Maiko Inagaki

Works (6)

Updated: July 11th, 2023 21:14

2019 journal article

Coordinating Tissue Regeneration Through Transforming Growth Factor-beta Activated Kinase 1 Inactivation and Reactivation

STEM CELLS, 37(6), 766–778.

By: H. Hsieh, S. Agarwal *, D. Cholok *, S. Loder *, K. Kaneko *, A. Huber *, M. Chung *, K. Ranganathan * ...

Contributors: H. Hsieh, S. Agarwal *, D. Cholok *, S. Loder *, K. Kaneko *, A. Huber *, M. Chung *, K. Ranganathan * ...

author keywords: Cellular proliferation; Differentiation; Progenitor cells; Proliferation; Stem; progenitor cell; Tissue regeneration
MeSH headings : Animals; Bone Regeneration / drug effects; Bone Regeneration / genetics; Cell Differentiation / drug effects; Cell Proliferation / drug effects; DNA Nucleotidyltransferases / genetics; DNA Nucleotidyltransferases / metabolism; Female; Founder Effect; Fractures, Bone / drug therapy; Fractures, Bone / enzymology; Fractures, Bone / genetics; Fractures, Bone / pathology; Gene Expression Regulation; Integrases / genetics; Integrases / metabolism; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / genetics; Male; Mesenchymal Stem Cells / cytology; Mesenchymal Stem Cells / drug effects; Mesenchymal Stem Cells / enzymology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Osteoblasts / cytology; Osteoblasts / drug effects; Osteoblasts / enzymology; Primary Cell Culture; Protein Kinase Inhibitors / pharmacology; Signal Transduction; Skull / drug effects; Skull / injuries; Skull / metabolism; Wound Healing / drug effects; Wound Healing / genetics
TL;DR: It is demonstrated that loss of transforming growth factor‐β activated kinase 1 (TAK1) signaling reduces inappropriate tissue formation (heterotopic ossification) through reduced cellular differentiation, and the importance of both the “drug on” and "drug off" states during regenerative therapy is revealed. (via Semantic Scholar)
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3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: July 22, 2019

2014 journal article

Tak1, Smad4 and Trim33 redundantly mediate TGF-beta 3 signaling during palate development

DEVELOPMENTAL BIOLOGY, 398(2), 231–241.

By: J. Lane*, K. Yumoto*, M. Azhar *, J. Ninomiya-Tsuji n , M. Inagaki n, Y. Hu*, C. Deng *, J. Kim *, Y. Mishina *, V. Kaartinen *

Contributors: J. Lane*, K. Yumoto*, M. Azhar *, J. Ninomiya-Tsuji n , M. Inagaki n, Y. Hu*, C. Deng *, J. Kim *, Y. Mishina *, V. Kaartinen *

author keywords: TGF-beta 3 signaling; Palatogenesis; Tak1; Smad4; Trim33
MeSH headings : Animals; Apoptosis / genetics; Cell Fusion; Cell Proliferation; Crosses, Genetic; Embryo, Mammalian / metabolism; Enzyme Activation; Epithelial Cells / metabolism; Epithelium / metabolism; Female; Gene Deletion; Gene Expression Regulation, Developmental; MAP Kinase Kinase Kinases / metabolism; Male; Matrix Metalloproteinase 13 / metabolism; Mice, Knockout; Models, Biological; Mutation / genetics; Organ Specificity; Palate / abnormalities; Palate / embryology; Palate / enzymology; Palate / metabolism; Signal Transduction; Smad4 Protein / metabolism; Transcription Factors / metabolism; Transforming Growth Factor beta3 / metabolism
TL;DR: The data reveal added complexity in TGF-β signaling during palatogenesis and demonstrate that functionally redundant pathways involving Smad4, Tak1 and Trim33 regulate palatal epithelial fusion. (via Semantic Scholar)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2013 journal article

TGF-beta-activated Kinase 1 (Tak1) Mediates Agonist-induced Smad Activation and Linker Region Phosphorylation in Embryonic Craniofacial Neural Crest-derived Cells

JOURNAL OF BIOLOGICAL CHEMISTRY, 288(19), 13467–13480.

By: K. Yumoto*, P. Thomas*, J. Lane*, K. Matsuzaki*, M. Inagaki n, J. Ninomiya-Tsuji n , G. Scott*, M. Ray* ...

Contributors: K. Yumoto*, P. Thomas*, J. Lane*, K. Matsuzaki*, M. Inagaki n, J. Ninomiya-Tsuji n , G. Scott*, M. Ray* ...

