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Article ; Online: Mutational spectrum of hepatitis C virus in patients with chronic hepatitis C determined by single molecule real-time sequencing.

Nakamura, Fumiyasu / Takeda, Haruhiko / Ueda, Yoshihide / Takai, Atsushi / Takahashi, Ken / Eso, Yuji / Arasawa, Soichi / Iguchi, Eriko / Shimizu, Takahiro / Mishima, Masako / Kumagai, Ken / Yamashita, Taiki / Uemoto, Shinji / Kato, Nobuyuki / Marusawa, Hiroyuki / Sekine, Akihiro / Seno, Hiroshi

Scientific reports

2022 Volume 12, Issue 1, Page(s) 7083

Abstract: The emergence of hepatitis C virus (HCV) with resistance-associated substitution (RAS), produced ... substitutions, especially A>G and U>C, occurred prominently under DAAs in both non-transplant and post ... transition mutations, notably A>G and U>C substitutions. However, RASs are acquired by both transition and ...

Abstract	The emergence of hepatitis C virus (HCV) with resistance-associated substitution (RAS), produced by mutations in the HCV genome, is a major problem in direct acting antivirals (DAA) treatment. This study aimed to clarify the mutational spectrum in HCV-RNA and the substitution pattern for the emergence of RASs in patients with chronic HCV infection. HCV-RNA from two HCV replicon cell lines and the serum HCV-RNA of four non-liver transplant and four post-liver transplant patients with unsuccessful DAA treatment were analyzed using high-accuracy single-molecule real-time long-read sequencing. Transition substitutions, especially A>G and U>C, occurred prominently under DAAs in both non-transplant and post-transplant patients, with a mutational bias identical to that occurring in HCV replicon cell lines during 10-year culturing. These mutational biases were reproduced in natural courses after DAA treatment. RASs emerged via both transition and transversion substitutions. NS3-D168 and NS5A-L31 RASs resulted from transversion mutations, while NS5A-Y93 RASs was caused by transition substitutions. The fidelity of the RNA-dependent RNA polymerase, HCV-NS5B, produces mutational bias in the HCV genome, characterized by dominant transition mutations, notably A>G and U>C substitutions. However, RASs are acquired by both transition and transversion substitutions, and the RASs-positive HCV clones are selected and proliferated under DAA treatment pressure.
MeSH term(s)	Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Drug Resistance, Viral/genetics ; Genotype ; Hepacivirus/genetics ; Hepatitis C ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/genetics ; Humans ; Mutation ; RNA ; Viral Nonstructural Proteins/genetics
Chemical Substances	Antiviral Agents ; Viral Nonstructural Proteins ; RNA (63231-63-0)
Language	English
Publishing date	2022-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-11151-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Intracellular Major Histocompatibility Complex Class II and C-X-C Motif Chemokine Ligand 10-Expressing Neutrophils Indicate the State of Anti-Tumor Activity Induced by

Biomedicines

2023 Volume 11, Issue 11

Abstract: 1) Background: Inflammatory responses induce the formation of both anti-tumor and pro-tumor neutrophils known as myeloid-derived suppressor cells (MDSCs). Intermittent intravesical infusion ... ...

Abstract	(1) Background: Inflammatory responses induce the formation of both anti-tumor and pro-tumor neutrophils known as myeloid-derived suppressor cells (MDSCs). Intermittent intravesical infusion of
Language	English
Publishing date	2023-11-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11113062
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Article: Clinical and Molecular Basis of Hepatocellular Carcinoma after Hepatitis C Virus Eradication.

Oe, Natsumi / Takeda, Haruhiko / Eso, Yuji / Takai, Atsushi / Marusawa, Hiroyuki

Pathogens (Basel, Switzerland)

2022 Volume 11, Issue 4

Abstract: ... hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV ...

Abstract	Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues.
Language	English
Publishing date	2022-04-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens11040430
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Article ; Online: Deoxygenative Insertion of Carbonyl Carbon into a C(sp

Asako, Sobi / Ishihara, Seina / Hirata, Keiya / Takai, Kazuhiko

Journal of the American Chemical Society

2019 Volume 141, Issue 25, Page(s) 9832–9836

Abstract: A simple deoxygenation reagent prepared in situ from commercially available Mo(CO) ...

