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An overlapped natural antisense lncRNA FCER1A-AS controls anaphylactic reaction by promoting FcεRIα expression

ABSTRACT: An overlapped natural antisense lncRNA FCER1A-AS controls anaphylactic reaction by promoting FcεRIα expression

PROVIDER: PRJNA820637 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18502311_1.fastq.gz	Fastqsanger.gz
	SRR18502311_2.fastq.gz	Fastqsanger.gz
	SRR18502312_1.fastq.gz	Fastqsanger.gz
	SRR18502312_2.fastq.gz	Fastqsanger.gz

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An overlapped natural antisense lncRNA FCER1A-AS controls anaphylactic reaction by promoting FcεRIα expression

Project description:Functioned as α-subunit of the high-affinity immunoglobulin E receptor (FcεRIα), FcεRIα plays a central role in the pathogenesis of Ig-E-mediated allergy and other IgE-related disorders. FcεRIα is normally expressed only in limited spectrum of cells like basophils and mast cells, but the mechanism of controlling FcεRIα expression in these cells is less well understood. In this study, we found fully overlapped natural antisense transcript (NATs) of FcεRIα (FCER1A-AS) is co-expressed with cognate sense transcript (FCER1A-S) in IL-3 induced FcεRIα-expressing cells or in high FcεRIα-expressing cell line MC/9. When FCER1A-AS is selectively knocked down by CRISPR/RfxCas13d (CasRx) approach in MC/9, expression of mRNA and proteins of FCER1A-S is also markedly decreased. Furthermore, deficiency of FCER1A-AS along with lack of FCER1A-S expression is found in two different lines of gene-targeted mice in which FCER1A locus is disturbed at different sites. More importantly, the FCER1A-AS-deficient homozygous mice display similarly diminished anaphylactic reaction as FCER1A gene knockout mice. Thus, we uncovered in this investigation that the expression of FCER1A-S is positively regulated by co-expressed fully overlapped antisense transcript.

2022-10-02 | GSE199532 | GEO

Intronic natural antisense transcripts in glioma patient biopsies

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lncRNA TINCR antisense pulldown of interacting RNAs

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lncRNA TINCR antisense pulldown of interacting RNAs

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Oncogenic Antisense LncRNA P14AS Regulates Expression of ANRIL through AUF1 Binding

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A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability.

Project description:The human genome encodes thousands of long noncoding RNA (lncRNA) genes; the function of majority of them is poorly understood. Aberrant expression of a significant number of lncRNAs is observed in various diseases, including cancer. To gain insights into the role of lncRNAs in breast cancer progression, we performed genome-wide transcriptome analyses in an isogenic, triple negative breast cancer (TNBC/basal-like) progression cell lines using a 3D cell culture model. We identified significantly altered expression of 1853 lncRNAs, including ~500 natural antisense transcript (NATs) lncRNAs. A significant number of breast cancer-deregulated NATs displayed co-regulated expression with oncogenic and tumor suppressor protein-coding genes in cis. Further studies on one such NAT, PDCD4-AS1 lncRNA reveal that it positively regulates the expression and activity of the tumor suppressor PDCD4 in mammary epithelial cells. Both PDCD4-AS1 and PDCD4 show reduced expression in TNBC cell lines and in patients, and depletion of PDCD4-AS1 compromised the cellular levels and activity of PDCD4. Further, tumorigenic properties of PDCD4-AS1-depleted TNBC cells were rescued by exogenous expression of PDCD4, implying that PDCD4-AS1 acts upstream of PDCD4. Mechanistically, PDCD4-AS1 stabilizes PDCD4 RNA by forming RNA duplex and controls the interaction between PDCD4 RNA and RNA decay promoting factors such as HuR. Our studies demonstrate crucial roles played by NAT lncRNAs in regulating post-transcriptional gene expression of key oncogenic or tumor suppressor genes, thereby contributing to TNBC progression.

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Endothelial protein interaction partners of the lncRNA PCAT19

Project description:PCAT19 is an endothelial-enriched lncRNA that contributes to the proliferation-quiescence switch in a cell density-dependent manner. Here we performed an antisense-oligonucleotide pulldown of the PCAT19 lncRNA followed by mass spectrometry to identify protein interaction partners of PCAT19. Interaction partners were further analysed for their potential role with PCAT19.

2022-09-29 | PXD032669 | Pride

Antisense lncRNA transcription mediates DNA demethylation to drive stochastic Protocadherin α promoter choice

Project description:Stochastic activation of clustered Protocadherin (Pcdh) α, β, and γ genes generates a cell-surface identity code in individual neurons that functions in neural circuit assembly. Here, we show that Pcdhα gene choice involves the activation of an antisense promoter located in the first exon of each Pcdhα alternate gene. Transcription of an antisense long noncoding RNA (lncRNA) from this antisense promoter extends through the sense promoter, leading to DNA demethylation of the CTCF binding sites proximal to each promoter. Demethylation-dependent CTCF binding to both promoters facilitates cohesin-mediated DNA looping with a distal enhancer (HS5-1), locking in the transcriptional state of the chosen Pcdhα gene. Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. Thus, antisense transcription-mediated promoter demethylation functions as a mechanism for distance-independent enhancer/promoter DNA looping to ensure stochastic Pcdhα promoter choice.

2019-04-15 | GSE115862 | GEO

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