Interaction between the human cytomegalovirus-encoded UL142 and cellular Snapin proteins

Liu, Chang; Ma, Yanping; He, Rong; Sun, Zhengrong; Huang, Yujing; Ji, Yaohua; Ruan, Qiang

doi:10.3892/mmr.2014.2829

Cited by 6 publications

(3 citation statements)

References 34 publications

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“…Functionally, this reduced both CD8 + T and NK cell activation. The effect of UL148 was greatest on NK cell activation in the context of antibody dependent cellular cytotoxicity (ADCC), which is consistent with reports that the CD2:CD58 pathway contributes significantly to this process ( 54 ). Perhaps even more significantly for the host, ADCC was detected against Merlin-infected cells regardless of a full complement of NK evasion genes.…”

Section: Introductionsupporting

confidence: 89%

HCMV-Encoded NK Modulators: Lessons From in vitro and in vivo Genetic Variation

et al. 2018

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Human cytomegalovirus (HCMV) is under constant selective pressure from the immune system in vivo. Study of HCMV genes that have been lost in the absence of, or genetically altered by, such selection can focus research toward findings of in vivo significance. We have been particularly interested in the most pronounced change in the highly passaged laboratory strains AD169 and Towne—the deletion of 13–15 kb of sequence (designated the UL/b′ region) that encodes up to 22 canonical genes, UL133-UL150. At least 5 genes have been identified in UL/b′ that inhibit NK cell function. UL135 suppresses formation of the immunological synapse (IS) by remodeling the actin cytoskeleton, thereby illustrating target cell cooperation in IS formation. UL141 inhibits expression of two activating ligands (CD155, CD112) for the activating receptor CD226 (DNAM-1), and two receptors (TRAIL-R1, R2) for the apoptosis-inducing TRAIL. UL142, ectopically expressed in isolation, and UL148A, target specific MICA allotypes that are ligands for NKG2D. UL148 impairs expression of CD58 (LFA-3), the co-stimulatory cell adhesion molecule for CD2 found on T and NK cells. Outside UL/b′, studies on natural variants have shown UL18 mutants change affinity for their inhibitory ligand LIR-1, while mutations in UL40's HLA-E binding peptide differentially drive NKG2C+ NK expansions. Research into HCMV genomic stability and its effect on NK function has provided important insights into virus:host interactions, but future studies will require consideration of genetic variability and the effect of genes expressed in the context of infection to fully understand their in vivo impact.

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Section: Introductionsupporting

confidence: 89%

HCMV-Encoded NK Modulators: Lessons From in vitro and in vivo Genetic Variation

et al. 2018

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“…Another study showed that snapin acts as a dynein motor adaptor and coordinates retrograde transport and late endosomal–lysosomal trafficking, thereby maintaining efficient autophagy–lysosomal function in neurons ( Cai and Sheng, 2011 ). It has been reported that the viral proteins pul130, ul70, ul105, and UL142 interact with the host protein snapin and affect viral DNA replication in human cytomegalovirus infection ( Shen et al, 2011 ; Luo et al, 2013 ; Liu et al, 2015 ; Wang et al, 2016 ). After infection in bees, DWV can cause abnormal neural activity and movement.…”

Section: Discussionmentioning

confidence: 99%

Interaction between the VP2 protein of deformed wing virus and host snapin protein and its effect on viral replication

Sun¹,

Li²,

Ma³

et al. 2023

Front. Microbiol.

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IntroductionDeformed wing virus (DWV) is one of the causative agents of colony collapse disorder. The structural protein of DWV plays a vital role in the process of viral invasion and host infection; however, there is limited research on DWV.Methods and ResultsIn this study, we screened the host protein snapin, which can interact with the VP2 protein of DWV, using the yeast two-hybrid system. Through computer simulation and GST pull-down and CO-IP assays, an interaction between snapin and VP2 was confirmed. Furthermore, immunofluorescence and co-localization experiments revealed that VP2 and snapin primarily co-localized in the cytoplasm. Consequently, RNAi was used to interfere with the expression of snapin in worker bees to examine the replication of DWV after the interference. After silencing of snapin, the replication of DWV in worker bees was significantly downregulated. Hence, we speculated that snapin was associated with DWV infection and involved in at least one stage of the viral life cycle. Finally, we used an online server to predict the interaction domains between VP2 and snapin, and the results indicate that the interaction domain of VP2 was approximately located at 56–90, 136–145, 184–190, and 239–242 aa and the snapin interaction domain was approximately located at 31–54 and 115–136 aa.ConclusionThis research confirmed that DWV VP2 protein could interacts with the snapin of host protein, which provides a theoretical basis for further investigation of its pathogenesis and development of targeted therapeutic drugs.

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“…Interacts with Snapin [408]; Downregulates ULBP3, protects cells from NK cytotoxicity [409] Immune evasion [406,407,409]…”

Section: Ul145mentioning

confidence: 99%

Insights into the Transcriptome of Human Cytomegalovirus: A Comprehensive Review

Zeng

Cao

Yang

et al. 2023

Viruses

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Human cytomegalovirus (HCMV) is a widespread pathogen that poses significant risks to immunocompromised individuals. Its genome spans over 230 kbp and potentially encodes over 200 open-reading frames. The HCMV transcriptome consists of various types of RNAs, including messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), with emerging insights into their biological functions. HCMV mRNAs are involved in crucial viral processes, such as viral replication, transcription, and translation regulation, as well as immune modulation and other effects on host cells. Additionally, four lncRNAs (RNA1.2, RNA2.7, RNA4.9, and RNA5.0) have been identified in HCMV, which play important roles in lytic replication like bypassing acute antiviral responses, promoting cell movement and viral spread, and maintaining HCMV latency. CircRNAs have gained attention for their important and diverse biological functions, including association with different diseases, acting as microRNA sponges, regulating parental gene expression, and serving as translation templates. Remarkably, HCMV encodes miRNAs which play critical roles in silencing human genes and other functions. This review gives an overview of human cytomegalovirus and current research on the HCMV transcriptome during lytic and latent infection.

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Interaction between the human cytomegalovirus-encoded UL142 and cellular Snapin proteins

Cited by 6 publications

References 34 publications

HCMV-Encoded NK Modulators: Lessons From in vitro and in vivo Genetic Variation

HCMV-Encoded NK Modulators: Lessons From in vitro and in vivo Genetic Variation

Interaction between the VP2 protein of deformed wing virus and host snapin protein and its effect on viral replication

Insights into the Transcriptome of Human Cytomegalovirus: A Comprehensive Review

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