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Formaldehyde-fixed RNA-Immunoprecipitation (fRIP for heterogenous ribonucleoprotein K (hnRNP K)

ABSTRACT: Formaldehyde-fixed RNA-Immunoprecipitation (fRIP for heterogenous ribonucleoprotein K (hnRNP K)

PROVIDER: PRJNA522053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8569440.fastq.gz	Fastqsanger.gz
	SRR8569441.fastq.gz	Fastqsanger.gz
	SRR8569436.fastq.gz	Fastqsanger.gz
	SRR8569437.fastq.gz	Fastqsanger.gz
	SRR8569438.fastq.gz	Fastqsanger.gz

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Formaldehyde-fixed RNA-Immunoprecipitation (fRIP for heterogenous ribonucleoprotein K (hnRNP K)

Project description:fRIP experiments were performed in OCI-AML3 cells to identify transcripts that bind to hnRNP K.

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Heterogenous nuclear ribonucleoprotein D-like controls endothelial cell functions

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LCDR maintains the integrity of lysosomal membrane by hnRNP K-stabilized LAPTM5 transcript and promotes cell survival

Project description:Lysosome plays important roles in cellular homeostasis and its dysregulation is associated with cancer. However, the regulation and underlying mechanism of lysosome in cancer survival remain incompletely understood. Here, we reveal a role for a histone acetylation-regulated long non-coding RNA termed as lysosome cell death regulator (LCDR) in lung cancer cell survival, knockdown of which promotes apoptosis. Mechanistically, LCDR binds to heterogenous nuclear ribonucleoprotein K (hnRNP K) to regulate the stability of lysosomal-associated protein transmembrane 5 (LAPTM5) transcript that maintain integrity of lysosomal membrane. Consequently, knockdown of LCDR, hnRNP K or LAPTM5 promotes lysosomal membrane permeabilization and lysosomal cell death-mediated apoptosis. LAPTM5 overexpression or cathepsin B inhibitor partially restores the effects of this axis on lysosomal cell death. Clinically, LCDR/hnRNP K/LAPTM5 are upregulated in lung cancer tissues and coexpression of this axis shows the increased diagnostic value for lung cancer. These findings shed light on LCDR/hnRNP K/LAPTM5 as potential therapeutic targets and targeting lysosome is a promising strategy in cancer treatment.

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Expression signatures of human HeLa cells with RNAi targetting A1 hnRNP, FUS, H hnRNP and p68-DDX5

Project description:Transcription profiling of human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs cloned into the pSuper expression vector compared to emprty vector negative controls for transfection. Four different RNA interference treatments targetted: A1 hnRNP (HNRNPA1, Heterogeneous nuclear ribonucleoprotein A1); FUS (fusion gene, involved in t(12;16) in malignant liposarcoma); H hnRNP (HNRNPH1); and p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5). Keywords: genetic modification

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Muscle Developmental Defects in Heterogeneous Nuclear Ribonucleoprotein A1 Knockout Mice

Project description:Transcriptome analysis of total RNA samples from heart tissue of knockout mice Alternative splicing is the main mechanism to increase protein diversity from an mRNA. Heterogeneous ribonucleoprotein (hnRNP) family members are vital regulators of alternative splicing. The hnRNP A1 is the most well-known protein in this family, but its role in embryonic development is not well understood. We generated hnRNP A1 knockout mice to study the function of hnRNP A1 in vivo. The hnRNP A1-depleted mice showed embryonic lethality because of muscle developmental defects. In a previous study, cellular hnRNP A2/B1 was reported to be capable of compensating for the expression of hnRNP A1. However, this phenomenon did not occur in the hnRNP A1 heterozygous mice in vivo. We demonstrated that hnRNP A1 regulated muscle-related genes expression and alternative splicing. In summary, our data demonstrated that hnRNP A1 plays a critical role in embryonic muscle development. Understanding the effects of hnRNP A1 in vivo may help to define the function of hnRNP A1 in alternative splicing.

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Aurora B phosphorylates hnRNP U/SAF-A to facilitate XIST RNA removal from the inactive X chromosome during mitosis

Project description:We show that Aurora-B phosphorylates heterogeneous nuclear ribonucleoprotein U (hnRNP U) in the SAP domain to dissociate hnRNP U from chromatin during mitosis. We use RNA-seq to show that hnRNP U associates with hundreds of mRNAs and lncRNAs during interphase and mitosis.

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Analysis of RNA quantitation in formaldehyde-fixed cells

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40S hnRNP particles are a novel class of nuclear biomolecular condensates

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2022-05-30 | PXD031677 | Pride

Metastasis-repressive CircRNA MASCOT Regulates Distribution of the Splicing Factor hnRNP M

Project description:Alternative splicing (AS) diversifies the transcriptome complexity and is usually hijacked by cancer cells. Here, we identified heterogeneous nuclear ribonucleoprotein M (hnRNP M) as an indispensable contributor to EMT-related AS reprogramming, whose sub-nuclear distribution of hnRNP M is altered in metastatic tumors. Upon TGFβ stimulation, hnRNP M trends to disassociate with a circRNA called MASCOT (hnRNP M-ASsociated Circular RNA Of TGFβ) that demonstrated an impressive inhibitory effect on EMT process and tumor metastasis. Mechanistically, the anti-metastatic effect of MASCOT is attributed to not only its competition with U2 RNA splicing factors to recruit hnRNP M in the nucleoplasm, but also the anchorage of hnRNP M with nucleolin into the nucleolus to cause a temporospatial separation of hnRNP M from spliceosome. Moreover, the correlation between MASCOT expression and hnRNP M sub-nuclear localization was validated in clinical specimens. Our study deciphers the regulatory codes controlling AS networks and highlights MASCOT as a promising therapeutic to treat metastasis.

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