Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290340 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2107160_1.fastq.gz | Fastqsanger.gz | |||
| SRR2107160_2.fastq.gz | Fastqsanger.gz | |||
| SRR2107161_1.fastq.gz | Fastqsanger.gz | |||
| SRR2107161_2.fastq.gz | Fastqsanger.gz | |||
| SRR2107162_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA was isolated from and YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 deficient human HeLa cells using the TRIzol (Invitrogen) reagent by following the company manual. For all samples the RNA integrity was checked using an Agilent Bioanalyzer 2100. All samples showed a RIN (RNA integrity number) of higher than 9. Approximately 2.5 µg of total RNA was then used for library preparation using a TruSeqâ?¢ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturerâ??s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read or paired-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. Examination of gene expressive levels in normal and YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 or SRSF10 deficient Human HeLa cells
2016-02-17 | E-GEOD-71095 | biostudies-arrayexpress
Project description:Label the cells overexpressed Flag tagged YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 with 4-SU, the RNA bound by YTHDC1 and SRSF proteins can be got by Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeq⢠RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturerâs protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. Discovery of the binding motif of YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 or SRSF10 in overexpressed Human HeLa cells
2016-02-17 | E-GEOD-71096 | biostudies-arrayexpress
Project description:RNA was isolated from and YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 deficient human HeLa cells using the TRIzol (Invitrogen) reagent by following the company manual. For all samples the RNA integrity was checked using an Agilent Bioanalyzer 2100. All samples showed a RIN (RNA integrity number) of higher than 9. Approximately 2.5 µg of total RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read or paired-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane.
2016-02-17 | GSE71095 | GEO
Project description:Label the cells overexpressed Flag tagged YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 with 4-SU, the RNA bound by YTHDC1 and SRSF proteins can be got by Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 101 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane.
2016-02-17 | GSE71096 | GEO
Project description:PAR-CLIP analysis of YTHDC1, SRSF1, SRSF3, SRSF7, SRSF9 and SRSF10 in human HeLa cells
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Project description:To understand the role of trans factors in the regulation of splicing and alternative splicing, we knocked-down 22 RNA-binding proteins previously shown or suspected to be involved in the regulation of splicing (“splicing factors”). We performed knockdown experiments in triplicate in the Hapmap lymphoblastoid cell line GM19238 using small interfering RNAs (siRNAs). RNA was extracted 72 hours after knockdown for RNA-seq library preparation. The following splicing factors were analyzed: ACIN1, ADAR, HNRPA2B1, HNRPF, HNRPH1, HNRPH2, HNRPK, HNRPL, HNRPR, PCBP2, PTBP1, RBM23, RBM39, RBMX, RNPS1, SRSF1, SRSF3, SRSF4, SRSF8, SRSF9, SRSF10 and SYNCRIP. Seven controls were generated with non-specific siRNA probes transfection. RNA-seq libraries were multiplexed and sequenced on 3 different flow-cells on an Illumina HiSeq 2000 sequencer (single-end 107 bp long reads).
2014-12-01 | GSE52834 | GEO
Project description:To evaluate the role of alternative splicing in cellular senescence, we analyzed transcriptomics by RNAseq in SRSF3 and SRSF7 suppressed human diploid fibroblasts.
2023-04-27 | GSE230443 | GEO
Project description:Human Microprocessor cleaves pri-miRNAs to initiate miRNA biogenesis. The accuracy and efficiency of Microprocessor cleavage ensure appropriate miRNA sequence and expression and thus its proper gene regulation. However, Microprocessor cleaves many pri-miRNAs incorrectly, so it requires assistance from its many cofactors. For example, SRSF3 enhances Microprocessor cleavage by interacting with the CNNC motif in pri-miRNAs. However, whether SRSF3 can function with other motifs and/or requires the motifs in a certain secondary structure is unknown. In addition, the function of SRSF7 (a paralog of SRSF3) in miRNA biogenesis still needs to be discovered. Here, we demonstrated that SRSF7 could stimulate Microprocessor cleavage. In addition, by conducting high-throughput pri-miRNA cleavage assays for Microprocessor and SRSF7 or SRSF3, we demonstrated that SRSF7 and SRSF3 function with the CRC and CNNC motifs, adopting certain secondary structures. In addition, SRSF7 and SRSF3 affect the Microprocessor cleavage sites in human cells. Our findings demonstrate the roles of SRSF7 in miRNA biogenesis and provide a comprehensive view of the molecular mechanism of SRSF7 and SRSF3 in enhancing Microprocessor cleavage.
