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Article ; Online: Generation of Specific Aptamers.

Liu, Shuang / Suzuki, Yasuyuki / Inui, Makoto

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2766, Page(s) 129–137

Abstract: Nucleic acid aptamers are therapeutic agents consisting of short single-strand DNA or RNA oligonucleotides, which have the ability to bind to target therapeutic molecules with high affinity and specificity and have been developed as potent drugs for the ... ...

Abstract	Nucleic acid aptamers are therapeutic agents consisting of short single-strand DNA or RNA oligonucleotides, which have the ability to bind to target therapeutic molecules with high affinity and specificity and have been developed as potent drugs for the treatment of rheumatoid arthritis. Aptamers have unique and advantageous features over antibodies, such as superior affinity with nano- or pico-molar dissociation constants and ease of chemical synthesis, modification, and inactivation by designing antisense sequences. In this chapter, using a DNA-oligonucleotide pool, the technology of proteoliposome-systematic evolution of ligands by exponential enrichment (SELEX) is introduced. By using this technique, potential therapeutic agents with high affinity and specificity could be obtained.
MeSH term(s)	Humans ; Antibodies ; Arthritis, Rheumatoid ; DNA, Single-Stranded ; Molar ; Oligonucleotides
Chemical Substances	Antibodies ; DNA, Single-Stranded ; Oligonucleotides
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3682-4_13
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Article: [Mechanisms of heart muscle contraction and relaxation and its modulation].

Inui, Makoto

Nihon rinsho. Japanese journal of clinical medicine

2016 Volume 74 Suppl 4 Pt 1, Page(s) 43–48

MeSH term(s)	Animals ; Heart Failure/physiopathology ; Humans ; Muscle Relaxation/physiology ; Myocardial Contraction/physiology
Language	Japanese
Publishing date	2016-06-20
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390903-7
ISSN	0047-1852
ISSN	0047-1852
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Zs.A 429: Show issues

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Article ; Online: Postnatal Pdzrn3 deficiency causes acute muscle atrophy without alterations in endplate morphology.

Kawai-Takaishi, Minako / Miyagawa, Yoshihiro / Honda, Takeshi / Inui, Makoto / Hosoyama, Tohru

Biochemical and biophysical research communications

2024 Volume 696, Page(s) 149542

Abstract: PDZ domain-containing RING finger family protein 3 (PDZRN3) is expressed in various tissues, including the skeletal muscle. Although PDZRN3 plays a crucial role in the terminal differentiation of myoblasts and synaptic growth/maturation in myogenesis, ... ...

Abstract	PDZ domain-containing RING finger family protein 3 (PDZRN3) is expressed in various tissues, including the skeletal muscle. Although PDZRN3 plays a crucial role in the terminal differentiation of myoblasts and synaptic growth/maturation in myogenesis, the role of this molecule in postnatal muscles is completely unknown despite its lifelong expression in myofibers. In this study, we aimed to elucidate the function of PDZRN3 in mature myofibers using myofiber-specific conditional knockout mice. After tamoxifen injection, PDZRN3 deficiency was confirmed in both fast and slow myofibers of Myf6-CreER
MeSH term(s)	Mice ; Animals ; Muscle, Skeletal/metabolism ; Muscular Atrophy/metabolism ; Neuromuscular Junction/pathology ; Sarcopenia/pathology ; Myoblasts/metabolism ; Mice, Knockout ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	PDZRN3 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2024.149542
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Article ; Online: PDZRN3 protects against apoptosis in myoblasts by maintaining cyclin A2 expression.

Honda, Takeshi / Inui, Makoto

Scientific reports

2020 Volume 10, Issue 1, Page(s) 1140

Abstract: PDZRN3 is a PDZ domain-containing RING-finger family protein that functions in various developmental processes. We previously showed that expression of PDZRN3 is induced together with that of MyoD during the early phase of skeletal muscle regeneration in ...

