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Страница 1 од 300 резултати
[Expressions of hepatitis B virus x protein and hypoxia-inducible factor-1alpha in hepatocellular carcinoma and their possible relationships].
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OBJECTIVE
To investigate the expressions of hepatitis B virus x protein (HBx) and hypoxia-inducible factor-1alpha (HIF-1alpha) in hepatocellular carcinoma (HCC) tissues and HepG2 cells under normoxic and hypoxic conditions.
METHODS
Immunohistochemistry was used to detect the expressions of HBx and
Hypoxia impairs anti-viral activity of natural killer (NK) cells but has little effect on anti-fibrotic NK cell functions in hepatitis C virus infection.
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OBJECTIVE
Natural killer (NK) cells have been shown to exert anti-viral as well as anti-fibrotic functions in hepatitis C virus (HCV) infection. Previous studies, however, analyzed NK cell functions exclusively under atmospheric oxygen conditions despite the fact that the liver microenvironment is
[Hepatitis B x protein activated vascular endothelial growth factor expression through hypoxia inducible factor-1 pathway].
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OBJECTIVE
To investigate whether hepatitis B x protein (HBx) stimulates vascular endothelial growth factor (VEGF) through hypoxia inducible factor-1 (HIF-1 alpha) pathway.
METHODS
Two plasmids including pIRES-EGFP-HBx and pTK-Hyg were co-transfected to a hepatocellular carcinoma cell line SMMC-7721.
Hepatitis B virus induces hypoxia-inducible factor-2α expression through hepatitis B virus X protein.
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A growing number of studies suggest that the hepatitis B virus X protein (HBx) enhances the protein stability of the hypoxia-inducible factor-1α (HIF-1α). However, the relationship between hepatitis B virus (HBV), HBx and hypoxia-inducible factor-2α (HIF-2α) has not yet been fully elucidated.
[Characteristics of functional and morphologic liver changes in toxic hepatitis with differing resistance to hypoxia].
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The functional and structural changes in the liver of white rats both low- and high-resistant to hypoxia, have been studied using the biochemical and morphological methods. It has been found that intensity and degree of the liver injury in experimental toxic hepatitis depend on the systemic
Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea.
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Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory
Role of hypoxia-inducible factor-alpha in hepatitis-B-virus X protein-mediated MDR1 activation.
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The transition from chemotherapy-responsive cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multi-drug resistance 1 (MDR1). We found that hepatitis-B-virus X protein (HBx) increases the transcriptional activity and protein level of MDR1 in a
Arterial flow focalization could increase tissue oxygen partial pressure, or trigger endothelial shear stress - a new concept to overcome cancer hypoxia-induced radiotherapy resistance, or stimulate liver regeneration during fulminant hepatitis.
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Malignant tumor hypoxia, which occurs due to abnormal and poor circulation of the tumoral vasculature, is the major cause of tumor aggressivity and failure of oncology therapeutics, particularly radiotherapy. Indeed, radio-sensitivity is reduced up to 3-fold in tumoral tissues with a lower oxygen
Human hepatitis B virus X protein is a possible mediator of hypoxia-induced angiogenesis in hepatocarcinogenesis.
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The hepatitis B virus (HBV)-encoded transcriptional activator HBV-X protein (HBx) was known to be involved in hepatocarcinogenesis. Hepatocarcinogenesis generally included an active angiogenesis that was mainly considered to be due to a local hypoxia in liver tissues. However, the exact mechanisms
Hidden secret in hepatitis B viral X protein mutation and hypoxia-inducible factor-1α in hepatocarcinoma cancer.
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Hepatitis B type virus (HBV) is an old hepato oncogenic and hepatitis agent. Hepatitis B viral X protein (HBx)-induced malignant transformation requires the excess amounts of ATP level, inducing the extremely oxygen-deprived condition in the cancer tissues and vessels. To adapt, cells go to shift
The expression of hypoxia-inducible factor-1alpha in hepatitis B virus-related hepatocellular carcinoma: correlation with patients' prognosis and hepatitis B virus X protein.
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Hypoxia inducible factor-1alpha (HIF-1alpha) was well correlated with carcinogenesis and tumor progression in many kinds of cancer. In this study, high expression of HIF-1alpha was found in 37 of the 72 (51.39%) tumor specimens, and significantly correlated with venous invasion and lymphonode
The carboxy-terminus of the hepatitis B virus X protein is necessary and sufficient for the activation of hypoxia-inducible factor-1alpha.
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Hepatitis B virus X protein (HBx) of the hepatitis B virus is strongly implicated in angiogenesis and metastasis during hepatocarcinogenesis. Previously, we reported that HBx enhances activity of hypoxia-inducible factor-1alpha (HIF-1alpha), a potent transactivator that induces angiogenic factors.
Hepatitis C virus core protein induces hypoxia-inducible factor 1α-mediated vascular endothelial growth factor expression in Huh7.5.1 cells.
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Hepatitis C virus (HCV) infection is one of the major causes of hepatocellular carcinoma (HCC). It has been demonstrated that the overexpression of angiogenic factors are associated with the maintenance of liver neoplasia. Hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor
Hepatitis C virus core protein upregulates the expression of vascular endothelial growth factor via the nuclear factor-κB/hypoxia-inducible factor-1α axis under hypoxic conditions.
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OBJECTIVE
Hepatitis C virus (HCV) core protein critically contributes to hepatocarcinogenesis, which is often observed in liver cirrhosis. Since the liver cirrhosis microenvironment is affected by hypoxia, we focused on the possible driving force of HCV core protein on signal relay from
Hypoxia-induced human deoxyribonuclease I is a cellular restriction factor of hepatitis B virus.
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Numerous human APOBEC3 cytidine deaminases have proven to be, inter alia, host cell restriction factors for retroviruses and hepadnaviruses. Although they can bind to genomic RNA and become encapsidated, they are only catalytically active on single-stranded DNA. As there are many cellular
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