Performance information

• CRISPRi knockdown of the cyabrB1 gene induces the divergently transcribed icfG and sll1783 operons related to carbon metabolism in the cyanobacterium Synechocystis sp. PCC 6803
  Atsuko Hishida; Ryo Shirai; Akiyoshi Higo; Minenosuke Matsutani; Kaori Nimura-Matsune; Tomoko Takahashi; Satoru Watanabe; Shigeki Ehira; Yukako Hihara
  The Journal of General and Applied Microbiology, Jul. 2024, [Reviewed]
  Microbiology Research Foundation, Scientific journal
  DOI：https://doi.org/10.2323/jgam.2024.01.001
  DOI ID：10.2323/jgam.2024.01.001, ISSN：0022-1260, eISSN：1349-8037
• microRNA-guided immunity against respiratory virus infection in human and mouse lung cells
  Ayaka Shibamoto; Yoshiaki Kitsu; Keiko Shibata; Yuka Kaneko; Harune Moriizumi; Tomoko Takahashi
  Biology Open, Volume：13, Number：6, Jun. 2024, [Reviewed], [Corresponding]
  ABSTRACT
  
  Viral infectivity depends on multiple factors. Recent studies showed that the interaction between viral RNAs and endogenous microRNAs (miRNAs) regulates viral infectivity; viral RNAs function as a sponge of endogenous miRNAs and result in upregulation of its original target genes, while endogenous miRNAs target viral RNAs directly and result in repression of viral gene expression. In this study, we analyzed the possible interaction between parainfluenza virus RNA and endogenous miRNAs in human and mouse lungs. We showed that the parainfluenza virus can form base pairs with human miRNAs abundantly than mouse miRNAs. Furthermore, we analyzed that the sponge effect of endogenous miRNAs on viral RNAs may induce the upregulation of transcription regulatory factors. Then, we performed RNA-sequence analysis and observed the upregulation of transcription regulatory factors in the early stages of parainfluenza virus infection. Our studies showed how the differential expression of endogenous miRNAs in lungs could contribute to respiratory virus infection and species- or tissue-specific mechanisms and common mechanisms could be conserved in humans and mice and regulated by miRNAs during viral infection.
  The Company of Biologists, Scientific journal
  DOI：https://doi.org/10.1242/bio.060172
  DOI ID：10.1242/bio.060172, eISSN：2046-6390
• Caspase-mediated processing of TRBP regulates apoptosis during viral infection
  Keiko Shibata; Harune Moriizumi; Koji Onomoto; Yuka Kaneko; Takuya Miyakawa; Shuhei Zenno; Masaru Tanokura; Mitsutoshi Yoneyama; Tomoko Takahashi; Kumiko Ui-Tei
  Nucleic Acids Research, Volume：52, Number：9, First page：5209, Last page：5225, Apr. 2024, [Reviewed], [Corresponding]
  Abstract
  
  RNA silencing is a post-transcriptional gene-silencing mechanism mediated by microRNAs (miRNAs). However, the regulatory mechanism of RNA silencing during viral infection is unclear. TAR RNA-binding protein (TRBP) is an enhancer of RNA silencing that induces miRNA maturation by interacting with the ribonuclease Dicer. TRBP interacts with a virus sensor protein, laboratory of genetics and physiology 2 (LGP2), in the early stage of viral infection of human cells. Next, it induces apoptosis by inhibiting the maturation of miRNAs, thereby upregulating the expression of apoptosis regulatory genes. In this study, we show that TRBP undergoes a functional conversion in the late stage of viral infection. Viral infection resulted in the activation of caspases that proteolytically processed TRBP into two fragments. The N-terminal fragment did not interact with Dicer but interacted with type I interferon (IFN) signaling modulators, such as protein kinase R (PKR) and LGP2, and induced ER stress. The end results were irreversible apoptosis and suppression of IFN signaling. Our results demonstrate that the processing of TRBP enhances apoptosis, reducing IFN signaling during viral infection.
