Arl4cのがんにおける発現とその機能
キーワード:Arl4c、がん
2012.04.
藤井 慎介(ふじい しんすけ) | データ更新日:2024.04.19 |
主な研究テーマ
Wntシグナルが唾液腺の発生に与える影響
キーワード:Wntシグナル、唾液腺
2011.04~2016.05.
キーワード:Wntシグナル、唾液腺
2011.04~2016.05.
トランスフォーミング増殖因子ベータ1(TGF-β1)がヒト歯根膜細胞の増殖および分化に与える影響
キーワード:トランスフォーミング増殖因子ベータ1、歯根膜細胞
2008.04.
キーワード:トランスフォーミング増殖因子ベータ1、歯根膜細胞
2008.04.
ヒト歯根膜前駆細胞株の樹立およびその特徴付け
キーワード:前駆細胞、歯根膜細胞
2006.04~2008.03.
キーワード:前駆細胞、歯根膜細胞
2006.04~2008.03.
ヒト歯根膜細胞の不死化
キーワード:不死化、歯根膜
2003.04~2006.03.
キーワード:不死化、歯根膜
2003.04~2006.03.
従事しているプロジェクト研究
細胞外環境が口腔癌に与える影響の解析
2017.06~2020.06.
2017.06~2020.06.
研究業績
主要原著論文
1. | Shinsuke Fujii, Kana Hasegawa, Takashi Maehara, Kari J Kurppa, Kristiina Heikinheimo, Kristy A. Warner, Satoshi Maruyama, Yudai Tajiri, Jacques E. Nör, Jun-ichi Tanuma, Shintaro Kawano, Tamotsu Kiyoshima, Wnt/β-catenin-C-kit axis may play a role in adenoid cystic carcinoma prognostication, Pathology - Research and Practice, 10.1016/j.prp.2024.155148, 155148-155148, 2024.01. |
2. | Thinh Thi Kim Truong, Shinsuke Fujii, Ryoko Nagano, Kana Hasegawa, Megumi Kokura, Yuta Chiba, Keigo Yoshizaki, Satoshi Fukumoto, Tamotsu Kiyoshima, Arl4c is involved in tooth germ development through osteoblastic/ameloblastic differentiation., Biochemical and biophysical research communications, 10.1016/j.bbrc.2023.09.014, 679, 167-174, 2023.09, Murine tooth germ development proceeds in continuous sequential steps with reciprocal interactions between the odontogenic epithelium and the adjacent mesenchyme, and several growth factor signaling pathways and their activation are required for tooth germ development. The expression of ADP-ribosylation factor (Arf)-like 4c (Arl4c) has been shown to induce cell proliferation, and is thereby involved in epithelial morphogenesis and tumorigenesis. In contrast, the other functions of Arl4c (in addition to cellular growth) are largely unknown. Although we recently demonstrated the involvement of the upregulated expression of Arl4c in the proliferation of ameloblastomas, which have the same origin as odontogenic epithelium, its effect on tooth germ development remains unclear. In the present study, single-cell RNA sequencing (scRNA-seq) analysis revealed that the expression of Arl4c, among 17 members of the Arf-family, was specifically detected in odontogenic epithelial cells, such as those of the stratum intermedium, stellate reticulum and outer enamel epithelium, of postnatal day 1 (P1) mouse molars. scRNA-seq analysis also demonstrated the higher expression of Arl4c in non-ameloblast and inner enamel epithelium, which include immature cells, of P7 mouse incisors. In the mouse tooth germ rudiment culture, treatment with SecinH3 (an inhibitor of the ARNO/Arf6 pathway) reduced the size, width and cusp height of the tooth germ and the thickness of the eosinophilic layer, which would involve the synthesis of dentin and enamel matrix organization. In addition, loss-of-function experiments using siRNAs and shRNA revealed that the expression of Arl4c was involved in cell proliferation and osteoblastic cytodifferentiation in odontogenic epithelial cells. Finally, RNA-seq analysis with a gene set enrichment analysis (GSEA) and Gene Ontology (GO) analysis showed that osteoblastic differentiation-related gene sets and/or GO terms were downregulated in shArl4c-expressing odontogenic epithelial cells. These results suggest that the Arl4c-ARNO/Arf6 pathway axis contributes to tooth germ development through osteoblastic/ameloblastic differentiation.. |
