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RNA-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

ABSTRACT: RNA-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

PROVIDER: PRJNA729719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14521883_1.fastq.gz	Fastqsanger.gz
	SRR14521883_2.fastq.gz	Fastqsanger.gz
	SRR14521884_1.fastq.gz	Fastqsanger.gz
	SRR14521884_2.fastq.gz	Fastqsanger.gz
	SRR14521885_1.fastq.gz	Fastqsanger.gz

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CLIP-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

Project description:CLIP-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

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RNA-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

Project description:We report the upregulated genes by the expression of LIN28A or loss of function mutant of LIN28A for 293FTcells..

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CLIP-Seq for LIN28A or LIN28A loss of function mutant expressing 293FT cells

Project description:We report the direct target genes by LIN28A or loss of function mutant of LIN28A for 293FTcells using CLIP-Seq

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. Given that Lin28a can bind to diverse mRNA to regulate their abundance and/or translation, we conducted RNA-seq to profile the cardiac transcriptome alteration without Lin28a under pressure overload. It showed that metabolic pathways, including glycolysis and biosynthetic pathway, were remarkedly affected. Thus, our study identifies Lin28a as a crucial regulator of cardiac hypertrophy via its role in metabolic programming.

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Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

Project description:Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

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Seizure-induced LIN28A disrupts pattern separation via aberrant hippocampal neurogenesis

Project description:Prolonged seizures can disrupt stem cell behavior in the adult hippocampus, an important brain structure for spatial memory. Here, using a mouse model of pilocarpine-induced status epilepticus (SE), we characterized spatiotemporal expression of Lin28a mRNA and proteins after SE. Unlike Lin28a transcripts, induction of LIN28A protein after SE was detected mainly in the subgranular zone, where immunoreactivity was found in progenitors, neuroblasts, and immature and mature granule neurons. To investigate roles of LIN28A in epilepsy, we generated Nestin-Cre::Lin28aloxP/loxP (cKO) and Nestin-Cre::Lin28a+/+ (WT) mice to block LIN28A upregulation in all neuronal lineages after acute seizure. Adult-generated neuron- and hippocampus-associated cognitive impairments were absent in epileptic LIN28A cKO mice as evaluated by pattern separation and contextual fear conditioning tests, respectively, while sham-manipulated WT and cKO animals showed comparable memory function. Moreover, numbers of hilar PROX1-expressing ectopic granule cells (EGCs), together with PROX1/NEUN+ mature EGCs, were significantly reduced in epileptic cKO mice. Transcriptomic analysis and immunohistochemical validation at 3 d post-pilocarpine provided potential LIN28A downstream targets such as serotonin receptor 4. Collectively, our findings indicate that LIN28A is a novel target for regulation of newborn neuron-associated memory dysfunction in epilepsy by modulating seizure-induced aberrant neurogenesis.

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Expression of circular RNAs in human HT29, 293FT and HeLa cells

Project description:Deep sequencing datasets are used for circRNA expression analysis in human HT29, 293FT and HeLa cells.

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DNA methylation statuses of 293FT cells with TET depletion and NOC18 treatment

Project description:DNA methylation statuses of 293FT cells with TET depletion and NOC18 treatment

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Expression profiling in LIN28A, SET7/9, and TUT4 depleted H9 cells, or in the silent mutations (siR) of LIN28A and LIN28A-K135R overexpressed H9 cells

Project description:A developmentally regulated RNA binding protein, LIN28A and its homolog LIN28B may share a similar mechanism to regulate the processing of let-7 microRNAs (miRNAs) in embryonic stem cells (ESCs) or certain cancer cells, although their predominant localization is different in cells. However, little is known about the regulatory mechanism of LIN28A for miRNA processing in the nucleus. Here, we show that SET7/9, a known histone methyltransferase, associates with LIN28A in vivo and in vitro. SET7/9-mediated methylation significantly leads to the nuclear retention and protein stability of LIN28A, and remarkably regulated RNA binding ability of LIN28A to pri-let-7. Using RNAi knockdown approach, we find that the methylated nuclear form of LIN28A may function in the nucleoli by sequestering the primary let-7 miRNA to block their processing through a Tut4 (Zcchc11)-independent mechanism to regulate human ESC pluripotency. We propose a new insight toward the understanding of the molecular mechanism for post-translational methylation of nuclear LIN28A along modulating pluripotency by regulating pri-let-7 miRNAs in human ESCs.

2016-12-05 | GSE53038 | GEO

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