Keio University · Medicine
Professor Masato Yano's research lab focuses on the molecular mechanisms underlying post-transcriptional gene regulation, particularly through RNA-binding proteins (RBPs), in neural development and disease. The lab investigates how RBPs such as Hu, Quaking, and Elavl family members control alternative splicing, mRNA stability, and translation during neuronal differentiation and in neurodevelopmental disorders. A central theme is understanding the role of signaling pathways—such as BMP/TGF-β—interconnected with RNA regulation in both normal development and pathological conditions like heterotopic ossification and cancer. The lab employs advanced techniques including HITS-CLIP, RNA-Seq, and conditional knockout models to decode RBP functions at the transcriptome level.
Figures are computed from collected data and may differ slightly.
The Hu family is a group of neuronal RNA-binding proteins required for neuronal differentiation in the developing nervous system. Previously, Hu proteins have been shown to enhance the stabilization and/or translation of target mRNAs, such as p21 (CIP1), by binding to AU-rich elements in untranslated regions (UTRs). In this study, we show that Hu induces p21 expression, cell cycle arrest, and neuronal differentiation in mouse neuroblastoma N1E-115 cells. p21 expression is also up-regulated durin
The transforming growth factor (TGF)-β family members, bone morphogenetic protein (BMP)-2 and TGF-β that signal via the receptor-regulated Smads (R-Smads) induce bone formation in vivo. The inhibitory Smads (I-Smads), Smad6 and Smad7, negatively regulate TGF-β family ligand signaling by competing with R-Smads for binding to activated type I receptors, and preventing R-Smad activation, Hence, the I-Smads potentially act as suppressors of bone formation although their effects on phenotypic changes
RNA regulation participates in many aspects of brain development. There is substantial evidence that RNA dysregulation is critical in the pathogenesis of neurodevelopmental disorders, neurological diseases, and cancer. Several gene families encode RNA-binding proteins (RNABPs) that bind directly to RNA and orchestrate the post-transcriptional regulation of gene expression, including pre-mRNA splicing, stability, and poly(A) site usage. Among neural RNABPs, the Elavl and Msi families are the focu
Fibrodysplasia ossificans progressiva is characterized by extensive ossification within muscle tissues, and its molecular pathogenesis is responsible for the constitutively activating mutation (R206H) of the bone morphogenetic protein type 1 receptor, activin-like kinase 2 (ALK2). In this study, we investigated the effects of implanting ALK2 (R206H)-transfected myoblastic C2C12 cells into nude mice on osteoclast formation during heterotopic ossification in muscle and subcutaneous tissues. The im
RNA-binding proteins (RBPs) control many types of post-transcriptional regulation, including mRNA splicing, mRNA stability, and translational efficiency, by directly binding to their target RNAs and their mutation and dysfunction are often associated with several human neurological diseases and tumorigenesis. Crosslinking immunoprecipitation (CLIP), coupled with high-throughput sequencing (HITS-CLIP), is a powerful technique for investigating the molecular mechanisms underlying disease pathogene
A set of tissue-specific splicing factors are thought to govern alternative splicing events during neural progenitor cell (NPC)-to-neuron transition by regulating neuron-specific exons. Here, we propose one such factor, RNA-binding protein Quaking 5 (Qki5), which is specifically expressed in the early embryonic neural stem cells. We performed mRNA-SEQ (Sequence) analysis using mRNAs obtained by developing cerebral cortices in <i>Qk</i> (<i>Quaking</i>) conditional knockout (cKO) mice. As expecte
The HMM-based method along with the conventional pattern matching approach can contribute to reducing costly and laborious wet-lab experiments to perform functional analysis on a given set of potential G-quadruplexes of interest. The C++ and Perl programs are available at http://tcs.cira.kyoto-u.ac.jp/~ykato/program/g4hmm/.
Microprocessor complex, including DiGeorge syndrome critical region gene 8 (DGCR8) and DROSHA, recognizes and cleaves primary transcripts of microRNAs (pri-miRNAs) in the maturation of canonical miRNAs. The study of DGCR8 haploinsufficiency reveals that the efficiency of this activity varies for different miRNA species. It is thought that this variation might be associated with the risk of schizophrenia with 22q11 deletion syndrome caused by disruption of the DGCR8 gene. However, the underlying
Nanosheet-derived H<i><sub>x</sub></i>(Ni<sub>1/3</sub>Co<sub>1/3</sub>Mn<sub>1/3</sub>)O₂ was prepared by restacking (Ni<sub>1/3</sub>Co<sub>1/3</sub>Mn<sub>1/3</sub>)O₂ nanosheets with large or small lateral sizes and their electrochemical properties in a 1 M KOH aqueous solution; microstructural factors were compared with those of bulk H<i><sub>x</sub></i>(Ni<sub>1/3</sub>Co<sub>1/3</sub>Mn<sub>1/3</sub>)O₂ (HNCM). The electrodes composed of small nanosheets exhibited very large capacitances
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