 could be due to abnormal neuronal connections as a result of alterations in cytoskeleton function.
2012-08-01 | GSE38175 | GEO