Abstract	PDZRN3 is a PDZ domain-containing RING-finger family protein that functions in various developmental processes. We previously showed that expression of PDZRN3 is induced together with that of MyoD during the early phase of skeletal muscle regeneration in vivo. We here show that PDZRN3 suppresses apoptosis and promotes proliferation in myoblasts in a manner dependent on cyclin A2. Depletion of PDZRN3 in mouse C2C12 myoblasts by RNA interference reduced the proportion of Ki-67-positive cells and the level of Akt phosphorylation, implicating PDZRN3 in regulation of both cell proliferation and apoptosis. Exposure of C2C12 cells as well as of C3H10T1/2 mesenchymal stem cells and NIH-3T3 fibroblasts to various inducers of apoptosis including serum deprivation resulted in a greater increase in the amount of cleaved caspase-3 in PDZRN3-depleted cells than in control cells. The abundance of cyclin A2 was reduced in PDZRN3-depleted C2C12 myoblasts, as was that of Mre11, which contributes to the repair of DNA damage. Overexpression of cyclin A2 restored the expression of Mre11 and Ki-67 as well as attenuated caspase-3 cleavage in PDZRN3-depleted cells deprived of serum. These results indicate that PDZRN3 suppresses apoptosis and promotes proliferation in myoblasts and other cell types by maintaining cyclin A2 expression.
MeSH term(s)	Animals ; Apoptosis/physiology ; Cell Adhesion ; Cell Cycle ; Cell Division ; Cells, Cultured ; Cyclin A2/biosynthesis ; Cyclin A2/genetics ; DNA Damage ; Down-Regulation ; Gene Expression Regulation ; Genomic Instability ; Mesenchymal Stem Cells/metabolism ; Mice ; Myoblasts/cytology ; Myoblasts/metabolism ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Ubiquitin-Protein Ligases/physiology
Chemical Substances	CCNA2 protein, mouse ; Cyclin A2 ; RNA, Messenger ; RNA, Small Interfering ; PDZRN3 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2020-01-24
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/s41598-020-58116-1
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Article ; Online: PDZRN3 regulates differentiation of myoblasts into myotubes through transcriptional and posttranslational control of Id2.

Honda, Takeshi / Inui, Makoto

Journal of cellular physiology

2018 Volume 234, Issue 3, Page(s) 2963–2972

Abstract: PDZRN3 (also known as LNX3) is a member of the PDZ domain-containing RING finger protein family. We previously showed that PDZRN3 is essential for differentiation of myoblasts into myotubes and that depletion of PDZRN3 inhibits such differentiation ... ...

Abstract	PDZRN3 (also known as LNX3) is a member of the PDZ domain-containing RING finger protein family. We previously showed that PDZRN3 is essential for differentiation of myoblasts into myotubes and that depletion of PDZRN3 inhibits such differentiation downstream of the upregulation of myogenin, a basic helix-loop-helix (bHLH) transcription factor required for completion of the differentiation process. However, the mechanism by which PDZRN3 controls this process has remained unclear. Myogenin is rendered active during the late stage of myogenic differentiation by the downregulation of Id2, a negative regulator of bHLH transcription factors. We now show that depletion of PDZRN3 inhibits the differentiation of C2C12 cells by inducing the upregulation of Id2 and thereby delaying its downregulation. Knockdown of Id2 by RNA interference restores the differentiation of PDZRN3-depleted cells. Luciferase reporter assays revealed that a putative binding site for STAT5b in the Id2 gene promoter is required for the upregulation of Id2 expression by PDZRN3 depletion. In addition, the amount of phosphorylated Id2 was reduced and that of the nonphosphorylated protein concomitantly increased in PDZRN3-depleted cells, with the inhibitory effect of Id2 on bHLH transcription factors having previously been shown to be attenuated by phosphorylation of Id2 catalyzed by the complex of Cdk2 with cyclin A2 or E1. Indeed, the expression of cyclin A2, but not that of cyclin E1, was reduced in PDZRN3-depleted cells. Our results thus indicate that PDZRN3 plays a key role in the differentiation of myoblasts into myotubes by regulating Id2 at both transcriptional and posttranslational levels.
MeSH term(s)	Animals ; Binding Sites ; Cell Differentiation/genetics ; Cell Line ; Cyclin A2/genetics ; DNA-Binding Proteins/genetics ; Humans ; Inhibitor of Differentiation Protein 2/genetics ; Mice ; Muscle Development/genetics ; Muscle Fibers, Skeletal/metabolism ; Myoblasts/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Processing, Post-Translational/genetics ; STAT5 Transcription Factor/genetics ; Transcription, Genetic ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Cyclin A2 ; DNA-Binding Proteins ; Idb2 protein, mouse ; Inhibitor of Differentiation Protein 2 ; STAT5 Transcription Factor ; Stat5b protein, mouse ; PDZRN3 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2018-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.27113
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Article ; Online: Calcium/calmodulin-dependent regulation of Rac GTPases and Akt in histamine-induced chemotaxis of mast cells.