  Oxford University Press (OUP), Scientific journal
  DOI：https://doi.org/10.1093/nar/gkae246
  DOI ID：10.1093/nar/gkae246, ISSN：0305-1048, eISSN：1362-4962
• AraC-induced neuron-like differentiation of human NTERA2/D1 cells and quantification of endogenous pre-mir-106b and 19b levels　　　　　　　　　　　　　　　
  Yuka Kaneko; Tomoko Takahashi
  MicroPubl. Biol., Jul. 2023, [Reviewed], [Corresponding]
  English
  DOI：https://doi.org/10.17912/micropub.biology.000803
  DOI ID：10.17912/micropub.biology.000803
• The regulation of persistent Borna disease virus infection by RNA silencing factors in human cells　　　　　　　　　　　　　　　
  Yuka Kaneko; Yuui Naito; Rie Koide; Nicholas F. Parrish; Tomoko Takahashi
  Biochemical and Biophysical Research Communications, Volume：658, First page：122, Last page：127, May 2023, [Reviewed], [Corresponding]
  Elsevier BV, Scientific journal
  DOI：https://doi.org/10.1016/j.bbrc.2023.03.069
  DOI ID：10.1016/j.bbrc.2023.03.069, ISSN：0006-291X
• Mammalian antiviral systems directed by small RNA
  Tomoko Takahashi; Steven M. Heaton; Nicholas F. Parrish
  PLOS Pathogens, Volume：17, Number：12, First page：e1010091, Last page：e1010091, Dec. 2021, [Reviewed], [Lead, Corresponding]
  There are strong incentives for human populations to develop antiviral systems. Similarly, genomes that encode antiviral systems have had strong selective advantages. Protein-guided immune systems, which have been well studied in mammals, are necessary for survival in our virus-laden environments. Small RNA–directed antiviral immune systems suppress invasion of cells by non-self genetic material via complementary base pairing with target sequences. These RNA silencing-dependent systems operate in diverse organisms. In mammals, there is strong evidence that microRNAs (miRNAs) regulate endogenous genes important for antiviral immunity, and emerging evidence that virus-derived nucleic acids can be directly targeted by small interfering RNAs (siRNAs), PIWI-interacting RNAs (piRNAs), and transfer RNAs (tRNAs) for protection in some contexts. In this review, we summarize current knowledge of the antiviral functions of each of these small RNA types and consider their conceptual and mechanistic overlap with innate and adaptive protein-guided immunity, including mammalian antiviral cytokines, as well as the prokaryotic RNA-guided immune system, CRISPR. In light of recent successes in delivery of RNA for antiviral purposes, most notably for vaccination, we discuss the potential for development of small noncoding RNA–directed antiviral therapeutics and prophylactics.
  Public Library of Science (PLoS), Scientific journal
  DOI：https://doi.org/10.1371/journal.ppat.1010091
  DOI ID：10.1371/journal.ppat.1010091, eISSN：1553-7374
• Establishing an efficient protoplast transient expression system for investigation of floral thermogenesis in aroids
  Haruhiko Maekawa; Miyabi Otsubo; Mitsuhiko P. Sato; Tomoko Takahashi; Koichiro Mizoguchi; Daiki Koyamatsu; Takehito Inaba; Yasuko Ito-Inaba
  Plant Cell Reports, Volume：41, Number：1, First page：263, Last page：275, Oct. 2021, [Reviewed]
  Springer Science and Business Media LLC, Scientific journal
  DOI：https://doi.org/10.1007/s00299-021-02806-1
  DOI ID：10.1007/s00299-021-02806-1, ISSN：0721-7714, eISSN：1432-203X
• Mutual Regulation of RNA Silencing and the IFN Response as an Antiviral Defense System in Mammalian Cells
  Tomoko Takahashi; Kumiko Ui-Tei
  International Journal of Molecular Sciences, Volume：21, Number：4, First page：1348, Last page：1348, Feb. 2020, [Reviewed], [Lead, Corresponding]
  RNA silencing is a posttranscriptional gene silencing mechanism directed by endogenous small non-coding RNAs called microRNAs (miRNAs). By contrast, the type-I interferon (IFN) response is an innate immune response induced by exogenous RNAs, such as viral RNAs. Endogenous and exogenous RNAs have typical structural features and are recognized accurately by specific RNA-binding proteins in each pathway. In mammalian cells, both RNA silencing and the IFN response are induced by double-stranded RNAs (dsRNAs) in the cytoplasm, but have long been considered two independent pathways. However, recent reports have shed light on crosstalk between the two pathways, which are mutually regulated by protein–protein interactions triggered by viral infection. This review provides brief overviews of RNA silencing and the IFN response and an outline of the molecular mechanism of their crosstalk and its biological implications. Crosstalk between RNA silencing and the IFN response may reveal a novel antiviral defense system that is regulated by miRNAs in mammalian cells.