3. | Shinsuke Fujii, Tamotsu Kiyoshima, The role of Wnt, ARL4C, and Sema3A in developmental process and disease pathogenesis., Pathology international, 10.1111/pin.13325, 73, 6, 217-233, 2023.06, Various types of tumors, including malignant and benign ones, occur in the oral cavity. These arise from the mucosal epithelium, odontogenic epithelium, and salivary gland. To date, few major driver events in oral tumors have been identified. Accordingly, molecular targets in anti-tumor therapy for oral tumors are lacking. We focused on elucidating the function of aberrantly activated signal transduction related to oral tumor formation, especially in oral squamous cell carcinoma, ameloblastoma, and adenoid cystic carcinoma, which are raised as common oral tumors. Wnt/β-catenin-dependent pathway is involved in the developmental process, organ homeostasis and disease pathogenesis through regulating various cellular functions by enhancing transcriptional activity. Recently, we identified ADP-ribosylation factor (ARF)-like 4c (ARL4C) and Semaphorin 3A (Sema3A), the expression of which is regulated by Wnt/β-catenin-dependent pathway, and characterized their functions in the developmental process and tumor formation. This review highlights the recent advances in understanding the roles of Wnt/β-catenin-dependent pathway, ARL4C and Sema3A, as determined by pathological and experimental studies.. |
4. | Dania Zuhier Ragheb Alkhatib, Thinh Thi Kim Truong, Shinsuke Fujii, Kana Hasegawa, Ryoko Nagano, Yudai Tajiri, Tamotsu Kiyoshima, Stepwise activation of p63 and the MEK/ERK pathway induces the expression of ARL4C to promote oral squamous cell carcinoma cell proliferation., Pathology, research and practice, 10.1016/j.prp.2023.154493, 246, 154493-154493, 2023.06, Carcinogenesis is a multistep process wherein cells accumulate multiple genetic alterations and progress to a more malignant phenotype. It has been proposed that sequential accumulation of gene abnormalities in specific genes drives the transition from non-tumorous epithelia through a preneoplastic lesion/benign tumor to cancer. Histologically, oral squamous cell carcinoma (OSCC) progresses in multiple ordered steps that begin with mucosal epithelial cell hyperplasia, which is followed by dysplasia, carcinoma in situ and invasive carcinoma. It is therefore hypothesized that genetic alteration-mediated multistep carcinogenesis would be involved in the development of OSCC; however, the detailed molecular mechanisms are unknown. We clarified the comprehensive gene expression patterns and carried out an enrichment analysis using DNA microarray data from a pathological specimen of OSCC (including a non-tumor region, carcinoma in situ lesion and invasive carcinoma lesion). The expression of numerous genes and signal activation were altered in the development of OSCC. Among these, the p63 expression was increased and the MEK/ERK-MAPK pathway was activated in carcinoma in situ lesion and in invasive carcinoma lesion. Immunohistochemical analyses revealed that p63 was initially upregulated in carcinoma in situ and ERK was sequentially activated in invasive carcinoma lesions in OSCC specimens. ADP-ribosylation factor (ARF)-like 4c (ARL4C), the expression of which is reportedly induced by p63 and/or the MEK/ERK-MAPK pathway in OSCC cells, has been shown to promote tumorigenesis. Immunohistochemically, in OSCC specimens, ARL4C was more frequently detected in tumor lesions, especially in invasive carcinoma lesions, than in carcinoma in situ lesions. Additionally, ARL4C and phosphorylated ERK were frequently merged in invasive carcinoma lesions. Loss-of-function experiments using inhibitors and siRNAs revealed that p63 and MEK/ERK-MAPK cooperatively induce the expression of ARL4C and cell growth in OSCC cells. These results suggest that the stepwise activation of p63 and MEK/ERK-MAPK contributes to OSCC tumor cell growth through regulation of ARL4C expression.. |
5. | Nagano, Ryoko; Fujii, Shinsuke; Hasegawa, Kana; Maeda, Hidefumi; Kiyoshima, Tamotsu, Wnt signaling promotes tooth germ development through YAP1-TGF- βsignaling, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 10.1016/j.bbrc.2022.09.012, 630, 64-70, 2022.11. |