Honda, Takeshi / Nishio, Yusuke / Sakai, Hiroki / Asagiri, Masataka / Yoshimura, Kiyoshi / Inui, Makoto / Kuramasu, Atsuo

Cellular signalling

2021 Volume 83, Page(s) 109973

Abstract: Histamine induces chemotaxis of mast cells through the histamine ... ...

Abstract	Histamine induces chemotaxis of mast cells through the histamine H
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Signaling/drug effects ; Calmodulin/metabolism ; Chemotaxis/drug effects ; Female ; Histamine/metabolism ; Histamine/pharmacology ; Mice ; Mice, Inbred BALB C ; Neuropeptides/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein/metabolism ; RAC2 GTP-Binding Protein
Chemical Substances	Calmodulin ; Neuropeptides ; Rac1 protein, mouse ; Histamine (820484N8I3) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; rac GTP-Binding Proteins (EC 3.6.5.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2021.109973
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Article ; Online: Distinct Roles of Small GTPases Rac1 and Rac2 in Histamine H

Kuramasu, Atsuo / Wakabayashi, Mie / Inui, Makoto / Yanai, Kazuhiko

The Journal of pharmacology and experimental therapeutics

2018 Volume 367, Issue 1, Page(s) 9–19

Abstract: Histamine induces chemotaxis of mast cells through the ... ...

Abstract	Histamine induces chemotaxis of mast cells through the H
MeSH term(s)	Animals ; Calcium/metabolism ; Chemotaxis ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Gene Knockdown Techniques ; Histamine/metabolism ; Mast Cells/cytology ; Mice ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/metabolism ; RNA, Small Interfering/genetics ; Receptors, Histamine H4/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/deficiency ; rac GTP-Binding Proteins/genetics ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein/deficiency ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism ; RAC2 GTP-Binding Protein
Chemical Substances	RNA, Small Interfering ; Receptors, Histamine H4 ; Histamine (820484N8I3) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; rac GTP-Binding Proteins (EC 3.6.5.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-07-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.118.249706
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Article ; Online: Generation of Specific Aptamers.

Liu, Shuang / Suzuki, Yasuyuki / Inui, Makoto

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1868, Page(s) 113–121

Abstract: Nucleic acid aptamers are therapeutic agents consisting of short single-strand DNA or RNA oligonucleotides, which have the ability to bind to target therapeutic molecules with high affinity and specificity, and have been developed as potent drugs for the ...

Abstract	Nucleic acid aptamers are therapeutic agents consisting of short single-strand DNA or RNA oligonucleotides, which have the ability to bind to target therapeutic molecules with high affinity and specificity, and have been developed as potent drugs for the treatment of rheumatoid arthritis. Aptamers have unique and advantageous features over antibodies, such as superior affinity with nano- or pico-molar dissociation constants, and ease of chemical synthesis, modification, and inactivation by designing antisense sequences. In this chapter, using a DNA-oligonucleotide pool, the technology of proteoliposome-systematic evolution of ligands by exponential enrichment (SELEX) is introduced. By using this technique, potential therapeutic agents with high affinity and specificity could be obtained.
MeSH term(s)	Aptamers, Nucleotide/metabolism ; DNA, Single-Stranded/metabolism ; Oligonucleotides/metabolism ; Proteolipids/metabolism ; SELEX Aptamer Technique/methods
Chemical Substances	Aptamers, Nucleotide ; DNA, Single-Stranded ; Oligonucleotides ; Proteolipids ; proteoliposomes
Language	English
Publishing date	2018-09-22
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8802-0_11
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Article: Local immune checkpoint blockade therapy by an adenovirus encoding a novel PD-L1 inhibitory peptide inhibits the growth of colon carcinoma in immunocompetent mice.

