Identification of host cellular proteins LAGE3 and IGFBP6 that interact with orf virus protein ORFV024

Long, Mingjian; Wang, Yuanyuan; Chen, Daxiang; Wang, Yong; Gong, Daozhi; He, Hongqing; Rock, Daniel L.; Hao, Wenbo; Luo, Shuhong

doi:10.1016/j.gene.2018.03.089

Cited by 7 publications

(3 citation statements)

References 23 publications

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“…NACA [ 32 ] and HAT1 [ 33 ] are potential host factors for Hepatitis B virus (HBV) replication. IGFBP6 can bind physically with the Orf virus (ORFV) ORFV024 protein, which can suppress the NF-kB signaling pathway and function as a critical regulator for early immune responses [ 34 ]. IL-11 is an anti-inflammatory factor, and its expression becomes elevated by virus infection and could be a potential target for novel antiviral development [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Rashid,

Coombs

2024

Viruses

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(1) Background: Influenza A Virus (IAV) uses host cellular proteins during replication in host cells. IAV infection causes elevated expression of chloride intracellular channel protein 1 (CLIC1) in lung epithelial cells, but the importance of this protein in IAV replication is unknown. (2) In this study, we determined the role of CLIC1 in IAV replication by investigating the effects of CLIC1 knockdown (KD) on IAV viral protein translation, genomic RNA transcription, and host cellular proteome dysregulation. (3) Results: CLIC1 KD in A549 human lung epithelial cells resulted in a significant decrease in progeny supernatant IAV, but virus protein expression was unaffected. However, a significantly larger number of viral RNAs accumulated in CLIC1 KD cells. Treatment with a CLIC1 inhibitor also caused a significant reduction in IAV replication, suggesting that CLIC1 is an important host factor in IAV replication. SomaScan®, which measures 1322 proteins, identified IAV-induced dysregulated proteins in wild-type cells and in CLIC1 KD cells. The expression of 116 and 150 proteins was significantly altered in wild-type and in CLIC1 KD cells, respectively. A large number of the dysregulated proteins in CLIC1 KD cells were associated with cellular transcription and predicted to be inhibited during IAV replication. (4) Conclusions: This study suggests that CLIC1 is involved in later stages of IAV replication. Further investigation should clarify mechanism(s) for the development of anti-IAV drugs targeting CLIC1 protein.

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Section: Discussionmentioning

confidence: 99%

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Rashid,

Coombs

2024

Viruses

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“…LAGE3 belongs to the NY-ESO gene family, a component of the EKC/KEOPS complex. This complex is required for the formation of a threonylcarbamoyl group on adenosine at position 37 (t6A37) in tRNAs that read codons beginning with adenine (55,56). Some researchers have reported that the EKC/KEOPS complex is linked with the protein synthesis machinery and cell growth (57).…”

Section: Discussionmentioning

confidence: 99%

Effect of eleutheroside B1 on non‑coding RNAs and protein profiles of influenza A virus‑infected A549 cells

et al. 2020

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Influenza viruses often pose a serious threat to animals and human health. In an attempt to explore the potential of herbal medicine as a treatment for influenza virus infection, eleutheroside B1, a coumarin compound extracted from herba sarcandrae, was identified, which exhibited antiviral and anti-inflammatory activities against influenza A virus. In this study, high-throughput RNA sequencing and isobaric tags for relative and absolute quantification (iTRAQ) assays were performed to determine alterations in the non-coding RNA (ncRNA) transcriptome and proteomics. Bioinformatics and target prediction analyses were used to decipher the potential roles of altered ncRNAs in the function of eleutheroside B1. Furthermore, long ncRNA (lncRNA) and mRNA co-expressing networks were constructed to analyze the biological functions by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The analysis of RNA sequencing data revealed that 5 differentially expressed ncRNAs were upregulated and 3 ncRNAs were downregulated in the A549 cells infected with A/PR8/34/H1N1, with or without eleutheroside B1 treatment (PR8+eleu and PR8, respectively). Nuclear paraspeckle assembly transcript 1 (NEAT1) was differentially expressed between the PR8 and A549 cell groups. GO and KEGG pathway analyses indicated that eleutheroside B1 took advantage of the host cell biological processes and molecular function for its antiviral and anti-inflammatory activities, as well as for regulating cytokine-cytokine receptor interaction in the immune system, consistent with previous findings. The results of the iTRAQ assays indicated that L antigen family member 3 (LAGE3) protein, essential for tRNA processing, tRNA metabolic processes and ncRNA processing, was downregulated in the PR8+eleu compared with the PR8 group. In the present study, these comprehensive, large-scale data analysis enhanced the understanding of multiple aspects of the transcriptome and proteomics that are involved in the antiviral and anti-inflammatory activities of eleutheroside B1. These findings demonstrate the potential of eleutheroside B1 for use in the prevention and treatment of influenza A virus-mediated infections.

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“…L antigen family member 3 (LAGE3), a 14,804-Da intracellular protein, is known as a component of the kinase, endopeptidase and other proteins of small size/endopeptidase-like and kinase associated to transcribed chromatin (KEOPS/EKC) complex ( 6 , 7 ). LAGE3 protein plays an important role in the regulation of RNA polymerase II-mediated positive transcription, translation as well as tRNA threonyl carbamoyl adenosine metabolic processes ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

Analysis of L Antigen Family Member 3 as a Potential Biomarker and Therapeutic Target Associated With the Progression of Hepatocellular Carcinoma

Chen

Xie

et al. 2022

Front. Oncol.

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BackgroundHepatocellular carcinoma (HCC) is the third cause of cancer-related deaths worldwide. L antigen family member 3 (LAGE3) is a prognostic biomarker and associated with progression in a variety of tumors. However, little has been reported about the role and potential mechanism of LAGE3 in HCC.MethodsThe clinical value and function of LAGE3 in HCC were obtained from multiple online databases. The potential functions and pathways of LAGE3 in HCC were analysed by R package of “clusterProfiler”. LAGE3 knockdown cells were constructed in HepG2, HuH7 and MHCC97H cell lines, respectively. The biological roles of LAGE3 were examined by in vitro and in vivo experiments.ResultsLAGE3 was upregulated in HCC tissues compared with normal tissues, and high expression of LAGE3 was significantly associated with several clinical characteristics and indicated a worse prognosis of HCC. The co-expressed genes of LAGE3 could be enriched in the mTOR signaling pathway in HCC. LAGE3 was upregulated in HCC cell lines. Functionally, knocking down LAGE3 expression not only increased apoptosis and inhibited growth rate, cell death mediated by T cells, colony formation, migration and invasion ability of HCC cell lines in vitro, but also reduced the progression of HCC in the subcutaneous xenotransplanted tumor model.ConclusionOur results suggested that LAGE3 served as an oncogenic factor of HCC and could be a potential biomarker and therapeutic target for HCC.

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Identification of host cellular proteins LAGE3 and IGFBP6 that interact with orf virus protein ORFV024

Cited by 7 publications

References 23 publications

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Effect of eleutheroside B1 on non‑coding RNAs and protein profiles of influenza A virus‑infected A549 cells

Analysis of L Antigen Family Member 3 as a Potential Biomarker and Therapeutic Target Associated With the Progression of Hepatocellular Carcinoma

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