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25 papers found.
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Mianserin suppresses R-spondin 2-induced activation of Wnt/β-catenin signaling in chondrocytes and prevents cartilage degradation in a rat model of osteoarthritis

Aberrant activation of the Wnt/β-catenin signaling pathway promotes the progression of osteoarthritis (OA). We previously reported that R-spondin 2 (Rspo2), an activator of the Wnt/β-catenin signaling, facilitates differentiation of proliferating chondrocytes into hypertrophic chondrocytes by enhancing Wnt/β-catenin signaling in endochondral ossification. However, the role of...

Lack of Fgf18 causes abnormal clustering of motor nerve terminals at the neuromuscular junction with reduced acetylcholine receptor clusters

FGF receptor 2 is involved in the formation of the neuromuscular junction (NMJ), but its in vivo ligand remains to be determined. Laser capture microdissection of the mouse spinal motor neurons (SMNs) revealed that Fgf18 mRNA is highly expressed in SMNs in adults. Expression of Fgf18 mRNA was the highest in the spinal cord at embryonic day (E) 15.5, which gradually decreased to...

Fluoxetine ameliorates cartilage degradation in osteoarthritis by inhibiting Wnt/β-catenin signaling

Contributions Conceptualization: Kentaro Miyamoto, Bisei Ohkawara, Kinji Ohno. Data curation: Kentaro Miyamoto, Bisei Ohkawara. Formal analysis: Kentaro Miyamoto, Bisei Ohkawara, Mikako Ito, Akio Masuda ... , Akihiro Hirakawa. Methodology: Bisei Ohkawara, Mikako Ito, Akio Masuda, Akihiro Hirakawa. Project administration: Bisei Ohkawara. Resources: Tadahiro Sakai, Hideki Hiraiwa, Takashi Hamada. Supervision

Wnt/β-catenin signaling suppresses expressions of Scx, Mkx, and Tnmd in tendon-derived cells

acquisition: Yasuzumi Kishimoto, Naoki Ishiguro, Kinji Ohno. Investigation: Yasuzumi Kishimoto, Bisei Ohkawara. Methodology: Yasuzumi Kishimoto, Mikako Ito, Akio Masuda, Chisa Shukunami, Denitsa Docheva ... . Project administration: Bisei Ohkawara, Tadahiro Sakai, Kinji Ohno. Resources: Chisa Shukunami, Denitsa Docheva. Supervision: Tadahiro Sakai, Mikako Ito, Akio Masuda, Naoki Ishiguro, Chisa Shukunami

Global identification of hnRNP A1 binding sites for SSO-based splicing modulation

Background Many pathogenic genetic variants have been shown to disrupt mRNA splicing. Besides splice mutations in the well-conserved splice sites, mutations in splicing regulatory elements (SREs) may deregulate splicing and cause disease. A promising therapeutic approach is to compensate for this deregulation by blocking other SREs with splice-switching oligonucleotides (SSOs...

Correction: Zonisamide Enhances Neurite Elongation of Primary Motor Neurons and Facilitates Peripheral Nerve Regeneration In Vitro and in a Mouse Model

, Kyotaro Ohta, Akio Masuda, Shiro Imagama, Naoki Ishiguro, Kinji Ohno OPEN ACCESS Regeneration In Vitro and in a Mouse Model. PLoS medium; provided the original author and source are - Fig 4 is incorrect

Zonisamide Enhances Neurite Elongation of Primary Motor Neurons and Facilitates Peripheral Nerve Regeneration In Vitro and in a Mouse Model

No clinically applicable drug is currently available to enhance neurite elongation after nerve injury. To identify a clinically applicable drug, we screened pre-approved drugs for neurite elongation in the motor neuron-like NSC34 cells. We found that zonisamide, an anti-epileptic and anti-Parkinson’s disease drug, promoted neurite elongation in cultured primary motor neurons and...

Collagen Q and anti-MuSK autoantibody competitively suppress agrin/LRP4/MuSK signaling

Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, JapanKenji Otsuka, Mikako Ito, Bisei Ohkawara, Akio Masuda, Yu Kawakami & Kinji OhnoDepartment of Neurology, Aichi Medical ... • PubMed • Google ScholarSearch for Mikako Ito in:Nature Research journals • PubMed • Google ScholarSearch for Bisei Ohkawara in:Nature Research journals • PubMed • Google ScholarSearch for Akio Masuda

Verapamil Protects against Cartilage Degradation in Osteoarthritis by Inhibiting Wnt/β-Catenin Signaling

In past years, the canonical Wnt/β-catenin signaling pathway has emerged as a critical regulator of cartilage development and homeostasis. FRZB, a soluble antagonist of Wnt signaling, has been studied in osteoarthritis (OA) animal models and OA patients as a modulator of Wnt signaling. We screened for FDA-approved drugs that induce FRZB expression and suppress Wnt/β-catenin...

