About: miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling
Creator	Qu, Liandong Li, Zhijie Tian, Jin Huang, Jiapei Yin, Hang Zhang, Jikai
topic	covid:37215fa618869df1820d22f28bace99ea9ceb1fc#this
Source	PMC
abstract	In response to viral infection, host cells activate various antiviral responses to inhibit virus replication. While feline herpesvirus 1 (FHV-1) manipulates the host early innate immune response in many different ways, the host could activate the antiviral response to counteract it through some unknown mechanisms. MicroRNAs (miRNAs) which serve as a class of regulatory factors in the host, participate in the regulation of the host innate immune response against virus infection. In this study, we found that the expression levels of miR-26a were significantly upregulated upon FHV-1 infection. Furthermore, FHV-1 infection induced the expression of miR-26a via a cGAS-dependent pathway, and knockdown of cellular cGAS significantly blocked the expression of miR-26a induced by poly (dA:dT) or FHV-1 infection. Next, we investigated the biological function of miR-26a during viral infection. miR-26a was able to increase the phosphorylation of STAT1 and promote type I IFN signaling, thus inhibiting viral replication. The mechanism study showed that miR-26a directly targeted host SOCS5. Knockdown of SOCS5 increased the phosphorylation of STAT1 and enhanced the type I IFN-mediated antiviral response, and overexpression of suppressor of the cytokine signalling 5 (SOCS5) decreased the phosphorylation of STAT1 and inhibited the type I IFN-mediated antiviral response. Meanwhile, with the knockdown of SOCS5, the upregulated expression of phosphorylated STAT1 and the anti-virus effect induced by miR-26a were significantly inhibited. Taken together, our data demonstrated a new strategy of host miRNAs against FHV-1 infection by enhancing IFN antiviral signaling.
has issue date	2019-12-18(xsd:dateTime)
bibo:doi	10.3390/v12010002
bibo:pmid	31861450
has license	cc-by
sha1sum (hex)	37215fa618869df1820d22f28bace99ea9ceb1fc
schema:url	https://doi.org/10.3390/v12010002
resource representing a document's title	miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling
has PubMed Central identifier	PMC7020096
has PubMed identifier	31861450
schema:publication	Viruses
resource representing a document's body	covid:37215fa618869df1820d22f28bace99ea9ceb1fc#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/37215fa618869df1820d22f28bace99ea9ceb1fc
is schema:about of	named entity 'VIRUS' named entity 'IFN' named entity 'PROMOTE' named entity 'INCREASED' named entity 'SUPPRESSOR' named entity 'CYTOKINE ' named entity 'MEDIATED' named entity 'SIGNALING' named entity 'MIR-26A' named entity 'LEVELS' named entity 'OVEREXPRESSION' named entity 'INDUCED' named entity 'PHOSPHORYLATION OF STAT1' named entity 'TARGETED' named entity 'UNKNOWN' named entity 'VARIOUS' named entity 'EXPRESSION' named entity 'CGAS' named entity 'INFECTION' named entity 'TO INCREASE' named entity 'MIRNAS' named entity 'FHV' named entity 'ENHANCING' named entity 'PROMOTING' named entity 'SOCS5' named entity 'MIR-26A' named entity 'VIRAL REPLICATION' named entity 'PHOSPHORYLATED' named entity 'DEMONSTRATED' named entity 'VIRAL INFECTION' named entity 'DEPENDENT' named entity 'HOST CELLS' named entity 'POLY' named entity 'ENHANCED' named entity 'RESPONSE TO' named entity 'BLOCKED' named entity 'A CLASS' named entity 'PATHWAY' named entity 'CELLULAR' named entity 'SIGNALLING' named entity 'DIRECTLY' named entity 'DIFFERENT' named entity 'NEW' named entity 'SOCS5' named entity 'ANTIVIRAL RESPONSE' covid:arg/37215fa618869df1820d22f28bace99ea9ceb1fc named entity 'FELINE HERPESVIRUS 1' named entity 'TYPE I INTERFERON' named entity 'RESPONSES' named entity 'ACTIVATE' named entity 'UPREGULATED' named entity 'DECREASED' named entity 'TYPE I' named entity 'MECHANISMS' named entity 'MECHANISM' named entity 'INHIBITED' named entity 'ANTIVIRAL' named entity 'BIOLOGICAL FUNCTION' named entity 'STUDY' named entity 'TO INHIBIT' named entity 'FOUND' named entity 'OUR' named entity 'REGULATORY' named entity 'HOST' named entity 'INNATE IMMUNE RESPONSE' named entity 'VIRUS REPLICATION' named entity 'REPLICATION' named entity 'INTERFERON SIGNALING' named entity 'TARGETING' named entity 'EFFECT' named entity 'INHIBITING' named entity 'REGULATION' named entity 'INVESTIGATED' named entity 'MICRORNAS'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software