Hepatitis B Virus X gene in Hepatocellular Carcinoma: Difference between revisions

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==Hepatitis B Virus Protein x in Hepatocellular Carcinoma==
==Hepatitis B Virus Protein x in Hepatocellular Carcinoma==


Hepatocellular carcinoma (HCC) is among the most frequently diagnosed cancers worldwide. For over forty years physicians and researchers have observed an association between HBV infection and development of HCC. Of the seven HBV genes, hepatitis b virus x protein (HBx, 17.5 kDa) is the smallest and required extensive efforts to characterize; its elusiveness is represented by its designation “X.” The protein functions as a transcriptional transactivator of both viral and cellular transcripts, in addition inducing cytoplasmic signal transduction pathways [enigmatic]. Interestingly, HBx was a more potent inducer of transcription upon deletion of its N-terminal 1 to 50-amino-acid fragment, suggesting this domain may function as a negative regulatory element [enigmatic]. In vitro, HBx binds eukaryotic basal transcription factors essential for proper RNAP II-DNA interactions and promoter escape, including TATA-binding protein (TBP), TFIIB, TFIIH, and the RNAP subunit RPB5 [TATA paper, enigmatic]. HBx has been shown to suppress apoptosis of hepatocytes via induction of survivin, disruption of the tumor suppressor p53, and activation of c-jun N-terminal kinases [ .., …, activated ras concogene]. In infected cells, HBx induces overexpression of a cellular target, HBXIP, which functions as a regulator of centrosome dynamics and cytokinesis – critical aspects of mitosis. Furthermore, it was reported that HBx activates src and the ras/raf/ERK (extracellular signal-regulated kinase) pathway, which leads to proliferation of quiescent cells [activated ras oncogene].  
Hepatocellular carcinoma (HCC) is among the most frequently diagnosed cancers worldwide. For over forty years physicians and researchers have observed an association between HBV infection and development of HCC. Of the seven HBV genes, hepatitis b virus x protein (HBx, 17.5 kDa) is the smallest and required extensive efforts to characterize; its elusiveness is represented by its designation “X.” The protein functions as a transcriptional transactivator of both viral and cellular transcripts, in addition inducing cytoplasmic signal transduction pathways [enigmatic]. Interestingly, HBx was a more potent inducer of transcription upon deletion of its N-terminal 1 to 50-amino-acid fragment, suggesting this domain may function as a negative regulatory element [enigmatic]. In vitro, HBx binds eukaryotic basal transcription factors essential for proper RNAP II-DNA interactions and promoter escape, including TATA-binding protein (TBP), TFIIB, TFIIH, and the RNAP subunit RPB5 [TATA paper, enigmatic]. HBx has been shown to suppress apoptosis of hepatocytes via induction of survivin, disruption of the tumor suppressor p53, and activation of c-jun N-terminal kinases [ .., …, activated ras concogene]. In infected cells, HBx induces overexpression of a cellular target, HBXIP, which functions as a regulator of centrosome dynamics and cytokinesis – critical aspects of mitosis. Furthermore, it was reported that HBx activates src and the ras/raf/ERK (extracellular signal-regulated kinase) pathway, which leads to proliferation of quiescent cells [activated ras oncogene]. In recent years miRNA…
      In recent years miRNA…

Revision as of 21:56, 11 November 2012

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A Viral Biorealm page on the family Hepatitis B Virus X gene in Hepatocellular Carcinoma

miRNAs are short, endogenous RNA molecules of 19- to 24- nucleotides in length that are expressed widely in eukaryotes that [1]. The main function of a miRNA is to bind its complementary (target) mRNA sequence and inhibit translation, a process known as RNA silencing. Since plants, fungi, and animals have evolved RNA silencing as an innate antiviral mechanism, it is not surprising that an infecting virus can induce changes in cellular miRNA or synthesize viral miRNA the antiviral activities of its host [2]. A common goal of many hepatitis B virus (HBV) researchers is to identify the roles of host miRNAs in replication an pathogenesis of the virus. Furthermore, particular interactions between host miRNAs and HBV have been correlated with instance and _____ of hepatocellular carcinoma.


Figure 1. Transmission electron micrograph of Ebola virus. [1].





First subtopic

hep b infection, HCC

Hepatitis B Virus Protein x in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is among the most frequently diagnosed cancers worldwide. For over forty years physicians and researchers have observed an association between HBV infection and development of HCC. Of the seven HBV genes, hepatitis b virus x protein (HBx, 17.5 kDa) is the smallest and required extensive efforts to characterize; its elusiveness is represented by its designation “X.” The protein functions as a transcriptional transactivator of both viral and cellular transcripts, in addition inducing cytoplasmic signal transduction pathways [enigmatic]. Interestingly, HBx was a more potent inducer of transcription upon deletion of its N-terminal 1 to 50-amino-acid fragment, suggesting this domain may function as a negative regulatory element [enigmatic]. In vitro, HBx binds eukaryotic basal transcription factors essential for proper RNAP II-DNA interactions and promoter escape, including TATA-binding protein (TBP), TFIIB, TFIIH, and the RNAP subunit RPB5 [TATA paper, enigmatic]. HBx has been shown to suppress apoptosis of hepatocytes via induction of survivin, disruption of the tumor suppressor p53, and activation of c-jun N-terminal kinases [ .., …, activated ras concogene]. In infected cells, HBx induces overexpression of a cellular target, HBXIP, which functions as a regulator of centrosome dynamics and cytokinesis – critical aspects of mitosis. Furthermore, it was reported that HBx activates src and the ras/raf/ERK (extracellular signal-regulated kinase) pathway, which leads to proliferation of quiescent cells [activated ras oncogene]. In recent years miRNA…