  MDPI AG, Scientific journal
  DOI：https://doi.org/10.3390/ijms21041348
  DOI ID：10.3390/ijms21041348, eISSN：1422-0067
• TRBP–Dicer interaction may enhance HIV-1 TAR RNA translation via TAR RNA processing, repressing host-cell apoptosis
  Chiaki Komori; Tomoko Takahashi; Yuko Nakano; Kumiko Ui-Tei
  Biology Open, Jan. 2020, [Reviewed]
  The transactivating response (TAR) RNA-binding protein (TRBP) has been identified as a double-stranded RNA (dsRNA)-binding protein, which associates with a stem-loop region known as the TAR element in human immunodeficiency virus-1 (HIV-1). However, TRBP is also known to be an enhancer of RNA silencing, interacting with Dicer, an enzyme that belongs to the RNase III family. Dicer cleaves long dsRNA into small dsRNA fragments called small interfering RNA or microRNA (miRNA) to mediate RNA silencing. During HIV-1 infection, TAR RNA-mediated translation is suppressed by the secondary structure of 5'UTR TAR RNA. However, TRBP binding to TAR RNA relieves its inhibitory action of translation and Dicer processes HIV-1 TAR RNA to generate TAR miRNA. However, whether the interaction between TRBP and Dicer is necessary for TAR RNA translation or TAR miRNA processing remains unclear. In this study, we constructed TRBP mutants that were unable to interact with Dicer by introducing mutations into amino acid residues necessary for the interaction. Furthermore, we established cell lines expressing such TRBP mutants. Then, we revealed that the TRBP–Dicer interaction is essential for both the TAR-containing RNA translation and the TAR miRNA processing in HIV-1.
  The Company of Biologists, Scientific journal
  DOI：https://doi.org/10.1242/bio.050435
  DOI ID：10.1242/bio.050435, eISSN：2046-6390
• LGP2 virus sensor enhances apoptosis by upregulating apoptosis regulatory genes through TRBP-bound miRNAs during viral infection
  Tomoko Takahashi; Yuko Nakano; Koji Onomoto; Mitsutoshi Yoneyama; Kumiko Ui-Tei
  Nucleic Acids Research, Volume：48, Number：3, First page：1494, Last page：1507, Dec. 2019, [Reviewed], [Lead]
  Abstract
  
  During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or retinoic acid-inducible gene I-like receptors (RLRs) in mammalian cells. Activation of these virus sensor proteins induces type-I interferon production and represses viral replication. Recently, we reported that an RLR family member, laboratory of genetics and physiology 2 (LGP2), modulates RNA silencing by interacting with an RNA silencing enhancer, TAR-RNA binding protein (TRBP). However, the biological implications remained unclear. Here, we show that LGP2 enhances apoptosis by upregulating apoptosis regulatory genes during viral infection. Sendai virus (SeV) infection increased LGP2 expression approximately 900 times compared to that in non-virus-infected cells. Then, the induced LGP2 interacted with TRBP, resulting in the inhibition of maturation of the TRBP-bound microRNA (miRNA) and its subsequent RNA silencing activity. Gene expression profiling revealed that apoptosis regulatory genes were upregulated during SeV infection: caspases-2, -8, -3 and -7, four cysteine proteases with key roles in apoptosis, were upregulated directly or indirectly through the repression of a typical TRBP-bound miRNA, miR-106b. Our findings may shed light on the mechanism of apoptosis, induced by the TRBP-bound miRNAs through the interaction of TRBP with LGP2, as an antiviral defense system in mammalian cells.
