About: Glucose-regulated protein 78 demonstrates antiviral effects but is more suitable for hepatocellular carcinoma prevention in hepatitis B

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

About: Glucose-regulated protein 78 demonstrates antiviral effects but is more suitable for hepatocellular carcinoma prevention in hepatitis B 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	Glucose-regulated protein 78 demonstrates antiviral effects but is more suitable for hepatocellular carcinoma prevention in hepatitis B
Creator	Xu, Hai Huang, Ming Peng, Xiao Zheng, Nai Zheng, Zi
Source	Medline; PMC
abstract	BACKGROUND: Hepatitis B virus (HBV) is the leading cause of liver cirrhosis and hepatocellular carcinoma in Asia and Africa. Existing antivirals cannot cure HBV or eliminate risk of hepatocellular carcinoma. Glucose-regulated protein 78 (GRP78) can inhibit HBV replication, but promote virion secretion and hepatocellular cancer cell invasion. For these reasons, the overall effect of GRP78 on HBV production and whether to utilize the HBV replication-inhibitory effect of GRP78 up-regulation or the hepatocellular cancer cell invasion-inhibitory effect of its down-regulation were further investigated in order to improve the efficacy of current antiviral therapy. METHODS: GRP78 regulations in HepG2.2.15 cells were conducted by transfections of expressing vector and small interfering RNA, respectively. The changes in HBV replication, hepatitis B e antigen (HBeAg) synthesis and hepatoma cell motility were monitored. RESULTS: GRP78 overall decreased HBV production due to its HBV replication-inhibitory effect time-dependently overwhelming virion secretion-promoting effect in HepG2.2.15 cells. Unlike the parental cells (HepG2), HepG2.2.15 cells demonstrated decreased expressions of the major genes in the interferon-β1-dependent pathway. Moreover, the expressions of these genes were not affected by GRP78 regulations. However, GRP78 was found to inhibit HBeAg secretion and to increase the retro-transportation of capsid assembly-interfering HBeAg precursor from the endoplasmic reticulum into the cytosol where new viral nucleocapsids formed. Furthermore, GRP78 overexpression promoted wound healing process (the motility) of HepG2.2.15 cells. In contrast, GRP78 knockdown enhanced HBV replication and HBeAg secretion, but they were abolished by entecavir and furin inhibitor, respectively. CONCLUSIONS: GRP78 mainly demonstrates anti-HBV effects, reducing HBV production and HBeAg secretion. With due regard to the hepatocellular cancer invasion risk of the overexpression and the rectifiability of the unpleasant effects of the knockdown, GRP78 down-regulation may be more suitable to serve as an additive strategy to cover the hepatocellular cancer prevention shortage of current antiviral therapy in the future.
has issue date	2017-04-13(xsd:dateTime)
bibo:doi	10.1186/s12985-017-0747-z
bibo:pmid	28407787
has license	cc-by
sha1sum (hex)	4fa344b02899cb75cb81db82d2cee5f624343c54
schema:url	https://doi.org/10.1186/s12985-017-0747-z
resource representing a document's title	Glucose-regulated protein 78 demonstrates antiviral effects but is more suitable for hepatocellular carcinoma prevention in hepatitis B
has PubMed Central identifier	PMC5390389
has PubMed identifier	28407787
schema:publication	Virol J
resource representing a document's body	covid:4fa344b02899cb75cb81db82d2cee5f624343c54#body_text
is schema:about of	named entity 'INVESTIGATED' named entity 'GLUCOSE-REGULATED PROTEIN 78' named entity 'REASONS' named entity 'CURE' named entity 'CURRENT' named entity 'EFFECTS' named entity 'GLUCOSE-REGULATED PROTEIN 78' named entity 'PREVENTION' named entity 'UP-REGULATION' named entity 'ORDER' named entity 'OVERALL' named entity 'GRP78' named entity 'ASIA' named entity 'HEPATOCELLULAR CARCINOMA' named entity 'BUT' named entity 'HEPATITIS B' named entity 'ANTIVIRAL' named entity 'DOWN-REGULATION' named entity 'EFFICACY' named entity 'CAUSE' named entity 'HEPATOCELLULAR CARCINOMA' named entity 'SECRETION' named entity 'HEPATOCELLULAR CANCER' named entity 'THESE' named entity 'ANTIVIRALS' named entity 'EFFECT' named entity 'AFRICA' named entity 'CELL INVASION' named entity 'VIRION' named entity 'BUT' named entity 'BACKGROUND' named entity 'PROMOTE' named entity 'PRODUCTION' named entity 'ITS' named entity 'OF LIVER CIRRHOSIS' named entity 'HEPATITIS B VIRUS' named entity 'INHIBITORY EFFECT' named entity 'RISK OF' named entity 'REPLICATION' named entity 'CANCER CELL' named entity 'HBV' named entity 'ANTIVIRAL THERAPY' named entity 'SUITABLE' named entity 'LEADING' covid:arg/4fa344b02899cb75cb81db82d2cee5f624343c54 named entity 'cell' named entity 'For' named entity 'Hepatitis B virus' named entity 'virion' named entity 'antiviral therapy' named entity 'HBV' named entity 'secretion' named entity 'down-regulation' named entity 'Asia' named entity 'GRP78' named entity 'Asia' named entity 'hepatocellular carcinoma' named entity 'Africa' named entity 'hepatitis' named entity 'hepatocellular carcinoma' named entity 'antiviral' named entity 'cell' named entity 'crystallization' named entity 'HCC' named entity 'GRP78' named entity 'virion' named entity 'HBeAg' named entity 'HBeAg' named entity 'polyvinylidene fluoride' named entity 'cytosolic' named entity 'signal sequence' named entity 'HBV' named entity 'HepG2' named entity 'stress conditions' named entity 'Southern blot' named entity 'Glucose-regulated protein' named entity 'digoxigenin'

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