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NF-kB essential modulator (NEMO) is essential for KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13- induced gene expression and its N-terminal 251 resdidues are sufficent for this process

ABSTRACT: We report here that KSHV viral infection targets the NF-kB pathway which is crucial for cell survival. KSHV protein vFLIP K13 is known to directly interact with cellular protein NEMO of the NF-kB pathway. We used gene expression array to suggets that the interaction of K13 with NEMO is important to activate NF-kB pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49245 | GEO | 2014/03/27

SECONDARY ACCESSION(S): PRJNA213382

REPOSITORIES: GEO

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NF-kB essential modulator (NEMO) is essential for KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13- induced gene expression and its N-terminal 251 resdidues are sufficent for this process

Project description:We report here that KSHV viral infection targets the NF-kB pathway which is crucial for cell survival. KSHV protein vFLIP K13 is known to directly interact with cellular protein NEMO of the NF-kB pathway. We used gene expression array to suggets that the interaction of K13 with NEMO is important to activate NF-kB pathway. We employed gene array analysis followed by bioinformatics analyses as well as biological pathways to determine the effect of K13 interaction with Nemo in Jurkat cell line system. Total RNA was isolated isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the Affymetrix Human Genome U133A 2.0 Array.

2014-03-27 | E-GEOD-49245 | biostudies-arrayexpress

A Computational Profiling of Changes in Gene Expression and Transcription Factors Induced by vFLIP K13 in Primary Effusion Lymphoma

Project description:Infection of Kaposi's sarcoma associated herpes virus (KSHV) has been linked to the development of primary effusion lymphoma (PEL), which is characterized by the loss of expression of B cell markers and effusions in the body cavities. This unique clinical feature of PEL has been attributed to their distinctive gene expression profile which shows overexpression of genes in various signaling pathways. KSHV-encoded latent protein vFLIP K13 has been shown to promote the survival and proliferation of PEL cells. In this study, we have employed gene array analysis followed by bioinformatics analysis of coordinated transcriptional factors network as well as biological pathways to characterize the effect of K13 on PEL-derived BCBL1 cells. We observed that genes associated with Cytokine signaling, Cell death, NF-kappaB and Cell adhesion pathways were differentially regulated by K13. We used computational approach complemented with microarrays to detail the global gene expression and identified distinct classes of differentially regulated genes in various cellular processes. We employed gene array analysis followed by bioinformatics analyses of coordinated transcriptional factors network as well as biological pathways to characterize the effect of K13 on in PEL-derived BCBL1 cells.

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A Computational Profiling of Changes in Gene Expression and Transcription Factors Induced by vFLIP K13 in Primary Effusion Lymphoma

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Transcription profiling of human HUVEC ells ectotopically expressing K13

Project description:Integrated microarray and multiplex cytokine analyses of Kaposi's Sarcoma Asssociated Herpesvirus viral FLICE Inhibitory Protein K13 affected genes and cytokines in human blood vascular endothelial cells. The KSHV-encoded K13 protein is one of the few proteins to be expressed in latently-infected spindle cells and the ectopic expression of K13 in human vascular endothelial cells is sufficient to transform them into spindle cells. Experiment Overall Design: We have examined the effect of ectopic K13 expression on global gene expression in human umbilical vein endothelial cells (HUVEC).

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Transcription profiling of human umbilical vein endothelial cells after transfection with the anti-apoptotic protein vFLIP/K13 of human herpesvirus type-8 (HHV-8)

Project description:Modulation of the transcriptome of human umbilical vein endothelial cells (HUVEC) by the anti-apoptotic protein vFLIP/K13 of human herpesvirus type-8 (HHV-8)

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Project description:Whole-transcriptome sequencing (RNA sequencing [RNA-seq]) was performed in the viral producer cell lines iSLK-RGB BAC16,iSLK-RGB-K9 mutant and iSLK-RGB-K13 mutant cells to uncover the global landscape of long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), mRNAs and microRNAs (miRNAs) in KSHV replication mediated by vIRF1 or vFLIP.

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Homo sapiens

Project description:NF-kB essential modulator (NEMO) is essential for KSHV-encoded viral FLICE inhibitory protein (vFLIP) K13- induced gene expression and its N-terminal 251 resdidues are sufficent for this process

| PRJNA213382 | ENA

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Project description:Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO.

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Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix)

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