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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RNA-seq]

ABSTRACT: RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RNA-seq]

PROVIDER: PRJNA878526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21491683_1.fastq.gz	Fastqsanger.gz
	SRR21491683_2.fastq.gz	Fastqsanger.gz
	SRR21491684_1.fastq.gz	Fastqsanger.gz
	SRR21491684_2.fastq.gz	Fastqsanger.gz
	SRR21491685_1.fastq.gz	Fastqsanger.gz

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma

Project description:RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RIP-seq]

Project description:RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RIP-seq]

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RIP-seq]

Project description:In order to clarify the post-transcriptional regulatory network of RPS27 in KS. We constructed a transcriptomic binding network using iRIP-seq. The KS lesions of the other two patients were used for separately.

2023-10-20 | GSE212960 | GEO

RNA-binding protein RPS27 and gene expression regulation in human umbilical vein endothelial cells (HUVECs)

Project description:RPS27, a significantly down-regulated and validated RBP in kaposi's sarcoma (KS), and known to be associated with viral infection. As KS is an endothelial cell cancer, we used HUVECs as the cell model to explore the functions of RPS27. RNA-seq technology was used to investigate the differentially expressed genes in HUVECs. By using small interference RNAs (siRNAs) to silence the expression of RPS27 (siRPS27), we detected significant decrease of RPS27 expression in RNA levels comparing with the negative control (siNC) samples.

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RNA-seq]

Project description:RNA-seq technology was used to investigate the differentially expressed genes and regulated alternative splicing events in Kaposi's sarcoma lesions and adjacent non-tumor tissues. We then performed gene expression profiling analysis using data obtained from RNA-seq.

2023-10-20 | GSE212961 | GEO

RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-20 | GSE212962 | GEO

RNA-seq of two Kaposi’s sarcoma tissue samples and the corresponding two normal tissue samples

Project description:We have reported that KSHV infection reprograms oral mesenchymal stem cells (MSCs) and transforms them to Kaposi sarcoma-like cells through mesenchymal-to-endothelial transition. To explore the mechanism of KSHV infection of MSCs, we compared the gene expression profiles of Kaposi’s sarcoma tissue and KSHV non-susceptible cells to explore potential host factors that contribute to KSHV infection.

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Kaposi’s Sarcoma-associated Herpesvirus Viral Protein Kinase Augments Cell Survival

Project description:Kaposi’s Sarcoma-associated Herpesvirus Viral Protein Kinase Augments Cell Survival

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Subfunctionalized expression drives evolutionary retention of ribosomal protein paralogs Rps27 and Rps27l in vertebrates

Project description:The formation of paralogs through gene duplication is a core evolutionary process. For paralogs that encode components of protein complexes such as the ribosome, a central question is whether they encode functionally distinct proteins, or whether they exist to maintain appropriate total expression of equivalent proteins. Here, we systematically tested evolutionary models of paralog function using the ribosomal protein paralogs Rps27 (eS27) and Rps27l (eS27L) as a case study. Evolutionary analysis suggests that Rps27 and Rps27l likely arose during whole-genome duplication(s) in a common vertebrate ancestor. We show that Rps27 and Rps27l have inversely correlated mRNA abundance across mouse cell types, with the highest Rps27 in lymphocytes and the highest Rps27l in mammary alveolar cells and hepatocytes. By endogenously tagging the Rps27 and Rps27l proteins, we demonstrate that Rps27- and Rps27l-ribosomes associate preferentially with different transcripts. Furthermore, murine Rps27 and Rps27l loss-of-function alleles are homozygous lethal at different developmental stages. However, strikingly, expressing Rps27 protein from the endogenous Rps27l locus or vice versa completely rescues loss-of-function lethality and yields mice with no detectable deficits. Together, these findings suggest that Rps27 and Rps27l are evolutionarily retained because their subfunctionalized expression patterns render both genes necessary to achieve the requisite total expression of two equivalent proteins across cell types. Our work represents the most in-depth characterization of a mammalian ribosomal protein paralog to date and highlights the importance of considering both protein function and expression when investigating paralogs.

2023-06-21 | GSE201845 | GEO

KSHV-induced iNOS in Kaposi’s Sarcoma tumors and mouse model

Project description:Kaposi’s Sarcoma (KS) is a heterogenous, multifocal vascular malignancy caused by the human herpesvirus 8 (HHV8), also known as Kaposi’s Sarcoma-Associated Herpesvirus (KSHV). Here, we show that KS lesions express iNOS/NOS2 broadly throughout KS lesions, with enrichment in LANA positive spindle cells. The iNOS byproduct 3-nitrotyrosine is also enriched in LANA positive tumor cells and colocalizes with a fraction of LANA-nuclear bodies. We show that iNOS is highly expressed in the L1T3 tumor model of KS. iNOS expression correlated with KSHV lytic cycle gene expression, which was elevated in late-stage tumors (>4 weeks) but to a lesser degree in early stage (1 week) xenografts. Further, we show that L1T3 tumor growth is sensitive to an inhibitor of nitric oxide, L-NMMA. These finding suggest that iNOS is expressed in KSHV infected endothelial-transformed tumor cells in KS, that iNOS expression depends on tumor microenvironment stress conditions, and that iNOS enzymatic activity contributes to KS tumor growth.

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