2021
DOI: 10.1007/s00705-020-04950-7
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C1QBP inhibits proliferation of porcine circovirus type 2 by restricting nuclear import of the capsid protein

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Cited by 5 publications
(5 citation statements)
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“…ON180781) propagated in PAMs were used in this study. The virus titer in PAMs was assessed through an indirect fluorescent antibody assay (IFA) conducted as previously described ( Ma et al, 2021 ), with PRRSV-N mAb (monoclonal antibody, gifted by Professor Shuqi Xiao from NWAFU) and Goat Anti-Mouse IgG H&L (Alexa Fluor® 488) (Abcam, Cambridge, United Kingdom) as primary and secondary antibody, respectively. The 50% tissue culture infective dose (TCID50) was calculated using the Reed-Muench method.…”
Section: Methodsmentioning
confidence: 99%
“…ON180781) propagated in PAMs were used in this study. The virus titer in PAMs was assessed through an indirect fluorescent antibody assay (IFA) conducted as previously described ( Ma et al, 2021 ), with PRRSV-N mAb (monoclonal antibody, gifted by Professor Shuqi Xiao from NWAFU) and Goat Anti-Mouse IgG H&L (Alexa Fluor® 488) (Abcam, Cambridge, United Kingdom) as primary and secondary antibody, respectively. The 50% tissue culture infective dose (TCID50) was calculated using the Reed-Muench method.…”
Section: Methodsmentioning
confidence: 99%
“…Further studies showed that the arginine-rich N-terminal NLS motif of PCV Cap could directly interact with the serine-48 residue at the N-terminal oligomerization domain of NPM1 [ 59 , 60 , 72 , 73 ]. Moreover, the C1QBP is a crucial mitochondrial matrix protein located on the cell surface, nucleus, and cytoplasm [ 74 , 75 , 76 ]. Therefore, C1QBP can interact with the NLS of viral Cap, thus inhibiting PCV proliferation by restricting the nuclear import [ 74 , 76 ].…”
Section: Crosstalk Between Pcv and Hostmentioning
confidence: 99%
“…Moreover, the C1QBP is a crucial mitochondrial matrix protein located on the cell surface, nucleus, and cytoplasm [ 74 , 75 , 76 ]. Therefore, C1QBP can interact with the NLS of viral Cap, thus inhibiting PCV proliferation by restricting the nuclear import [ 74 , 76 ]. C1QBP was downregulated at the early stage of PCV infection [ 74 , 76 ].…”
Section: Crosstalk Between Pcv and Hostmentioning
confidence: 99%
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“…Notably, PCV2 infection promoted IFN-β production via activating the cGAS/STING signaling, while IFN-α, IFN-β, IFN-γ, concanavalin A (ConA), and IL-2 can enhance PCV2 replication [3][4][5][6][7][8][9][10][11]. On the other hand, intracellular host restriction factors, such as 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), complement component 1Q subcomponent-binding protein (C1QBP), and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein (14-3-3β/α, YWHAB), play important roles in resisting virus infection [1,2,[12][13][14]. Among the intracellular host factors, tripartite motif proteins (TRIMs) are a kind of newly discovered host protein involved in various cellular functions, including cell cycles, immunity, carcinogenesis, apoptosis, as well as virus infection [15][16][17].…”
Section: Introductionmentioning
confidence: 99%