Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Keiko Tsuji Wakisaka"'
Publikováno v:
Mobile DNA, Vol 9, Iss 1, Pp 1-16 (2018)
Abstract Background P-element transposition in the genome causes P-M hybrid dysgenesis in Drosophila melanogaster. Maternally deposited piRNAs suppress P-element transposition in the progeny, linking them to P-M phenotypes; however, the role of zygot
Externí odkaz:
https://doaj.org/article/361dbe91c11e4e73824669cd60916be0
Publikováno v:
Mobile DNA, Vol 8, Iss 1, Pp 1-10 (2017)
Abstract Background Transposition of P elements in the genome causes P–M hybrid dysgenesis in Drosophila melanogaster. For the P strain, the P–M phenotypes are associated with the ability to express a class of small RNAs, called piwi-interacting
Externí odkaz:
https://doaj.org/article/674fd588a4264a599b6e5559fe40d079
Autor:
Ibuki Ueoka, Keiko Tsuji Wakisaka, Hideki Yoshida, Ikuko Mizuta, Yuuka Muraoka, Mizuki Yamaguchi, Jo Shimizu, Masamitsu Yamaguchi
Publikováno v:
NeuroReport. 30:1039-1047
AlkB family proteins are enzymes that repair alkylated DNA and RNA by oxidative demethylation. Nine homologs have been identified and characterized in mammals. ALKBH1 is conserved among metazoans including Drosophila. Although the ALKBH1 mouse homolo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5b020212cc91e420386dbb64f32aba90
https://doi.org/10.1097/wnr.0000000000001323
https://doi.org/10.1097/wnr.0000000000001323
Autor:
Takahiko Tokuda, Keiko Tsuji Wakisaka, Seiko Ohno, Kojiro Suda, Tomoki Hirashima, Hideki Yoshida, Ryo Tanaka, Masanobu Itoh, Yumiko Azuma, Yuuka Muraoka, Kenji Ichiyanagi, Satoshi Asada, Masamitsu Yamaguchi
Publikováno v:
Brain Research. 1708:207-219
piRNAs, small non-coding RNAs, were considered to be restricted to germline cells. Although they have recently been detected in somatic cells including neurons, it remains unclear how piRNA biogenesis is involved in neuronal diseases. We herein exami
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7f547e580025ef61107faaa3c906aa11
https://doi.org/10.1016/j.brainres.2018.12.028
https://doi.org/10.1016/j.brainres.2018.12.028
Publikováno v:
Methods in Molecular Biology ISBN: 9781071614945
Parkinson's disease (PD) is a neurodegenerative disorder that affects the motor system. PD is characterized by the accumulation of intracellular protein aggregates, Lewy bodies, and Lewy neurites, composed primarily of the protein α-synuclein. Thus,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::154ebf672ba611e460aecc144df415ac
https://doi.org/10.1007/978-1-0716-1495-2_11
https://doi.org/10.1007/978-1-0716-1495-2_11
Autor:
Keiko Tsuji Wakisaka, Yuzuru Imai
Publikováno v:
Frontiers in Bioscience. 24:1440-1451
Small non-coding PIWI-interacting RNAs (piRNAs) silence the expression of transposable elementsof eukaryotic genomes in germline cells. Additionally, piRNAs regulate chromatin modifications, such as trimethylation of histone H3 lysine 9 (H3K9me3) or
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b0d71533f7a082f3e98cf7138de675c
https://doi.org/10.2741/4789
https://doi.org/10.2741/4789
Publikováno v:
Mobile DNA
Mobile DNA, Vol 9, Iss 1, Pp 1-16 (2018)
Mobile DNA, Vol 9, Iss 1, Pp 1-16 (2018)
Background P-element transposition in the genome causes P-M hybrid dysgenesis in Drosophila melanogaster. Maternally deposited piRNAs suppress P-element transposition in the progeny, linking them to P-M phenotypes; however, the role of zygotic piRNAs
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::44feab159ef3338fd45132726d142c6c
https://doi.org/10.1186/s13100-018-0110-y
https://doi.org/10.1186/s13100-018-0110-y
Publikováno v:
Journal of the Yamashina Institute for Ornithology. 47:17-23
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5ffec4ab5473313268cbdd625f884c0c
https://doi.org/10.3312/jyio.47.17
https://doi.org/10.3312/jyio.47.17
Publikováno v:
Japanese Journal of Ornithology. 63:43-47
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8e3757b74771ac5fc30fcad06d1c2b0b
https://doi.org/10.3838/jjo.63.43
https://doi.org/10.3838/jjo.63.43
Autor:
Seiko Ohno, Takashi Ashihara, Kenichi Dochi, Takahiro Ishii, Hiroshi Matsuura, Keiko Tsuji-Wakisaka, Masaharu Akao, Takeru Makiyama, Minoru Horie, Futoshi Toyoda
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1812(11):1452-1459
Background. KCNQ1 gene encodes the delayed rectifier K+ channel in cardiac muscle, and its mutations cause long QT syndrome type 1 (LQT1). Especially exercise-related cardiac events predominate in LQT1. We previously reported that a KCNQ1 splicing mu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c17b5d7ee8b3a03929dd8b73d84c26fa