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The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 [RNA-seq]

ABSTRACT: The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 [RNA-seq]

PROVIDER: PRJNA566376 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10145074_1.fastq.gz	Fastqsanger.gz
	SRR10145074_2.fastq.gz	Fastqsanger.gz
	SRR10145075_1.fastq.gz	Fastqsanger.gz
	SRR10145075_2.fastq.gz	Fastqsanger.gz
	SRR10145076_1.fastq.gz	Fastqsanger.gz

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The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1

Project description:The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1

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The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 (RNA-seq data set)

Project description:The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 (RNA-seq data set)

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Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal. 2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging. 3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases. 4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.

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The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1

Project description:High triglycerides can lead to atherosclerotic cardiovascular disease. Long noncoding RNAs (lncRNAs) are currently consider to have vital and wide range of biological functions, but the molecular mechanism underlying TG metabolism remains poorly understood. To identify novel lncRNAs differentially expressed in rat liver with hypertriglyceridemia using transcriptome sequencing and elucidated the function role in TG metabolism. In our study, we identified a novel lncRNA, Lnc19959.2, which was highly expression in rat liver with hypertriglyceridemia. Knockdown of lnc19959.2 has profound TG lowering effects in vitro and vivo. Subsequently genome-wide analysis identified that knockdown of Lnc19959.2 caused deregulation of many genes during TG homeostasis. Further mechanism studies reveal that Lnc19959.2 specifically bound to Purb to up-regulate expression of Apoa4, while bound to hnRNPA2B1 to down-regulate the expression of Cpt1a, Tm7sf2 and Gpam, respectively. In the upstream pathway, palmitate acid up-regulated CCAAT/Enhancer-Binding Protein Beta (Cebpb) facilitates its binding to promoter region of Lnc19959.2, which resulted in significant promotion of lnc19959.2 transcriptional activity. Our findings provide novel insights into transcriptional regulation of TG homeostasis by a novel lncRNA. This newly identified lncRNA could be exploited as novel therapeutic targets for hypertriglyceridemia.

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The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 [RNA-seq]

2020-06-08 | GSE137712 | GEO

The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 (RNA-seq data set)

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Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion. Wild type MDA-MB-231 cells were subjected to the HITS-CLIP procedure on immunoprecipitated HNRNPA2B1 associated RNA obtained from the nuclear fraction (Licatalosi D, et al. 2008, Nature 456:464-U22). For RNA-seq, nuclear RNA was extracted from MDA-MB-231 or Hela cells knocked down for METTL3 or HNRNPA2B1.

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Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

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DRAIC mediates hnRNPA2B1 stability and m6A-modified IGF1R instability to inhibit tumor progression [RNA-seq]

Project description:Both N6-methyladenosine (m6A) mediates RNA fates and ubiquitin mediates protein fates play an important role in either physiology or pathology including cancer, yet how long noncoding RNAs (lncRNAs) are involved in a link of molecular fate between m6A and ubiquitin remains unknown. Here, we reveal a role for a lncRNA Downregulated RNA in Cancer (DRAIC) to suppress tumor growth and metastasis in clear cell Renal Carcinoma (ccRCC). Mechanistically, DRAIC physically interacts with heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) and enhances its protein stability by blocking E3 ligase F-box protein 11 (FBXO11)-mediated ubiquitin and proteasome-dependent degradation. Subsequently, hnRNPA2B1 destabilizes m6A modified-type 1 insulin-like growth factor receptor (IGF1R) to lead to inhibition of ccRCC progression. Moreover, four m6A modification sites of IGF1R are identified and results in its mRNA degradation. Collectively, our findings reveal that DRAIC/hnRNPA2B1 axis regulates IGF1R mRNA expression in an m6A-dependent manner and highlights an important mechanism of IGF1R fate. These findings shed light on DRAIC/hnRNPA2B1/FBXO11/IGF1R axis as potential therapeutic targets in ccRCC and build a link of molecular fate between m6A-modified RNA and ubiquitin-modified protein.

2024-01-07 | GSE244891 | GEO

The RNA binding protein HNRNPA2B1 regulates RNA abundance and motor protein activity in neurites

Project description:RNA molecules are localized to subcellular regions through interactions between localization-regulatory cis-elements and trans-acting RNA binding proteins (RBPs). However, the identities of RNAs whose localization is regulated by a specific RBP as well as the impacts of that RNA localization on cell function have generally remained unknown. Here, we demonstrate that the RBP HNRNPA2B1 acts to keep specific RNAs out of neuronal projections. Using subcellular fractionation, high-throughput sequencing, and single molecule RNA FISH, we find that hundreds of RNAs demonstrate markedly increased abundance in neurites in HNRNPA2B1 knockout cells. These RNAs often encode motor proteins and are enriched for known HNRNPA2B1 binding sites and motifs in their 3′ UTRs. The speed and processivity of microtubule-based transport is impaired in these cells, specifically in their neurites. HNRNPA2B1 point mutations that increase its cytoplasmic abundance relative to wildtype lead to stronger suppression of both RNA mislocalization and transport defects than seen with wildtype HNRNPA2B1. We further find that the subcellular localizations of HNRNPA2B1 target RNAs are sensitive to perturbations of RNA decay machinery, suggesting that it is HNRNPA2B1’s known role in regulating RNA stability that may explain these observations. These findings establish HNRNPA2B1 as a negative regulator of neurite RNA abundance and link the subcellular activities of motor proteins with the subcellular abundance of the RNAs that encode them.

2024-08-20 | GSE275212 | GEO

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