N-Acetylneuraminic Acid Synthase (NANS)

Betenbaugh, Michael J.; Yin, Bojiao; Blake, Emily; Kristoffersen, Linda; Narang, Someet; Viswanathan, Karthik

doi:10.1007/978-4-431-54240-7_11

Cited by 1 publication

(1 citation statement)

References 45 publications

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“…More specifically, both aforementioned viruses downregulated the expression of NANP gene encoding N -acylneuraminate 9-phosphatase responsible for dephosphorylation of sialic acid 9-phosphate to free sialic acid [ 47 ]. RVC infection also led to downregulation of expression of gene encoding N -acetylneuraminic acid 9-phosphate synthase (Neu5Ac-9-P synthase) which catalyses the primary synthesis of the most common sialic acid, N -acetylneuraminic acid (Neu5Ac, NeuNAc, or NeuAc) and SLC35A1 – gene encoding SA transporter—a transmembrane protein moving SA produced in nucleus into the Golgi apparatus, where SA is used as a substrate for sialylation by sialyltransferases [ 48 , 49 ]. While no significant effect on this gene expression was observed in PIEs infected with G9P[13], infection with this virus led to downregulation of expression of NAGK-encoding gene whose product provides the conversion of GlcNAc to GlcNAc-6-phosphate [ 50 ].…”

Section: Resultsmentioning

confidence: 99%

Differential transcriptome response following infection of porcine ileal enteroids with species A and C rotaviruses

Raev,

Raque,

Kick

et al. 2023

Virol J

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Background Rotavirus C (RVC) is the major causative agent of acute gastroenteritis in suckling piglets, while most RVAs mostly affect weaned animals. Besides, while most RVA strains can be propagated in MA-104 and other continuous cell lines, attempts to isolate and culture RVC strains remain largely unsuccessful. The host factors associated with these unique RVC characteristics remain unknown. Methods In this study, we have comparatively evaluated transcriptome responses of porcine ileal enteroids infected with RVC G1P[1] and two RVA strains (G9P[13] and G5P[7]) with a focus on innate immunity and virus-host receptor interactions. Results The analysis of differentially expressed genes regulating antiviral immune response indicated that in contrast to RVA, RVC infection resulted in robust upregulation of expression of the genes encoding pattern recognition receptors including RIG1-like receptors and melanoma differentiation-associated gene-5. RVC infection was associated with a prominent upregulation of the most of glycosyltransferase-encoding genes except for the sialyltransferase-encoding genes which were downregulated similar to the effects observed for G9P[13]. Conclusions Our results provide novel data highlighting the unique aspects of the RVC-associated host cellular signalling and suggest that increased upregulation of the key antiviral factors maybe one of the mechanisms responsible for RVC age-specific characteristics and its inability to replicate in most cell cultures.

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