  Oxford University Press (OUP), Scientific journal
  DOI：https://doi.org/10.1093/nar/gkz1143
  DOI ID：10.1093/nar/gkz1143, ISSN：0305-1048, eISSN：1362-4962
• Virus Sensor RIG-I Represses RNA Interference by Interacting with TRBP through LGP2 in Mammalian Cells
  Tomoko Takahashi; Yuko Nakano; Koji Onomoto; Mitsutoshi Yoneyama; Kumiko Ui-Tei
  Genes, Volume：9, Number：10, First page：511, Last page：511, Oct. 2018, [Reviewed], [Lead]
  Exogenous double-stranded RNAs (dsRNAs) similar to viral RNAs induce antiviral RNA silencing or RNA interference (RNAi) in plants or invertebrates, whereas interferon (IFN) response is induced through activation of virus sensor proteins including Toll like receptor 3 (TLR3) or retinoic acid-inducible gene I (RIG-I) like receptors (RLRs) in mammalian cells. Both RNA silencing and IFN response are triggered by dsRNAs. However, the relationship between these two pathways has remained unclear. Laboratory of genetics and physiology 2 (LGP2) is one of the RLRs, but its function has remained unclear. Recently, we reported that LGP2 regulates endogenous microRNA-mediated RNA silencing by interacting with an RNA silencing enhancer, TAR-RNA binding protein (TRBP). Here, we investigated the contribution of other RLRs, RIG-I and melanoma-differentiation-associated gene 5 (MDA5), in the regulation of RNA silencing. We found that RIG-I, but not MDA5, also represses short hairpin RNA (shRNA)-induced RNAi by type-I IFN. Our finding suggests that RIG-I, but not MDA5, interacts with TRBP indirectly through LGP2 to function as an RNAi modulator in mammalian cells.
  MDPI AG, Scientific journal
  DOI：https://doi.org/10.3390/genes9100511
  DOI ID：10.3390/genes9100511, eISSN：2073-4425
• LGP2 virus sensor regulates gene expression network mediated by TRBP-bound microRNAs
  Tomoko Takahashi; Yuko Nakano; Koji Onomoto; Fuminori Murakami; Chiaki Komori; Yutaka Suzuki; Mitsutoshi Yoneyama; Kumiko Ui-Tei
  Nucleic Acids Research, Volume：46, Number：17, First page：9134, Last page：9147, Jun. 2018, [Reviewed], [Lead]
  Oxford University Press (OUP), Scientific journal
  DOI：https://doi.org/10.1093/nar/gky575
  DOI ID：10.1093/nar/gky575, ISSN：0305-1048, eISSN：1362-4962
• Current Status for Application of RNA Interference Technology as Nucleic Acid Drug
  Tomoko Takahashi; Yuko Nakano; Kumiko Ui-Tei
  Gene Expression and Regulation in Mammalian Cells - Transcription From General Aspects, Feb. 2018, [Reviewed], [Lead]
  InTech, In book
  DOI：https://doi.org/10.5772/intechopen.71965
  DOI ID：10.5772/intechopen.71965
• Chemical Modification of the siRNA Seed Region Suppresses Off-Target Effects by Steric Hindrance to Base-Pairing with Targets
  Hanna Iribe; Kengo Miyamoto; Tomoko Takahashi; Yoshiaki Kobayashi; Jastina Leo; Misako Aida; Kumiko Ui-Tei
  ACS Omega, Volume：2, Number：5, First page：2055, Last page：2064, May 2017, [Reviewed]
  American Chemical Society (ACS), Scientific journal
  DOI：https://doi.org/10.1021/acsomega.7b00291
  DOI ID：10.1021/acsomega.7b00291, ISSN：2470-1343, eISSN：2470-1343
