Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1049742 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27128878_1.fastq.gz | Fastqsanger.gz | |||
| SRR27128878_2.fastq.gz | Fastqsanger.gz | |||
| SRR27128879_1.fastq.gz | Fastqsanger.gz | |||
| SRR27128879_2.fastq.gz | Fastqsanger.gz | |||
| SRR27128880_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq in KYSE30 and KYSE150 cells following KLF12 overexpression
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Project description:Background: Although adequate periconceptional folic acid (FA) supplementation has reduced the occurrence of neural tube defects (NTDs)-affected pregnancies, mechanisms underlie FA resistant NTDs are poorly understood, so that NTDs still remain a global public health concern now. It has been proven that high level of Krüppel-like factor 12 (KLF12) has bad effects on heath in most cases, but there is no evidence concerning its roles during development. Methods: We used KLF12-overexpression mice to study the effects of high level of KLF12 on neural tube development. Findings: We showed KLF12-overexpression fetuses died in utero at around 10.5 days post coitus with 100% cranial NTDs. Neither FA or formate benefited normal neural tube closure in mutant fetuses. Further anylasis revealed high level of KLF12 caused NTDs in mice via overactivating Sonic hedgehog (Shh) signaling pathway, leading to upregulation of Ptch1, Gli1, Hhip etc. PF-5274857, an antagonist of Shh signaling pathway could significantly promote dorsolateral hinge point formation and partially rescue the phynotype. Interpretation: The regulatory hierarchy between high level of KLF12 and FA-resistant NTDs might provide new insights for the diagnosis and treatment of unexplained NTDs in the future.
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Project description:The goal of this study is to determine the role of the transcription factor, Klf12, in mouse NK cells. Transcriptome profiling by RNA-Seq of wild-type and Klf12-deficient mouse CD4+ T cells, CD8+ T cells, B cells, and NK cells. We found that Klf12-deficient mouse NK cells express more transcripts of Btg3 and have a proliferative impairment compared to wild-type mouse NK cells in a competitive setting.
2020-04-13 | GSE128962 | GEO
Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3’-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.
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Project description:Purpose: To fully realize the potential molecular mechanism that LHX2 promotes ESCC progression Methods: Total RNA of LHX2-knockdown KYSE30/KYSE510 and control cells was extracted with TRIzol Reagent. RNA libraries were constructed using an Illumina TruSeq RNA Sample Preparation kit according to the manufacturer’s protocol. A total of 150 base paired-end reads were sequenced using the Novaseq 6000 S4 platform. Results: We identified 26008 transcripts in KYSE30 control and KYSE30 LHX2-knockdown cells ,and 25561 transcripts in KYSE510 control and KYSE510 LHX2-knockdown cells. Conclusions: Our study represents the analysis of LHX2-knockdown ESCC cells, generated by RNA-seq.
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