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Specialty: Chemistry
Infectious Disease: Hepatitis

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Total 4 results found since Jan 2013.

Ribonucleotide reductase M2 promotes RNA replication of hepatitis C virus by protecting NS5B protein from hPLIC1-dependent proteasomal degradation Microbiology
Hepatitis C virus (HCV) establishes a chronic infection that can lead to cirrhosis and hepatocellular carcinoma. The HCV life cycle is closely associated with host factors that promote or restrict viral replication, the characterization of which could help to identify potential therapeutic targets. To this end, here we performed a genome-wide microarray analysis and identified ribonucleotide reductase M2 (RRM2) as a cellular factor essential for HCV replication. We found that RRM2 is up-regulated in response to HCV infection in quiescent hepatocytes from humanized chimeric mouse livers. To elucidate the molecular basis of ...
Source: Journal of Biological Chemistry - April 11, 2019 Category: Chemistry Authors: Bouchra Kitab, Masaaki Satoh, Yusuke Ohmori, Tsubasa Munakata, Masayuki Sudoh, Michinori Kohara, Kyoko Tsukiyama-Kohara Tags: Microbiology Source Type: research

Heat shock proteins stimulate APOBEC-3-mediated cytidine deamination in the hepatitis B virus DNA and Chromosomes
Apolipoprotein B mRNA-editing enzyme catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively expressed. They are often up-regulated during carcinogenesis and candidate genes for causing the major single-base substitution in cancer-associated DNA mutations. Moreover, APOBEC-3s are involved in host innate immunity against many viruses. However, how APOBEC-3 mutational activity is regulated in normal and pathological conditions remains largely unknown. Heat shock protein levels are often elevated in both carcinogenesis and viral infection and are associated with DNA mutations. Here, ...
Source: Journal of Biological Chemistry - August 11, 2017 Category: Chemistry Authors: Zhigang Chen, Thomas L. Eggerman, Alexander V. Bocharov, Irina N. Baranova, Tatyana G. Vishnyakova, Roger Kurlander, Amy P. Patterson Tags: Molecular Bases of Disease Source Type: research

HCV-activated NLRP3 Inflammasome Regulates Lipid Metabolism Molecular Bases of Disease
In this study, we elucidate the potential link between chronic hepatitis C-associated inflammation and alteration of lipid homeostasis in infected cells. Our results reveal that the HCV-activated NLRP3 inflammasome is required for the up-regulation of lipogenic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty acid synthase, and stearoyl-CoA desaturase. Using pharmacological inhibitors and siRNA against the inflammasome components (NLRP3, apoptosis-associated speck-like protein containing a CARD, and caspase-1), we further show that the activation of the NLRP3 inflammasome plays a critical role in lipid d...
Source: Journal of Biological Chemistry - February 12, 2016 Category: Chemistry Authors: McRae, S., Iqbal, J., Sarkar-Dutta, M., Lane, S., Nagaraj, A., Ali, N., Waris, G. Tags: Microbiology Source Type: research

Nuclear Import of HBXIP Requires Collaboration with c-Fos Gene Regulation
Aberrant nuclear localization of oncogenic transcription factors and coactivators always leads to the development of cancer. We have reported that the oncoprotein hepatitis B X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. However, the mechanism of regulating the nuclear import of HBXIP remains unclear. In the present study, we found that HBXIP interacted with c-Fos through their leucine zipper domains in vitro and in vivo. Interestingly, the leucine zipper mutant of HBXIP (or c-Fos) was unavailable to bind to c-Fos (or HBXIP), resulti...
Source: Journal of Biological Chemistry - June 28, 2013 Category: Chemistry Authors: Zhang, Y., Zhao, Y., Li, H., Li, Y., Cai, X., Shen, Y., Shi, H., Li, L., Liu, Q., Zhang, X., Ye, L. Tags: Cell Biology Source Type: research