Ishiguro, Susumu / Upreti, Deepa / Bassette, Molly / Singam, E R Azhagiya / Thakkar, Ravindra / Loyd, Mayme / Inui, Makoto / Comer, Jeffrey / Tamura, Masaaki

Translational oncology

2022 Volume 16, Page(s) 101337

Abstract: A novel peptide that interferes with the PD-1/PD-L1 immune checkpoint pathway, termed PD-L1 inhibitory peptide 3 (PD-L1ip3), was computationally designed, experimentally validated for its specific binding to PD-L1, and evaluated for its antitumor effects ...

Abstract	A novel peptide that interferes with the PD-1/PD-L1 immune checkpoint pathway, termed PD-L1 inhibitory peptide 3 (PD-L1ip3), was computationally designed, experimentally validated for its specific binding to PD-L1, and evaluated for its antitumor effects in cell culture and in a mouse colon carcinoma syngeneic murine model. In several cell culture studies, direct treatment with PD-L1ip3, but not a similar peptide with a scrambled sequence, substantially increased death of CT26 colon carcinoma cells when co-cultured with murine CD8
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233
ISSN	1936-5233
DOI	10.1016/j.tranon.2021.101337
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Article ; Online: Peptide therapies for ocular surface disturbances based on fibronectin-integrin interactions.

Nishida, Teruo / Inui, Makoto / Nomizu, Motoyoshi

Progress in retinal and eye research

2015 Volume 47, Page(s) 38–63

Abstract: The condition of the corneal epithelium is a critical determinant of corneal transparency and clear vision. The corneal epithelium serves as a barrier to protect the eye from external insults, with its smooth surface being essential for its optical ... ...

Abstract	The condition of the corneal epithelium is a critical determinant of corneal transparency and clear vision. The corneal epithelium serves as a barrier to protect the eye from external insults, with its smooth surface being essential for its optical properties. Disorders of the corneal epithelium include superficial punctate keratopathy, corneal erosion, and persistent epithelial defects (PEDs). The prompt resolution of these disorders is important for minimization of further damage to the cornea. Currently available treatment modalities for corneal epithelial disorders are based on protection of the ocular surface in order to allow natural healing to proceed. PEDs remain among the most difficult corneal conditions to treat, however. On the basis of characterization of the pathobiology of PEDs at the cell and molecular biological levels, we have strived to develop new modes of treatment for these defects. These treatments rely on two key concepts: provision of a substrate, such as the adhesive glycoprotein fibronectin, for the attachment and migration of corneal epithelial cells, and activation of these cells by biological agents such as the combination of substance P and insulin-like growth factor-1 (IGF-1). Central to both approaches is the role of the fibronectin-integrin system in corneal epithelial wound healing. Determination of the minimum amino acid sequences required for the promotion of corneal epithelial wound closure by fibronectin (PHSRN) and by substance P (FGLM-amide) plus IGF-1 (SSSR) has led to the development of peptide eyedrops for the treatment of PEDs that are free of adverse effects of the parent molecules.
MeSH term(s)	Animals ; Corneal Diseases/drug therapy ; Corneal Diseases/physiopathology ; Disease Models, Animal ; Epithelium, Corneal/drug effects ; Epithelium, Corneal/physiopathology ; Fibronectins/physiology ; Fibronectins/therapeutic use ; Humans ; Insulin-Like Growth Factor I/physiology ; Integrins/physiology ; Integrins/therapeutic use ; Molecular Targeted Therapy/methods ; Peptides/therapeutic use ; Substance P/physiology ; Wound Healing/physiology
Chemical Substances	Fibronectins ; Integrins ; Peptides ; Substance P (33507-63-0) ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2015-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1182683-6
ISSN	1873-1635 ; 1350-9462
ISSN (online)	1873-1635
ISSN	1350-9462
DOI	10.1016/j.preteyeres.2015.01.004
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