hepatitis b/tyrosine

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Treatment of chronic hepatitis B patients with tyrosine-methionine-aspartate-aspartate mutations.

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Lamivudine is an antiviral used for the treatment of chronic hepatitis B. Several studies have reported various mutations that are induced by lamivudine therapy. These mutations in the tyrosine-methionine-aspartate-aspartate (YMDD) motif are necessary and sufficient to confer high-level lamivudine

Hepatitis B Virus Reactivation during Treatment with Multi-Tyrosine Kinase Inhibitor for Hepatocellular Carcinoma.

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Hepatitis B virus (HBV) reactivation is well documented in individuals with cancer who receive certain cytotoxic or immunosuppressive therapies including rituximab treatment. As a general rule, the risk is greatest upon withdrawal of chemotherapy. The risk ranges from approximately 20 to 50% among

Hepatitis B surface antibody purification with hepatitis B surface antibody imprinted poly(hydroxyethyl methacrylate-N-methacryloyl-L-tyrosine methyl ester) particles.

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Hepatitis B surface antibody imprinted poly(hydroxyethyl methacrylate-N-methacryloyl-L-tyrosine methyl ester) particles were prepared for the purification of hepatitis B surface antibody from human plasma. N-methacryloyl-L-tyrosine methyl ester was chosen as a complexing agent for hepatitis B

Fatal submassive hepatic necrosis associated with tyrosine-methionine-aspartate-aspartate-motif mutation of hepatitis B virus after long-term lamivudine therapy.

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We present a case of infection with lamivudine-resistant mutant hepatitis B virus (HBV) that fatally exacerbated hepatitis following the emergence of HBV with mutations in the tyrosine-methionine-aspartate-aspartate (YMDD) motif in an immunocompetent patient who was receiving long-term lamivudine

Reverse transcription in hepatitis B viruses is primed by a tyrosine residue of the polymerase.

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All known DNA polymerases require primers for the initiation of DNA synthesis. While cellular polymerases and reverse transcriptases use free hydroxyl groups of RNA or DNA, the DNA polymerases of certain animal viruses and bacteriophages depend upon hydroxyl groups of amino acid residues within

Nonreceptor protein tyrosine phosphatases (NRPTPs) gene family associates with the risk of hepatocellular carcinoma in a Chinese hepatitis B virus-related subjects

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Nonreceptor protein tyrosine phosphatases (NRPTPs) are reported to be associated with several human cancers, but their roles in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remain unclear. Here, we integrated bioinformatics tools, population association analyses, and biological

[Expression of insulin receptor substrate-2 and its tyrosine phosphorylation in the hepatic tissue of chronic hepatitis B patients].

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OBJECTIVE To observe the expression of insulin receptor substrate-2 (IRS-2) mRNA and protein, and its tyrosine phosphorylation in hepatic tissue of chronic hepatitis B (CHB) patients, and to explore the role of IRS-2 on insulin resistance in CHB patients. METHODS Eighteen patients with CHB were

Through induction of juxtaposition and tyrosine kinase activity of Jak1, X-gene product of hepatitis B virus stimulates Ras and the transcriptional activation through AP-1, NF-kappaB, and SRE enhancers.

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Here, based on the recent finding of HBx (X-gene product of hepatitis B virus) as the inducer of Jak1, we investigated the mechanism for the HBx-mediated host cell regulation and found that (i) HBx associates specifically with Jak1 in vivo; (ii) HBx itself forms a dimer which leads to juxtaposition

Clinical Outcomes and Prognosis Factors of Nivolumab Plus Chemotherapy or Multitarget Tyrosine Kinase Inhibitor in Multi-Line Therapy for Recurrent Hepatitis B Virus-Related Hepatocellular Carcinoma: A Retrospective Analysis

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Background: This study investigates the potential predictors of nivolumab plus chemotherapy or multitarget tyrosine kinase inhibitor (TKI) treatment response in patients with recurrent hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Methods: Patients with recurrent

The adjuvant effect of stearyl tyrosine on a recombinant subunit hepatitis B surface antigen.

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We describe the enhancement of the antibody response against hepatitis B surface Ag by octadecyl L-tyrosine, a synthetic adjuvant designed to exert its adjuvant effect in a manner similar to that of alum because it binds soluble Ag and releases it slowly from the site of injection. Our data

Incidence of hepatitis B reactivation during epidermal growth factor receptor tyrosine kinase inhibitor treatment in non-small-cell lung cancer patients.

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Reactivation of hepatitis B virus (HBV) is a documented risk during cytotoxic chemotherapy in patients with lung cancer. Cases of HBV reactivation in non-small-cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment

Hepatitis B reactivation in chronic myeloid leukemia patients receiving tyrosine kinase inhibitor.

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Hepatitis B virus (HBV) reactivation is a well-recognized complication in patients with chronic HBV infection receiving cytotoxic or immunosuppressive chemotherapy. Imatinib mesylate and nilotinib are selective Bcr/Abl tyrosine kinase inhibitors, which are now widely used in the treatment of

Activation and inhibition of cellular calcium and tyrosine kinase signaling pathways identify targets of the HBx protein involved in hepatitis B virus replication.

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Human hepatitis B virus (HBV) HBx protein is a multifunctional protein that activates cellular signaling pathways and is thought to be essential for viral infection. Woodchuck HBV mutants that lack HBx are unable to replicate in vivo or are severely impaired. HBV replication in HepG2 cells, a human

Suppression of hepatitis B viral gene expression by protein-tyrosine phosphatase PTPN3.

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Protein-tyrosine phosphatase PTPN3 is a membrane-associated non-receptor protein-tyrosine phosphatase. PTPN3 contains a N-terminal FERM domain, a middle PDZ domain, and a C-terminal phosphatase domain. Upon co-expression of PTPN3, the level of human hepatitis B viral (HBV) RNAs, 3.5 kb, 2.4/2.1 kb,

Low risk of hepatitis B virus reactivation in patients with resolved infection and chronic myeloid leukemia treated with tyrosine kinase inhibitors.

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