Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function. - Wikidata - wikimedia - TriplyDB

Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function.

Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function.

http://www.wikidata.org/entity/Q37418293

about

Methyltransferase PRMT1 is a binding partner of HBx and a negative regulator of hepatitis B virus transcription X region mutations of hepatitis B virus related to clinical severity Engineering Hepadnaviruses as Reporter-Expressing Vectors: Recent Progress and Future Perspectives The Epigenetic Control of Hepatitis B Virus Modulates the Outcome of Infection Intricate Roles of Mammalian Sirtuins in Defense against Viral Pathogens Potential mechanisms of hepatitis B virus induced liver injury Hepatitis B virus, HBx mutants and their role in hepatocellular carcinoma Molecular mechanisms underlying occult hepatitis B virus infection.Recent advances in understanding and diagnosing hepatitis B virus infection Roles of hepatocyte nuclear factors in hepatitis B virus infection Molecular biology of hepatitis B virus infection Current and future antiviral drug therapies of hepatitis B chronic infection Hepatitis B virus molecular biology and pathogenesis Genome-wide identification of direct HBx genomic targets The Role of cccDNA in HBV Maintenance.Detection of HBV Covalently Closed Circular DNA Hepatitis B Virus Immunopathology, Model Systems, and Current Therapies Occult HBV infection: a faceless enemy in liver cancer development.Interleukin-34 inhibits hepatitis B virus replication in vitro and in vivo.Proteins ZNF198 and SUZ12 are down-regulated in hepatitis B virus (HBV) X protein-mediated hepatocyte transformation and in HBV replication Molecular characterization of occult hepatitis B virus infection in patients with end-stage liver disease in Colombia.Hepatocarcinogenesis associated with hepatitis B, delta and C viruses.Baseline value of intrahepatic HBV DNA over cccDNA predicts patient's response to interferon therapy MicroRNAs associated with HBV infection and HBV-related HCC.Persistence of hepatitis B virus covalently closed circular DNA in hepatocytes: molecular mechanisms and clinical significance.Transcription of hepatitis B virus covalently closed circular DNA is regulated by CpG methylation during chronic infection DDX3 DEAD-box RNA helicase is a host factor that restricts hepatitis B virus replication at the transcriptional level Comparative analysis of CpG islands among HBV genotypes.Sirtuins are evolutionarily conserved viral restriction factors.Targeting Hepatitis B Virus With CRISPR/Cas9.Regulation of gene expression in HBV- and HCV-related hepatocellular carcinoma: integrated GWRS and GWGS analyses Alpha-interferon suppresses hepadnavirus transcription by altering epigenetic modification of cccDNA minichromosomes Somatic mutations, viral integration and epigenetic modification in the evolution of hepatitis B virus-induced hepatocellular carcinoma The roles of hepatitis B virus-encoded X protein in virus replication and the pathogenesis of chronic liver disease.The role of unintegrated DNA in HIV infection Antiviral therapies and prospects for a cure of chronic hepatitis B.The Tudor domain protein Spindlin1 is involved in intrinsic antiviral defense against incoming hepatitis B Virus and herpes simplex virus type 1 Search for a cure for chronic hepatitis B infection: How close are we?IL6 Inhibits HBV Transcription by Targeting the Epigenetic Control of the Nuclear cccDNA Minichromosome.RPB5-Mediating Protein Suppresses Hepatitis B Virus (HBV) Transcription and Replication by Counteracting the Transcriptional Activation of Hepatitis B virus X Protein in HBV Replication Mouse Model

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P2860

Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function.

http://www.wikidata.org/entity/Q37418293

description

2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

@zh-hans

2009年学术文章

@zh-my

2009年学术文章

@zh-sg

2009年學術文章

@yue

2009年學術文章

@zh

2009年學術文章

@zh-hant

name

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@en

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@nl

type

label

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@en

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@nl

prefLabel

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@en

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function.

@nl

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PNAS.0908365106

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Nuclear HBx binds the HBV mini ...... regulation of cccDNA function

@en

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Francesca De Nicola

http://www.w3.org/2001/XMLSchema#string

Giovanni Raimondo

http://www.w3.org/2001/XMLSchema#string

Giuseppina Raffa

http://www.w3.org/2001/XMLSchema#string

Laura Belloni

http://www.w3.org/2001/XMLSchema#string

Maurizio Fanciulli

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P2860

The enigmatic X gene of hepatitis B virus

Hepatitis B virus X protein stimulates viral genome replication via a DDB1-dependent pathway distinct from that leading to cell death.

The transcriptional transactivation function of HBx protein is important for its augmentation role in hepatitis B virus replication

Mapping chromosomal proteins in vivo by formaldehyde-crosslinked-chromatin immunoprecipitation.

Genetics of hepatocellular carcinoma.

Hepatitis B virus and hepatocellular carcinoma.

Hepatitis B virus infection: epidemiology and vaccination.

Enhancement of hepatitis B virus replication by the regulatory X protein in vitro and in vivo

The covalently closed duplex form of the hepadnavirus genome exists in situ as a heterogeneous population of viral minichromosomes.

A novel method for efficient amplification of whole hepatitis B virus genomes permits rapid functional analysis and reveals deletion mutants in immunosuppressed patients

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47

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106

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Francesca Guerrieri

Teresa Pollicino

Massimo Levrero

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2009-11-11T00:00:00Z

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38083504

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19906987

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2775998

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