Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus exp

StephenW

<http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02423.x/abstract>

Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus
expression

Iddo Bar-Yishay1, Yosef Shaul2, Amir Shlomai1Article first published online: 11
JAN 2011

DOI: 10.1111/j.1478-3231.2010.02423.x
© 2011 John Wiley & Sons A/S
Issue

Liver International
Early View (Articles online in advance of print)

Abstract
Hepatitis B virus (HBV) is a small DNA virus responsible for significant
morbidity and mortality worldwide. The liver, which is the main target organ for
HBV infection, provides the virus with the machinery necessary for persistent
infection and propagation, a process that might ultimately lead to severe liver
pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene
expression is regulated mainly at the transcriptional level by recruitment of a
whole set of cellular transcription factors (TFs) and co-activators to support
transcription. Over the years, many of these TFs were identified and
interestingly enough most are associated with the body's nutritional state.
These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X
receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding
protein (C/EBP) and glucocorticoid receptor TFs and the transcription
coactivator PPARγ coactivator-1α. Consequently, HBV gene expression is linked
to hepatic metabolic processes such as glucose and fat production and
utilization as well as bile acids' production and secretion. Furthermore, recent
evidence indicates that HBV actively interferes with some of these hepatic
metabolic processes by manipulating key TFs, such as CREB and C/EBP, to meet its
requirements. The discovery of the mechanisms by which HBV is controlled by the
hepatic metabolic milieu may broaden our understanding of the unique regulation
of HBV expression and may also explain the mechanisms by which HBV induces liver
pathologies. The emerging principle of the intimate link between HBV and liver
metabolism can be further exploited for host-targeted therapeutic strategies.

肝细胞代谢信号通路和调节乙型肝炎病毒
表达

易多扎Yishay1，优素福Shaul2，阿米尔Shlomai1Article首次出版在线：11
2011年1月

分类号：10.1111/j.1478-3231.2010.02423.x
© 2011年约翰Wiley＆Sons出版A / S公司
发行

国际肝病
厄尔利维尤（第预先在网上打印）

摘要
乙型肝炎病毒（HBV）是一种小DNA病毒重要的责任
全世界发病率和死亡率。肝，这是主要的靶器官
乙肝病毒感染，提供了必要的机械持续病毒
感染和传播，这一进程最终可能导致严重的肝脏
疾病，如慢性肝炎，肝硬化和肝癌。 HBV基因
表达是在转录水平调控主要是通过招聘
细胞转录因子（转录因子）和联合激活一整套支持
转录。多年来，许多人对这些转录因子识别和
有趣的是大多数都与人体的营养状况。
这些措施包括肝细胞核因子，叉头框弧菌，法尼醇X
受体，循环-腺苷反应元件结合（CREB）的，CCAAT /增强子结合
蛋白质（的C / EBP的）和糖皮质激素受体的转录因子和转录
激活PPARγ的激活-1α。因此，与乙肝病毒基因的表达
与肝代谢，如葡萄糖和脂肪的生产工艺和
利用以及胆汁酸的生产和分泌。此外，最近
证据表明，乙肝病毒与这些积极的一些干扰肝
通过控制关键转录因子CREB的等和C / EBP的，以满足其代谢过程
要求。该以何种病毒是由控制机制发现
肝脏代谢环境可能会扩大我们的独特理解规例
HBV的表达，并可能也解释了机制，乙肝病毒引起肝脏
病变。对乙肝病毒与肝之间的密切联系原则新兴
代谢能得到进一步开发为主机的靶向治疗策略。




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