• RNA干渉法の核酸医薬への利用（1）　　　　　　　　　　　　　　　
  高橋朋子; 程久美子
  Volume：21, First page：14, Last page：21, 2017, [Reviewed], [Lead]
• siRNAの利点と技術開発・安全性評価　　　　　　　　　　　　　　　
  中野悠子; 高橋朋子; 程久美子
  2017
• 核酸医薬とsmall RNA　　　　　　　　　　　　　　　
  高橋朋子; 程久美子
  2016, [Lead]
• The siRNA Non-seed Region and Its Target Sequences Are Auxiliary Determinants of Off-Target Effects
  Piotr J. Kamola; Yuko Nakano; Tomoko Takahashi; Paul A. Wilson; Kumiko Ui-Tei
  PLOS Computational Biology, Volume：11, Number：12, First page：e1004656, Last page：e1004656, Dec. 2015, [Reviewed]
  Public Library of Science (PLoS), Scientific journal
  DOI：https://doi.org/10.1371/journal.pcbi.1004656
  DOI ID：10.1371/journal.pcbi.1004656, eISSN：1553-7358
• Control of the localization and function of a miRNA silencing component TNRC6A by Argonaute protein
  Kenji Nishi; Tomoko Takahashi; Masataka Suzawa; Takuya Miyakawa; Tatsuya Nagasawa; Yvelt Ming; Masaru Tanokura; Kumiko Ui-Tei
  Nucleic Acids Research, First page：gkv1026, Last page：gkv1026, Oct. 2015, [Reviewed]
  Oxford University Press (OUP), Scientific journal
  DOI：https://doi.org/10.1093/nar/gkv1026
  DOI ID：10.1093/nar/gkv1026, ISSN：0305-1048, eISSN：1362-4962
• ノンコーディングRNAの生体機能と医薬応用の現状　　　　　　　　　　　　　　　
  程久美子; 高橋朋子
  2015
• Interactions between the non-seed region of siRNA and RNA-binding RLC/RISC proteins, Ago and TRBP, in mammalian cells
  Tomoko Takahashi; Shuhei Zenno; Osamu Ishibashi; Toshihiro Takizawa; Kaoru Saigo; Kumiko Ui-Tei
  Nucleic Acids Research, Volume：42, Number：8, First page：5256, Last page：5269, Feb. 2014, [Reviewed], [Lead]
  Oxford University Press (OUP), Scientific journal
  DOI：https://doi.org/10.1093/nar/gku153
  DOI ID：10.1093/nar/gku153, ISSN：0305-1048, eISSN：1362-4962
• miRBase 〜miRNAのデータベース〜　　　　　　　　　　　　　　　
  高橋朋子; 程久美子
  2014, [Lead]
• miRNAの標的予測ウェブサイト　　　　　　　　　　　　　　　
  高橋朋子; 程久美子
  2014, [Lead]
• Distinguishable In Vitro Binding Mode of Monomeric TRBP and Dimeric PACT with siRNA
  Tomoko Takahashi; Takuya Miyakawa; Shuhei Zenno; Kenji Nishi; Masaru Tanokura; Kumiko Ui-Tei
  PLoS ONE, Volume：8, Number：5, First page：e63434, Last page：e63434, May 2013, [Reviewed], [Lead]
  Public Library of Science (PLoS), Scientific journal
  DOI：https://doi.org/10.1371/journal.pone.0063434
  DOI ID：10.1371/journal.pone.0063434, eISSN：1932-6203
• Thermodynamic Control of Small RNA-Mediated Gene Silencing　　　　　　　　　　　　　　　
  Kumiko Ui-Tei; Kenji Nishi; Tomoko Takahashi; Tatsuya Nagasawa
  Frontiers in Genetics, Volume：3, Jun. 2012, [Reviewed]
  Frontiers Media SA, Scientific journal
  DOI：https://doi.org/10.3389/fgene.2012.00101
  DOI ID：10.3389/fgene.2012.00101, eISSN：1664-8021
• RNAi実験の準備と実践 3. 修飾基のついたsiRNAのRNAi効果とその選択　　　　　　　　　　　　　　　
  西賢二; 高橋朋子; 長沢達矢; 程久美子
  2012
• Role of Multiple HLR1 Sequences in the Regulation of the Dual Promoters of the psaAB Genes in Synechocystis sp. PCC 6803
  Tomoko Takahashi; Nanako Nakai; Masayuki Muramatsu; Yukako Hihara
  Journal of Bacteriology, Volume：192, Number：15, First page：4031, Last page：4036, Aug. 2010, [Reviewed], [Lead]
  ABSTRACT
  
