Expression data from YTHDF1 or YTHDF2 down-regulated PC9
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA720377 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The human YTH domain family protein (YTHDF) family is RNA binding protein which specifically recognizes N6-methyladenosine (m6A), and exerts distinct roles in eukaryocytes; YTHDF1 promotes the translation of m6A modified mRNAs collaborating with initiation factors, and YTHDF2 reduces the stability of the m6A-modified transcripts. We used the Nanostring nCounter to detail the differential gene expression by YTHDF1 and YTHDF2.
2021-08-24 | GSE171634 | GEO
Project description:To identify the target mRNAs of the m6A reader protein YTHDF1 and YTHDF2, we carired out anti YTHDF1 and anti YTHDF2 RNA Immunoprecipitation (RIP) followed by RNA-sequencencing. Using EZ-Magna RIP™ RNA-Binding Protein Immunoprecipitation Kit (Millipore), RNA from P6-P8 wild type mouse cerebellum was pulled down by rabbit polyclonal anti-YTHDF1 (proteintech) or polyclonal anti-YTHDF2 (proteintech) and then sequenced on Illumina HiSeq3000 platform. The filtered reads were mapped to the mouse reference genome (GRCm38) using STAR v2.5 with default parameters. The resulting bam files were fed to HTSeq tool to count the number of RNA-seq reads, which was further normalized to calculate FPKM. To determine which gene is enriched, we computed the FPKM from RIP elute to input and any fold change greater than 2 was considered enriched. Finally, Biological replicates of anti-YTHDF1 RIP-Seq and anti-YTHDF2 RIP-Seq identified 506 and 596 mRNAs transcripts, respectively. This study provides gene lists which shows mRNA binding with YTHDF1 and YTHDF2 in mouse cerebellum.
2021-12-10 | GSE153689 | GEO
Project description:To identify the target mRNAs of the m6A reader proteins YTHDF1 and YTHDF2, we carried out anti-YTHDF1 and anti-YTHDF2 RNA Immunoprecipitation (RIP) followed by RNA-sequencing. Using EZ-Magna RIP™ RNA-Binding Protein Immunoprecipitation Kit (Millipore), RNA from E12.5 wild-type mouse cortices and P0 wild-type mouse retinas was pulled down by rabbit polyclonal anti-YTHDF1 (proteintech) and rabbit polyclonal anti-YTHDF2 (proteintech), and then sequenced on Illumina HiSeq3000 platform. The filtered reads were mapped to the mouse reference genome (GRCm38) using STAR v2.5 with default parameters. The resulting bam files were fed to the HTSeq tool to count the number of RNA-seq reads, which was further normalized to calculate FPKM. To determine which gene is enriched, we computed the FPKM from RIP elute to input, and any fold change greater than 2 was considered enriched. From the embryonic cortex, we identified 986 and 1860 mRNAs by anti-YTHDF1 and anti-YTHDF2 RIP-seq, respectively. Anti-YTHDF1 and anti-YTHDF2 RIP-seq in mouse retina identified 2969 and 1638 mRNAs, respectively. This study provides the gene lists which show mRNAs binding with YTHDF1 and YTHDF2 in the mouse cortex and retina.
2022-08-05 | GSE199962 | GEO
Project description:m6A and YTHDF1, YTHDF2, YTHDF3 mapping of IAV RNA with PAR-CLIP and pA-m6A-seq
2017-10-17 | GSE98033 | GEO
Project description:Anti-YTHDF1 and anti-YTHDF2 RIP-Seq to identify the target mRNAs for YTHDF1 and YTHDF2, respectively
| PRJNA643706 | ENA
Project description:Silencing of MED13L impairs Mediator-regulated chromatin H3K27ac modification in NSCLC. Here, we performed H3K27ac ChIP-seq to investigate impacts of miR-4497 or knocking-down MED13L on chromatin H3K27ac modification in NSCLC PC9 cells.
2020-08-19 | GSE147120 | GEO
Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down
2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress
Project description:N6-methyladenosine (m6A), the most abundant modification in mRNAs, has been defined as a crucial modulator in the progression of acute myeloid leukemia (AML), while the detailed mechanism remains elusive. Here we report that YTHDF1, an m6A reader protein, is overexpressed in human AML samples with enrichment in leukemia stem cells (LSCs). Whereas YTHDF1 is dispensable for normal hematopoiesis in mice, depletion of YTHDF1 attenuates self-renewal and proliferation of patient-derived LSCs, and impedes leukemia establishment in immunodeficient mice. Mechanistically, YTHDF1 promotes the translation of diverse m6A-modified oncogene mRNAs particularly cyclin E2. We applied a structure-based virtual screening of FDA-approved drugs and identified tegaserod as a potential YTHDF1 inhibitor. Tegaserod blocks the direct binding of YTHDF1 with m6A-modified mRNAs and inhibits YTHDF1-regulated mRNA translation. Moreover, tegaserod inhibits leukemogenesis in vitro and in mice, phenocopying the loss of YTHDF1. Together, our study defines YTHDF1 as an integral regulator of AML progression at the translational level and identifies tegaserod as a potential therapeutic agent for AML by targeting YTHDF1.
2021-09-28 | GSE184842 | GEO
Project description:N6-methyladenosine (m6A), the most abundant reversible modification on eukaryote messenger RNA, is recognized by a series of readers, including the YT521-B homology domain family (YTHDF) proteins, which are coupled to perform physiological functions. Here, we report that YTHDF2 and YTHDF3, but not YTHDF1, are required for reprogramming of somatic cells into induced pluripotent stem cells (iPSCs). Mechanistically, we found that YTHDF3 recruits the PAN2-PAN3 deadenylase complex and conduces to reprogramming by promoting mRNA clearance of somatic genes, including Tead2 and Tgfb1, which parallels the activity of the YTHDF2-CCR4-NOT deadenylase complex. Ythdf2/3 deficiency further represses mesenchymal-to-epithelial transition (MET) and chromatin silencing at loci containing the TEAD motif, contributing to decreased reprogramming efficiency. Moreover, RNA interference of Tgfb1 or the Hippo signaling effectors Yap1, Taz, and Tead2 rescues Ythdf2/3-defective reprogramming. Overall, YTHDF2/3 couple RNA deadenylation and regulation with the clearance of somatic genes provides insights into iPSC reprogramming at the posttranscriptional level.
2020-08-19 | GSE156437 | GEO
Project description:Analysis of gefitinib short-term resistance at gene expression level. The hyposthesis tested in the present study was that short-term resistance towards gefitinib in NSCLC cells influences pathways that associates with resistance towards EGFR-TKI treatment. Results provide important information of the response of EGFR mutant NSCLC cells to gefitinib and also to resistance towards gefitinib resistance, up-or down-regulated specific resistance pathways and cellular functions. Total RNA obtained from PC9 cell line (n=3), co-cultured PC9 (with MRC-5 cells)(n=3), gefitinib treated (0.5µM) PC9 (n=3), and co-cultured (MRC-5) + gefitinib treated PC9 cells (n=3) for 48h after gefitinib treatment
2016-07-01 | E-GEOD-75308 | biostudies-arrayexpress