Abstract	A simple deoxygenation reagent prepared in situ from commercially available Mo(CO)
Language	English
Publishing date	2019-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3155-0
ISSN	1520-5126 ; 0002-7863
ISSN (online)	1520-5126
ISSN	0002-7863
DOI	10.1021/jacs.9b05428
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Article ; Online: Novel function of the C-terminal region of the Hsp110 family member Osp94 in unfolded protein refolding.

Kojima, Ryoji / Takai, Shinichi / Osada, Hinako / Yamamoto, Lina / Furukawa, Misa / Gullans, Steven R

Journal of cell science

2022 Volume 135, Issue 6

Abstract: ... has a longer C-terminus than found in Hsc70/Hsp70 family proteins, composed of the loop region ... with a partial substrate-binding domain (SBD) β (L), and the SBDα and the C-terminal extension (H ... reactivation of heat-inactivated Luc. These results indicate that Osp94 acts as a holdase, and that the C ...

Abstract	Osp94 (also known as HSPA4L or HSPH3), a member of the Hsp110/Sse1 family of heat-shock proteins, has a longer C-terminus than found in Hsc70/Hsp70 family proteins, composed of the loop region with a partial substrate-binding domain (SBD) β (L), and the SBDα and the C-terminal extension (H), but the functions of these domains are poorly understood. Here, we found that Osp94 suppressed heat-induced aggregation of luciferase (Luc). Osp94-bound heat-inactivated Luc was reactivated in the presence of rabbit reticulocyte lysate (RRL) and/or a combination of Hsc70 and Hsp40 (also known as HSPA8 and DNAJB1, respectively). Targeted deletion mutagenesis revealed that the SBDβ and H domains of Osp94 are critical for protein disaggregation and RRL-mediated refolding. Reactivation of Hsp90-bound heat-inactivated Luc was abolished in the absence of RRL but compensated for by PA28α (also known as PSME1), a proteasome activator. Interestingly, the LH domain also reactivated heat-inactivated Luc, independently of PA28α. Biotin-tag cross-linking experiments indicated that the LH domain and PA28α interact with Luc bound by Hsp90 during refolding. A chimeric protein in which the H domain was exchanged for PA28α also mediated disaggregation and reactivation of heat-inactivated Luc. These results indicate that Osp94 acts as a holdase, and that the C-terminal region plays a PA28α-like role in the refolding of unfolded proteins.
MeSH term(s)	Animals ; Family ; HSC70 Heat-Shock Proteins/metabolism ; HSP40 Heat-Shock Proteins/genetics ; HSP40 Heat-Shock Proteins/metabolism ; HSP70 Heat-Shock Proteins/genetics ; HSP70 Heat-Shock Proteins/metabolism ; Heat-Shock Proteins/metabolism ; Protein Refolding ; Rabbits
Chemical Substances	HSC70 Heat-Shock Proteins ; HSP40 Heat-Shock Proteins ; HSP70 Heat-Shock Proteins ; Heat-Shock Proteins
Language	English
Publishing date	2022-03-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.258542
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Article ; Online: Mutational spectrum of hepatitis C virus in patients with chronic hepatitis C determined by single molecule real-time sequencing

Fumiyasu Nakamura / Haruhiko Takeda / Yoshihide Ueda / Atsushi Takai / Ken Takahashi / Yuji Eso / Soichi Arasawa / Eriko Iguchi / Takahiro Shimizu / Masako Mishima / Ken Kumagai / Taiki Yamashita / Shinji Uemoto / Nobuyuki Kato / Hiroyuki Marusawa / Akihiro Sekine / Hiroshi Seno

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 13

Abstract: Abstract The emergence of hepatitis C virus (HCV) with resistance-associated substitution (RAS ... substitutions, especially A>G and U>C, occurred prominently under DAAs in both non-transplant and post ... transition mutations, notably A>G and U>C substitutions. However, RASs are acquired by both transition and ...