MeSH headings : Amino Acid Motifs; Animals; Cells, Cultured; Cleft Palate / enzymology; Cleft Palate / genetics; Ectoderm / cytology; Female; Gene Expression Regulation, Developmental; Head / embryology; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / physiology; Male; Mandible / abnormalities; Mice; Mice, Transgenic; Mitogen-Activated Protein Kinases / metabolism; Neural Crest / cytology; Phosphorylation; Protein Processing, Post-Translational; Protein Serine-Threonine Kinases / metabolism; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta / metabolism; Signal Transduction; Smad Proteins / metabolism; Smad Proteins, Receptor-Regulated / metabolism; TGF-beta Superfamily Proteins / physiology; Wnt1 Protein / genetics; Wnt1 Protein / metabolism
TL;DR: It is suggested that in neural crest-derived ecto-mesenchymal cells, Tak1 provides a critical point of intersection in a complex dialogue between the canonical and noncanonical arms of TGF-β superfamily signaling required for normal craniofacial development. (via Semantic Scholar)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2012 journal article

TAK1 (MAP3K7) Signaling Regulates Hematopoietic Stem Cells through TNF-Dependent and -Independent Mechanisms

PLoS ONE, 7(11), e51073.

By: G. Takaesu *, M. Inagaki n, K. Takubo *, Y. Mishina *, P. Hess n , G. Dean  n, A. Yoshimura *, K. Matsumoto * ...

Contributors: G. Takaesu *, M. Inagaki n, K. Takubo *, Y. Mishina *, P. Hess n , G. Dean  n, A. Yoshimura *, K. Matsumoto *, T. Suda *, J. Ninomiya-Tsuji n 

Ed(s): M. Tjwa

MeSH headings : Adaptor Proteins, Signal Transducing / metabolism; Animals; Antigens, Surface / metabolism; Bone Marrow Cells / enzymology; Cell Death; Cell Proliferation; Chimerism; Hematopoietic Stem Cells / cytology; Hematopoietic Stem Cells / enzymology; Humans; MAP Kinase Kinase Kinases / deficiency; MAP Kinase Kinase Kinases / metabolism; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; Receptors, Tumor Necrosis Factor, Type I / deficiency; Receptors, Tumor Necrosis Factor, Type I / metabolism; Time Factors; Tumor Necrosis Factor-alpha / metabolism
TL;DR: The results indicate that TAB1- or TAB2-dependent activation of TAK1 is required for maintenance of the hematopoietic system through two mechanisms: one is prevention of TNF-dependent cell death and the other is T NF-independent maintenance of long-term HSC. (via Semantic Scholar)
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3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, Crossref, NC State University Libraries, ORCID
Added: August 6, 2018

2008 journal article

Generation of a conditional mutant allele for Tab1 in mouse

GENESIS, 46(8), 431–439.

By: M. Inagaki n, Y. Komatsu *, G. Scott*, G. Yamada *, M. Ray*, J. Ninomiya-Tsuji n , Y. Mishina *

Contributors: M. Inagaki n, Y. Komatsu *, G. Scott*, G. Yamada *, M. Ray*, J. Ninomiya-Tsuji n , Y. Mishina *

author keywords: conditional gene knockout; MAP kinase; BMP; Tab1; TGF-beta
MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Animals; Exons; Gene Targeting; Integrases / metabolism; Mice; Mutation
TL;DR: It is demonstrated that Cre‐mediated recombination using Sox2‐Cre, a Cre line expressed in the epiblast during early embryogenesis, results in deletion of the gene and protein and homozygous Cre‐recombined null embryos display an identical phenotype to conventional null embryos. (via Semantic Scholar)
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UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2008 journal article

TAK1-binding Protein 1, TAB1, Mediates Osmotic Stress-induced TAK1 Activation but Is Dispensable for TAK1-mediated Cytokine Signaling

JOURNAL OF BIOLOGICAL CHEMISTRY, 283(48), 33080–33086.

By: M. Inagaki n, E. Omori n, J. Kim n, Y. Komatsu *, G. Scott*, M. Ray*, G. Yamada *, K. Matsumoto *, Y. Mishina *, J. Ninomiya-Tsuji n 

Contributors: M. Inagaki n, E. Omori n, J. Kim n, Y. Komatsu *, G. Scott*, M. Ray*, G. Yamada *, K. Matsumoto *, Y. Mishina *, J. Ninomiya-Tsuji n 

MeSH headings : Adaptor Proteins, Signal Transducing / genetics; Adaptor Proteins, Signal Transducing / metabolism; Animals; Cell Line; Cytokines / metabolism; Embryo, Mammalian / cytology; Embryo, Mammalian / metabolism; Enzyme Activation / physiology; Fibroblasts / cytology; Fibroblasts / metabolism; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Knockout; Osmotic Pressure / physiology; Protein Structure, Tertiary / physiology; Signal Transduction / physiology
TL;DR: It is found that TAK1 is spontaneously activated when the concentration is increased and that it is totally dependent on TAB1, and that the C-terminal 68 amino acids of TAB 1 were sufficient to mediate osmotic stress-induced TAK 1 activation. (via Semantic Scholar)
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Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

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