  Previously, we analyzed the promoter architecture of the psaAB genes encoding reaction center subunits of photosystem I (PSI) in the cyanobacterium Synechocystis sp. PCC 6803. There exist two promoters, P1 and P2, both of which show typical high-light (HL) response of PSI genes; their activities are high under low-light (LL) conditions but rapidly downregulated upon the shift to HL conditions. In this study, it was suggested that a response regulator RpaB binds to multiple high-light regulatory 1 (HLR1) sequences in the upstream region of the psaAB genes. We explored the regulatory role of cis -elements, including these HLR1 sequences on the individual activity of P1 and P2. Under LL conditions, the most influential cis -element is HLR1C (−62 to −45, relative to the transcriptional starting point of P1) working for positive regulation of P1. The other HLR1 sequences also affect the promoter activity under LL conditions; HLR1A (−255 to −238) is involved in repression of P1, whereas HLR1B (−153 to −126) works for activation of P2. Upon the shift to HL conditions, regulation via HNE2 located within the region from −271 to −177 becomes active in order to downregulate both P1 and P2 activities. A positive effect of HLR1B on P2 may persist under HL. These results suggest that cis -elements, including multiple HLR1 sequences, differently regulate the activities of dual promoters of the psaAB genes to achieve the fine-tuning of the gene expression.
  American Society for Microbiology, Scientific journal
  DOI：https://doi.org/10.1128/jb.00444-10
  DOI ID：10.1128/jb.00444-10, ISSN：0021-9193, eISSN：1098-5530
• The Response Regulator RpaB Binds to the Upstream Element of Photosystem I Genes To Work for Positive Regulation under Low-Light Conditions in Synechocystis sp. Strain PCC 6803
  Yurie Seino; Tomoko Takahashi; Yukako Hihara
  Journal of Bacteriology, Volume：191, Number：5, First page：1581, Last page：1586, Mar. 2009, [Reviewed]
  ABSTRACT
  
  The coordinated high-light response of genes encoding subunits of photosystem I (PSI) is achieved by the AT-rich region located just upstream of the core promoter in Synechocystis sp. strain PCC 6803. The upstream element enhances the basal promoter activity under low-light conditions, whereas this positive regulation is lost immediately after the shift to high-light conditions. In this study, we focused on a high-light regulatory 1 (HLR1) sequence included in the upstream element of every PSI gene examined. A gel mobility shift assay revealed that a response regulator RpaB binds to the HLR1 sequence in PSI promoters. Base substitution in the HLR1 sequence or decrease in copy number of the rpaB gene resulted in decrease in the promoter activity of PSI genes under low-light conditions. These observations suggest that RpaB acts as a transcriptional activator for PSI genes. It is likely that RpaB binds to the HLR1 sequence under low-light conditions and works for positive regulation of PSI genes and for negative regulation of high-light-inducible genes depending on the location of the HLR1 sequence within target promoters.