Abstract	Abstract The emergence of hepatitis C virus (HCV) with resistance-associated substitution (RAS), produced by mutations in the HCV genome, is a major problem in direct acting antivirals (DAA) treatment. This study aimed to clarify the mutational spectrum in HCV-RNA and the substitution pattern for the emergence of RASs in patients with chronic HCV infection. HCV-RNA from two HCV replicon cell lines and the serum HCV-RNA of four non-liver transplant and four post-liver transplant patients with unsuccessful DAA treatment were analyzed using high-accuracy single-molecule real-time long-read sequencing. Transition substitutions, especially A>G and U>C, occurred prominently under DAAs in both non-transplant and post-transplant patients, with a mutational bias identical to that occurring in HCV replicon cell lines during 10-year culturing. These mutational biases were reproduced in natural courses after DAA treatment. RASs emerged via both transition and transversion substitutions. NS3-D168 and NS5A-L31 RASs resulted from transversion mutations, while NS5A-Y93 RASs was caused by transition substitutions. The fidelity of the RNA-dependent RNA polymerase, HCV-NS5B, produces mutational bias in the HCV genome, characterized by dominant transition mutations, notably A>G and U>C substitutions. However, RASs are acquired by both transition and transversion substitutions, and the RASs-positive HCV clones are selected and proliferated under DAA treatment pressure.
Keywords	Medicine ; R ; Science ; Q
Subject code	360
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Structural Dynamics of the N-Extension of Cardiac Troponin I Complexed with Troponin C by Site-Directed Spin Labeling Electron Paramagnetic Resonance.

Zhao, Chenchao / Somiya, Takayasu / Takai, Shinji / Ueki, Shoji / Arata, Toshiaki

Scientific reports

2019 Volume 9, Issue 1, Page(s) 15259

Abstract: The secondary structure of the N-extension of cardiac troponin I (cTnI) was determined by measuring the distance distribution between spin labels attached to the i and i + 4 residues: 15/19, 23/27, 27/31, 35/39, and 43/47. All of the EPR spectra of these ...

Abstract	The secondary structure of the N-extension of cardiac troponin I (cTnI) was determined by measuring the distance distribution between spin labels attached to the i and i + 4 residues: 15/19, 23/27, 27/31, 35/39, and 43/47. All of the EPR spectra of these regions in the monomeric state were broadened and had a amplitude that was reduced by two-thirds of that of the single spin-labeled spectra and was fit by two residual distance distributions, with a major distribution one spreading over the range from 1 to 2.5 nm and the other minor peak at 0.9 nm. Only slight or no obvious changes were observed when the extension was bound to cTnC in the cTnI-cTnC complex at 0.2 M KCl. However, at 0.1 M KCl, residues 43/47, located at the PKC phosphorylation sites Ser42/44 on the boundary of the extension, exclusively exhibited a 0.9 nm peak, as expected from α-helix in the crystal structure, in the complex. Furthermore, 23/27, which is located on the PKA phosphorylation sites Ser23/24, showed that the major distribution was markedly narrowed, centered at 1.4 nm and 0.5 nm wide, accompanying the spin label immobilization of residue 27. Residues 35 and 69 at site 1 and 2 of cTnC exhibited partial immobilization of the attached spin labels upon complex formation. The results show that the extension exhibited a primarily partially folded or unfolded structure equilibrated with a transiently formed α-helix-like short structure over the length. We hypothesize that the structure binds at least near sites 1 and 2 of cTnC and that the specific secondary structure of the extension on cTnC becomes uncovered when decreasing the ionic strength demonstrating that only the phosphorylation regions of cTnI interact stereospecifically with cTnC.
MeSH term(s)	Animals ; Electron Spin Resonance Spectroscopy ; Macromolecular Substances/metabolism ; Models, Molecular ; Phosphorylation ; Protein Binding ; Spin Labels ; Troponin C/metabolism ; Troponin I/metabolism
Chemical Substances	Macromolecular Substances ; Spin Labels ; Troponin C ; Troponin I
Language	English
Publishing date	2019-10-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-51740-6
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Article ; Online: Mechanistic Insights into Rhenium-Catalyzed Regioselective C-Alkenylation of Phenols with Internal Alkynes.

Murai, Masahito / Yamamoto, Masaki / Takai, Kazuhiko

Chemistry (Weinheim an der Bergstrasse, Germany)

2019 Volume 25, Issue 66, Page(s) 15189–15197

Abstract: ... ortho-alkenylation (C-alkenylation) of unprotected phenols with alkynes. The reaction exclusively ...

