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alpha mannosidase/هپاتیت

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مقالاتآزمایشات بالینیحق ثبت اختراع
صفحه 1 از جانب 20 نتایج

α-Mannosidase I Protein Expression in Peripheral Blood Mononuclear Cells Is Upregulated During Hepatitis B Virus Infection.

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Hepatitis B virus (HBV) has been reported to be recognized by dendritic cell-specific ICAM-3-grabbing nonintegrin in the presence of the α-mannosidase I inhibitor kifunensine, whereas native HBV is not. The aim of our study was to determine whether changes in α-mannosidase I expression in peripheral

Novel function of the endoplasmic reticulum degradation-enhancing α-mannosidase-like proteins in the human hepatitis B virus life cycle, mediated by the middle envelope protein.

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Cells replicating the human hepatitis B virus (HBV) express high levels of degradation-enhancing α-mannosidase-like proteins (EDEMs), a family of proteins involved in the endoplasmic reticulum associated degradation, one of the pathways activated during the unfolded protein response. Owing to their

Characterization of two differently glycosylated molecular species of yeast-derived hepatitis B vaccine carrying the pre-S2 region.

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Modified hepatitis B virus surface antigen M protein particles (HBsAg M-P31c) produced in yeast is mainly composed of two differently glycosylated proteins, GP37 and GP34. GP37 has an N-linked sugar chain and O-linked sugar chains; and GP34 has an N-linked sugar chain bound to the peptide backbone

No evidence of the unfolded protein response in patients with chronic hepatitis C virus infection.

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OBJECTIVE Hepatitis C virus (HCV) proteins activate the unfolded protein response (UPR) in experimental models. The role of the UPR in the pathogenesis of HCV-induced liver injury has not been determined. Our aim was to investigate the role of the UPR in the pathogenesis of chronic

Hepatitis B virus upregulates host expression of α-1,2-mannosidases via the PPARα pathway.

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OBJECTIVE To assess the effects of hepatitis B virus (HBV) on the expression of host α-1,2-mannosidases and determine the underlying mechanisms. METHODS We measured the expression levels of MAN1A1, MAN1A2, MAN1B1, and MAN1C1 in cell lines HepG2.2.15, HepN10, HepAD38 and HepG2 by Western blot. Viral

Identification and characterization of a 230-kDa Golgi-associated protein recognized by autoantibodies from a patient with HBV hepatitis.

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A serum from a patient with HBV hepatitis was found to contain autoantibodies reacting with various mammalian cells. Immunofluorescence staining of cultured cells with the autoantibodies revealed that the antigen was localized at perinuclear regions, where the Golgi markers alpha-mannosidase II and

Hepatitis C virus non-structural protein NS4B can modulate an unfolded protein response.

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Viral infection causes stress to the endoplasmic reticulum (ER). The response to endoplasmic reticulum stress, known as the unfolded protein response (UPR), is designed to eliminate misfolded proteins and allow the cell to recover. The role of hepatitis C virus (HCV) non-structural protein NS4B, a

MicroRNA-581 promotes hepatitis B virus surface antigen expression by targeting Dicer and EDEM1.

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Hepatitis B virus surface antigen (HBsAg) is an important risk factor for hepatocellular carcinoma (HCC) and is downregulated during hepatocarcinogenesis. MicroRNAs (miRNAs) are frequently deregulated in HCC tissues. However, whether the deregulation of certain miRNAs in HCC has an impact on HBsAg

Hepatitis C virus suppresses the IRE1-XBP1 pathway of the unfolded protein response.

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Hepatitis C virus (HCV) gene expression disrupts normal endoplasmic reticulum (ER) functions and induces ER stress. ER stress results from the accumulation of unfolded or misfolded proteins in the ER; cells can alleviate this stress by degrading or refolding these proteins. The IRE1-XBP1 pathway

Role of Dendritic Cell-Specific ICAM-3-Grabbing Nonintegrin on Dendritic Cells in the Recognition of Hepatitis B Virus.

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Dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) is an essential process for virus infection, such as HIV and hepatitis C, and plays a role in immune escape. However, the role of DC-SIGN in hepatitis B virus (HBV) infection is still unknown. The aim of this study was to investigate the

Age-related changes of glycosidases in human retinal pigment epithelium.

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This study was undertaken to determine whether there are age-related changes in the specific activities of several glycosidases in fresh retinal pigment epithelial cells (RPE) isolated from the posterior pole of human donor eyes. One hundred and twenty-one pairs of eyes from human donors, between

Branched oligosaccharide structures on HBV prevent interaction with both DC-SIGN and L-SIGN.

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Hepatitis B virus (HBV) is a DNA virus that infects the liver as primary target. Currently, a high affinity receptor for HBV is still unknown. The dendritic cell specific C-type lectin DC-SIGN is involved in pathogen recognition through mannose and fucose containing carbohydrates leading to the

[Value of serum glycosidase spectrum in the diagnosis of hepatocellular carcinoma].

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Activities of alpha-L-fucosidase (alpha-Fucase), N-acetyl-beta-D-glucosaminidase (beta-GlcNA-case), N-acetyl-beta-D-galactosaminidase (beta-GalNAcase) and alpha-mannosidase (alpha-Manase) in sera of normal adults, patients with hepatocellular carcinoma (HCC), benign liver diseases and non-liver

Whey Protein Concentrate WPC-80 Intensifies Glycoconjugate Catabolism and Induces Oxidative Stress in the Liver of Rats.

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The aim of this study was to evaluate the effect of whey protein concentrate (WPC-80) on glycoconjugate catabolism, selected markers of oxidative stress and liver inflammation. The experiment was conducted on male Wistar rats (n = 63). The animals from the study group were administered WPC-80 at a

Coronavirus interactions with the cellular autophagy machinery

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The COVID-19 pandemic, caused by the SARS-CoV-2 virus, is the most recent example of an emergent coronavirus that poses a significant threat to human health. Virus-host interactions play a major role in the viral life cycle and disease pathogenesis, and cellular pathways such as
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