2023-01-23 | GSE215790 | GEO
Project description:MicroRNAs (miRNAs) are short non-coding RNAs that play essential roles in RNA silencing and gene regulation. The human Microprocessor (MP) is the key factor to initiate miRNA biogenesis by cleaving primary microRNAs (pri-miRNAs). However, the Microprocessor alone cannot precisely and efficiently cleave all pri-miRNAs; thus, it requires cofactors to assist its cleavage. SRSF3 interacts with CNNC in pri-miRNAs, enhancing the MP cleavage. However, it is unknown if SRSF3 can function with other non-CNNC motifs and if secondary structure might influce CNNC function. In addition, function of SRSF7, a paralog of SRSF3, in the SR proteins family, in miRNA biogenesis is largely unknown. In this study, by conducting the high-throughput pri-miRNA cleavage assays for the MP with SRSF3 or SRSF7 and randomized pri-miRNAs, we discovered that SRSF7 also stimulate MP clevage. Futhermore, we found that both SRSF3 and SRSF7 can function with some non-CNNC motifs and with CNNC motifs with certain secondary structures. Furthermore, we also demonstrated that SRSF7 and SRSF3 governed the cleavage sites of the Microprocessor in human cells. Our findings disclose the roles SRSF7 in miRNA biogenesis, demonstrate a compresenhive moleucalr mechanism of SFSF3 and SRSF7 in enhancing cleavage of MP and described in more detail the RNA-binding features of SRSF7 and SRSF3.
2023-01-23 | GSE221996 | GEO
Project description:Alternative polyadenylation (APA) refers to the regulated selection of polyadenylation sites (PASs) in transcripts, which affects the length of their 3’ untranslated regions (3’UTRs). APA regulates stage- and tissue-specific gene expression by affecting the stability, subcellular localization or translation rate of transcripts. We have recently shown that SRSF3 and SRSF7, two closely related SR proteins, link APA to mRNA export. However, the underlying mechanism for APA regulation by SRSF3 and SRSF7 remained unknown. Here, we combined iCLIP and 3’-end sequencing to find that both proteins bind upstream of proximal PAS (pPAS), but exert opposing effects on 3’UTR length. We show that SRSF7 enhances pPAS usage in a splicing-independent and concentration-dependent manner by recruiting the cleavage factor FIP1, thereby generating short 3’UTRs. SRSF7-specific domains that are absent in SRSF3 are necessary and sufficient for FIP1 recruitment. SRSF3 promotes long 3’UTRs by maintaining high levels of the cleavage factor Im (CFIm) via alternative splicing. Using iCLIP, we show that CFIm binds before and after the pPASs of SRSF3 targets, which masks them and inhibits polyadenylation. In the absence of SRSF3, CFIm levels are strongly reduced, which exposes the pPASs and leads to shorter 3’UTRs. Conversely, during cellular differentiation, 3’UTRs are massively extended, while the levels of SRSF7 and FIP1 strongly decline. Altogether, our data suggest that SRSF7 acts as a sequence-specific enhancer of pPASs, while SRSF3 inhibits pPAS usage by controlling CFIm levels. Our data shed light on a long-standing puzzle of how one factor (CFIm) can inhibit and enhance PAS usage.
2021-09-09 | PXD018090 | Pride