  American Society for Microbiology, Scientific journal
  DOI：https://doi.org/10.1128/jb.01588-08
  DOI ID：10.1128/jb.01588-08, ISSN：0021-9193, eISSN：1098-5530

• The Molecular Biology Society of Japan
• The Japanese Society for Virology
• The RNA Society of Japan
• Nucleic Acids Therapeutics Society of Japan

• The Canon Foundation, Science and Technology that Achieve a Good Future　　　　　　　　　　　　　　　
  2023
  Tomoko Takahashi, Principal investigator
• The MSD Life Science Foundation　　　　　　　　　　　　　　　
  2023
  Tomoko Takahashi, Principal investigator
• The Takeda Science Foundation　　　　　　　　　　　　　　　
  2022
  Tomoko Takahashi, Principal investigator
• The Hitachi Global Foundation　　　　　　　　　　　　　　　
  2021
  Tomoko Takahashi, Principal investigator
• The Naito Foundation, The 52nd Naito Research Grant, Dec. 2020
  Tomoko Takahashi, Principal investigator
• The SECOM Science and Technology Foundation, The SECOM challenge grant, Apr. 2020
  Tomoko Takahashi, Principal investigator
• Antiviral gene expression network regulated by endogenous microRNAs in human cells　　　　　　　　　　　　　　　
  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Early-Career Scientists, 01 Apr. 2018 - 31 Mar. 2020
  Takahashi Tomoko
  Grant amount(Total)：4160000, Direct funding：3200000, Indirect funding：960000
  During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or RIG-I-like receptors (RLRs) in mammalian cells. Activation of these virus sensor proteins induces type-I interferon production and represses viral replication. We reported that an RLR family member, LGP2, modulates RNA silencing by interacting with an RNA silencing enhancer, TRBP and LGP2 enhances apoptosis by upregulating apoptosis regulatory genes during viral infection via the interaction. Our findings may shed light on the mechanism of apoptosis, induced by the TRBP-bound miRNAs through the interaction of TRBP with LGP2, as an antiviral defense system in mammalian cells.
  Grant number：18K15178
• Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for Young Scientists, Apr. 2018 - Mar. 2020
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• The Ito Science Foundation, The 53rd Research Grant, 2020
  Tomoko Takahashi, Principal investigator
• JGC-S Scholarship Foundation, The Research Grant 2020, 2020
  Tomoko Takahashi, Principal investigator
• The NOVARTIS Foundation (Japan) for the Promotion of Science, Novartis research grant, 2020
  Tomoko Takahashi, Principal investigator
• The Koyanagi foundation, The Research Grant 2020, 2020
  Tomoko Takahashi, Principal investigator
• Crosstalk between RNA silencing and antiviral response in mammalian cells　　　　　　　　　　　　　　　
  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Young Scientists (B), 01 Apr. 2015 - 31 Mar. 2017
  Takahashi Tomoko, The University of Tokyo
  Grant amount(Total)：4160000, Direct funding：3200000, Indirect funding：960000
  The siRNAs and miRNAs are small non-coding RNAs that mediate mRNA cleavage, degradation, and/or translational repression by a mechanism known as RNA silencing. RNA viruses infected into human cells are recognized by virus sensor proteins to activate interferon expression as an antiviral defense system. Here, we revealed that RNA silencing and antiviral defense system are mutually regulated by their components.
  Grant number：15K19124
• Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for Young Scientists (B), Apr. 2015 - Mar. 2017
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• The Uehara Memorial Foundation, The Research Incentive Grant, 2017
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• The Inamori Foundation, The Inamori Grant, 2016
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• The Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care, The Scholarship Grant for Research in Basic Medical Sciences and Medical Care, Apr. 2014
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for JSPS Fellows, Apr. 2011 - Mar. 2014
  Tomoko Takahashi, Principal investigator
  Competitive research funding
• 二本鎖ＲＮＡ結合タンパク質ＴＲＢＰの遺伝子サイレンシングにおける機能　　　　　　　　　　　　　　　
  2011 - 2013
  Grant amount(Total)：1900000, Direct funding：1900000
  Grant number：11J08395