Meclozine Facilitates Proliferation and Differentiation of Chondrocytes by Attenuating Abnormally Activated FGFR3 Signaling in Achondroplasia

Achondroplasia (ACH) is one of the most common skeletal dysplasias with short stature caused by gain-of-function mutations in FGFR3 encoding the fibroblast growth factor receptor 3. We used the drug repositioning strategy to identify an FDA-approved drug that suppresses abnormally activated FGFR3 signaling in ACH. We found that meclozine, an anti-histamine drug that has long been...

FUS-regulated region- and cell-type-specific transcriptome is associated with cell selectivity in ALS/FTLD

FUS is genetically and pathologically linked to amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). To clarify the RNA metabolism cascade regulated by FUS in ALS/FTLD, we compared the FUS-regulated transcriptome profiles in different lineages of primary cells from the central nervous system. The profiles of FUS-mediated gene expression and...

AG-dependent 3′-splice sites are predisposed to aberrant splicing due to a mutation at the first nucleotide of an exon

In pre-mRNA splicing, a conserved AG/G at the 3′-splice site is recognized by U2AF35. A disease-causing mutation abrogating the G nucleotide at the first position of an exon (E+1) causes exon skipping in GH1, FECH and EYA1, but not in LPL or HEXA. Knockdown of U2AF35 enhanced exon skipping in GH1 and FECH. RNA-EMSA revealed that wild-type FECH requires U2AF35 but wild-type LPL...

LRP4 third β-propeller domain mutations cause novel congenital myasthenia by compromising agrin-mediated MuSK signaling in a position-specific manner

Congenital myasthenic syndromes (CMS) are heterogeneous disorders in which the safety margin of neuromuscular transmission is compromised by one or more specific mechanisms. Using Sanger and exome sequencing in a CMS patient, we identified two heteroallelic mutations, p.Glu1233Lys and p.Arg1277His, in LRP4 coding for the postsynaptic low-density lipoprotein receptor-related...

Position-dependent FUS-RNA interactions regulate alternative splicing events and transcriptions

FUS is an RNA-binding protein that regulates transcription, alternative splicing, and mRNA transport. Aberrations of FUS are causally associated with familial and sporadic ALS/FTLD. We analyzed FUS-mediated transcriptions and alternative splicing events in mouse primary cortical neurons using exon arrays. We also characterized FUS-binding RNA sites in the mouse cerebrum with HITS...

CUGBP1 and MBNL1 preferentially bind to 3′ UTRs and facilitate mRNA decay

CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. We globally determined the in vivo RNA-binding sites of CUGBP1 and MBNL1. Interestingly, CUGBP1 and MBNL1 are both preferentially bound to 3′ UTRs. Analysis of CUGBP1- and MBNL1-bound 3′ UTRs demonstrated that both factors mediate accelerated mRNA decay...

Human branch point consensus sequence is yUnAy

Yeast carries a strictly conserved branch point sequence (BPS) of UACUAAC, whereas the human BPS is degenerative and is less well characterized. The human consensus BPS has never been extensively explored in vitro to date. Here, we sequenced 367 clones of lariat RT-PCR products arising from 52 introns of 20 human housekeeping genes. Among the 367 clones, a misincorporated...

Four parameters increase the sensitivity and specificity of the exon array analysis and disclose 25 novel aberrantly spliced exons in myotonic dystrophy

Tohru Matsuura Jun Shinmi Yoshinobu Amakusa Akio Masuda Mikako Ito Masanobu Kinoshita Hirokazu Furuya Koji Abe Tohru Ibi Ko Sahashi Kinji Ohno The authors of the above paper noticed an error in

hnRNP H enhances skipping of a nonfunctional exon P3A in CHRNA1 and a mutation disrupting its binding causes congenital myasthenic syndrome

In humans and great apes, CHRNA1 encoding the muscle nicotinic acetylcholine receptor α subunit carries an inframe exon P3A, the inclusion of which yields a nonfunctional α subunit. In muscle, the P3A(−) and P3A(+) transcripts are generated in a 1:1 ratio but the functional significance and regulation of the alternative splicing remain elusive. An intronic mutation (IVS3-8G>A...

Tannic acid facilitates expression of the polypyrimidine tract binding protein and alleviates deleterious inclusion of CHRNA1 exon P3A due to an hnRNP H-disrupting mutation in congenital myasthenic syndrome

We recently reported that the intronic splice-site mutation IVS3-8G>A of CHRNA1 that encodes the muscle nicotinic acetylcholine receptor α subunit disrupts binding of a splicing repressor, hnRNP H. This, in turn, results in exclusive inclusion of the downstream exon P3A. The P3A(+) transcript encodes a non-functional α subunit that comprises 50% of the transcripts in normal human...