Research Interests 【 display / non-display 】

Research Interests 【 display / non-display 】

Campus Career 【 display / non-display 】

Campus Career 【 display / non-display 】

• 2012.04

  -

  Now

  IWATE University   Faculty of Agriculture   Veterinary Medicine   Professor   [Duty]

External Career 【 display / non-display 】

External Career 【 display / non-display 】

• 2012.10

  　

  　

    Professor  

• 2010.04

  -

  2012.03

    Lecturer  

• 2000.04

  -

  2004.03

    Researcher  

• 1992.04

  -

  2000.03

    Researcher  

Research Areas 【 display / non-display 】

Research Areas 【 display / non-display 】

• Life Science / Veterinary medical science

• Life Science / Laboratory animal science

Course Subject 【 display / non-display 】

Course Subject 【 display / non-display 】

• 2012

  Laboratory Animal Science

• 2012

  Practical in Laboratory Animal Science

• 2013

  Experimental Animal Science

• 2013

  Animal Breeding and Genetics

• 2013

  Basic Veterinary Laboratory

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Published Papers 【 display / non-display 】

Published Papers 【 display / non-display 】

• Expression profiles of genes encoding glycosyltransferases synthesizing the glycosaminoglycan linker region during chondrogenic differentiation of ATDC5 cells

  Yamashita R, Lee E, Furuichi T

  Jpn J Vet Res   72   28 - 35   2024.06

  Academic Journal  Multiple authorship

  DOI

• Mice lacking nucleotide sugar transporter SLC35A3 exhibit lethal chondrodysplasia with vertebral anomalies and impaired glycosaminoglycan biosynthesis

  (46) Saito S, Mizumoto S, Yonekura T, Yamashita R, Nakano K, Okubo T, Yamada S, Okamura T, and Furuichi T.

  PLoS One   18   2023.04  [Refereed]

  Bulletin of University, Institute, etc.  Multiple authorship

  DOI

• CANT1 deficiency in a mouse model of Desbuquois dysplasia impairs glycosaminoglycan synthesis and chondrocyte differentiation in growth plate cartilage.

  Kodama K, Takahashi H, Oiji N, Nakano K, Okamura T, Niimi K, Takahashi E, Guo L, Ikegawa S, Furuichi T

  FEBS Open Bio     2020.04  [Refereed]

  Academic Journal  Multiple authorship

  DOI

• Crim1^C140S mutant mice reveal the importance of cysteine 140 in the internal region 1 of CRIM1 for its physiological functions

  Furuichi T, Tsukamoto M, Saito M, Sato Y, Oiji N, Yagami K, Fukumura R, Gondo Y, Guo L, Ikegawa S, Yamamori Y, Tomii K

  Mamma Genome   30   329 - 338   2019.12  [Refereed]

  Academic Journal  Multiple authorship

  Cysteine-rich transmembrane bone morphogenetic protein regulator 1 (CRIM1) is a type I transmembrane protein involved in the organogenesis of many tissues via its interactions with growth factors including BMP, TGF-β, and VEGF. In this study, we used whole-exome sequencing and linkage analysis to identify a novel Crim1 mutant allele generated by ENU mutagenesis in mice. This allele is a missense mutation that causes a cysteine-to-serine substitution at position 140, and is referred to as Crim1C140S. In addition to the previously reported phenotypes in Crim1 mutants, Crim1C140S homozygous mice exhibited several novel phenotypes, including dwarfism, enlarged seminal vesicles, and rectal prolapse. In vitro analyses showed that Crim1C140S mutation affected the formation of CRIM1 complexes and decreased the amount of the overexpressed CRIM1 proteins in the cell culture supernatants. Cys140 is located in the internal region 1 (IR1) of the N-terminal extracellular region of CRIM1 and resides

  DOI

• Disruption of the mouse Slc39a14 gene encoding zinc transporter ZIP14 is associated with decreased bone mass, likely caused by enhanced bone resorption

  Sasaki S, Tsukamoto M, Saito M, Hojyo S, Fukada T, Takami M and Furuichi T

  FEBS OPEN Bio   26   655 - 663   2018.04  [Refereed]

  Bulletin of University, Institute, etc.  Multiple authorship

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Review Papers 【 display / non-display 】

Review Papers 【 display / non-display 】

• Genetic skeletal disorders with collagen abnormalities and endoplasmic reticulum stress

  Tatsuya furuichi

  THE BONE ( メディカルレビュー社 )  32 ( 2 ) 209 - 214   2018.10

  Academic Journal  

Presentations 【 display / non-display 】

Presentations 【 display / non-display 】

• 新規Col2a1変異マウスを用いたトーランス型扁平椎異形成症の病態機序の検討

  Oral Presentation(General) 

  2016.05

  　

  　

• モデルマウスを用いたトーランス型扁平椎異形成症の病態機序の検討

  Oral Presentation(General) 

  2015.09

  -

  2016.09