Abstract	A (μ-aryloxo)rhenium complex was isolated and confirmed as a key precatalyst for rhenium-catalyzed ortho-alkenylation (C-alkenylation) of unprotected phenols with alkynes. The reaction exclusively provided ortho-alkenylphenols; the formation of para or multiply alkenylated phenols and hydrophenoxylation (O-alkenylation) products was not observed. Several mechanistic experiments excluded a classical Friedel-Crafts-type mechanism, leading to the proposed phenolic hydroxyl group assisted electrophilic alkenylation as the most plausible reaction mechanism. For this purpose, the use of rhenium, a metal between the early and late transition metals in the periodic table, was key for the activation of both the soft carbon-carbon triple bond of the alkyne and the hard oxygen atom of the phenol, at the same time. ortho-Selective alkenylation with allenes also provided the corresponding adducts with a substitution pattern different from that obtained by the addition reaction with alkynes.
Language	English
Publishing date	2019-10-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1478547-X
ISSN	1521-3765 ; 0947-6539
ISSN (online)	1521-3765
ISSN	0947-6539
DOI	10.1002/chem.201903910
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Article ; Online: Clinical and Molecular Basis of Hepatocellular Carcinoma after Hepatitis C Virus Eradication

Natsumi Oe / Haruhiko Takeda / Yuji Eso / Atsushi Takai / Hiroyuki Marusawa

Pathogens, Vol 11, Iss 430, p

2022 Volume 430

Abstract: ... hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV ...

Abstract	Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues.
Keywords	hepatitis C virus ; liver cancer ; SVR ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Oncogenic transcriptomic profile is sustained in the liver after the eradication of the hepatitis C virus.

Takeda, Haruhiko / Takai, Atsushi / Iguchi, Eriko / Mishima, Masako / Arasawa, Soichi / Kumagai, Ken / Eso, Yuji / Shimizu, Takahiro / Takahashi, Ken / Ueda, Yoshihide / Taura, Kojiro / Hatano, Etsuro / Iijima, Hiroko / Aoyagi, Haruyo / Aizaki, Hideki / Marusawa, Hiroyuki / Wakita, Takaji / Seno, Hiroshi

Carcinogenesis

2021 Volume 42, Issue 5, Page(s) 672–684

Abstract: Hepatocellular carcinoma (HCC) developing after hepatitis C virus (HCV) eradication is a serious ...

Abstract	Hepatocellular carcinoma (HCC) developing after hepatitis C virus (HCV) eradication is a serious clinical concern. However, molecular basis for the hepatocarcinogenesis after sustained virologic response (SVR) remains unclear. In this study, we aimed to unveil the transcriptomic profile of post-SVR liver tissues and explore the molecules associated with post-SVR carcinogenesis. We analysed 90 RNA sequencing datasets, consisting of non-cancerous liver tissues including 20 post-SVR, 40 HCV-positive and 7 normal livers, along with Huh7 cell line specimens before and after HCV infection and eradication. Comparative analysis demonstrated that cell cycle- and mitochondrial function-associated pathways were altered only in HCV-positive non-cancerous liver tissues, whereas some cancer-related pathways were up-regulated in the non-cancerous liver tissues of both post-SVR and HCV-positive cases. The persistent up-regulation of carcinogenesis-associated gene clusters after viral clearance was reconfirmed through in vitro experiments, of which, CYR61, associated with liver fibrosis and carcinogenesis in several cancer types, was the top enriched gene and co-expressed with cell proliferation-associated gene modules. To evaluate whether this molecule could be a predictor of hepatocarcinogenesis after cure of HCV infection, we also examined 127 sera from independent HCV-positive cohorts treated with direct-acting antivirals (DAAs), including 60 post-SVR-HCC patients, and found that the elevated serum Cyr61 was significantly associated with early carcinogenesis after receiving DAA therapy. In conclusion, some oncogenic transcriptomic profiles are sustained in liver tissues after HCV eradication, which might be a molecular basis for the liver cancer development even after viral clearance. Among them, up-regulated CYR61 could be a possible biomarker for post-SVR-HCC.
MeSH term(s)	Carcinogenesis/genetics ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Carcinoma, Hepatocellular/virology ; Cell Line, Tumor ; Cysteine-Rich Protein 61/genetics ; Databases, Genetic ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Hepacivirus/pathogenicity ; Hepatitis C/genetics ; Hepatitis C/pathology ; Hepatitis C/virology ; Humans ; Liver/metabolism ; Liver/pathology ; Liver/virology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Liver Neoplasms/virology ; Male ; RNA-Seq ; Sustained Virologic Response ; Transcriptome/genetics
Chemical Substances	CCN1 protein, human ; Cysteine-Rich Protein 61
Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgab014
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