6. | Shinsuke Fujii, Tatsufumi Fujimoto, Kana Hasegawa, Ryoko Nagano, Takuma Ishibashi, Kari J.Kurppa, Yurie Mikami, Megumi Kokura, Yudai Tajiri, Toshiro Kibe, Hiroko Wada, Naohisa Wada, Shosei Kishida, Yoshinori Higuchi, Tamotsu Kiyoshima., The Semaphorin 3A-AKT axis-mediated cell proliferation in salivary gland morphogenesis and adenoid cystic carcinoma pathogenesis, Pathology - Research and Practice, 10.1016/j.prp.2022.153991, 236 (2022) 153991, 2022.06. |
7. | Kana Hasegawa, Shinsuke Fujii, Kari J Kurppa, Takashi Maehara, Kazunari Oobu, Seiji Nakamura, Tamotsu Kiyoshima, Clear cell squamous cell carcinoma of the tongue exhibits characteristics as an undifferentiated squamous cell carcinoma, Pathology - Research and Practice, 10.1016/j.prp.2022.153909, 235, 153909, 2022.04. |
8. | Fujii, Shinsuke; Ishibashi, Takuma; Kokura, Megumi; Fujimoto, Tatsufumi; Matsumoto, Shinji; Shidara, Satsuki; Kurppa, Kari J.; Pape, Judith; Caton, Javier; Morgan, Peter R.; Heikinheimo, Kristiina; Kikuchi, Akira; Jimi, Eijiro; Kiyoshima, Tamotsu, RAF1-MEK/ERK pathway-dependent ARL4C expression promotes ameloblastoma cell proliferation and osteoclast formation, JOURNAL OF PATHOLOGY, 10.1002/path.5814, 256, 1, 119-133, 2022.01. |
9. | Kana Hasegawa, Shinsuke Fujii, Shinji Matsumoto, Yudai Tajiri, Akira Kikuchi and Tamotsu Kiyoshima, YAP signaling induces PIEZO1 to promote oral squamous cell carcinoma cell proliferation, JOURNAL OF PATHOLOGY, 10.1002/path.5553, 253, 1, 80-93, 2021.01, Most cancer cells are exposed to altered extracellular environments, such as an increase in extracellular matrix (ECM) stiffness and soluble signals consisting of growth factors and cytokines. It is therefore conceivable that changes in tumor extracellular environments affect tumor cell behavior. The Hippo pathway reportedly responds to the extracel- lular environment and regulates the nuclear localization of the transcription co-activator, yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ). Inactivation of the Hippo pathway with nuclear translocation of YAP/TAZ stimulates cell proliferation. Its pathway also regulates gene expression, but the precise molecule(s) meditating the cell-proliferating effect of YAP signaling on oral squamous cell carcinoma (OSCC) is unclear. First, we examined the effects of YAP signaling on OSCC tumorigenesis. Loss-of-function experiments using siRNA or an inhibitor, and immunohistochemical analyses of tissue specimens obtained from OSCC patients demon- strated that YAP signaling was involved in OSCC cell proliferation. Second, we identified Piezo-type mechanosensi- tive ion channel component 1 (PIEZO1), a Ca2+ channel, as a transcriptional target of YAP signaling and showed that elevated PIEZO1 was required for PIEZO1 agonist-dependent Ca2+ entry and cell proliferation in OSCC cells. Exper- iments using three-dimensional and suspension culture revealed that PIEZO1 was involved in OSCC cellular growth. Finally, YAP overexpression in the nucleus and/or cytoplasm was immunohistochemically detected in tumor lesions with frequent expression of both PIEZO1 and Ki-67, but not in non-tumor regions of OSCC specimens. These results suggest that the YAP/PIEZO1 axis promotes OSCC cell growth.. |
10. | Fujii S, Tajiri Y, Hasegawa K, Matsumoto S, Yoshimoto RU, Wada H, Kishida S, Kido MA, Yoshikawa H, Ozeki S, Kiyoshima T, The TRPV4-AKT axis promotes oral squamous cell carcinoma cell proliferation via CaMKII activation., Lab Invest, 2019.12. |
11. | Fujii, Shinsuke; Nagata, Kengo; Matsumoto, Shinji; Kohashi, Ken-ichi; Kikuchi, Akira; Oda, Yoshinao; Kiyoshima, Tamotsu; Wada, Naohisa, Wnt/beta-catenin signaling, which is activated in odontomas, reduces Sema3A expression to regulate odontogenic epithelial cell proliferation and tooth germ development, SCIENTIFIC REPORTS, 10.1038/s41598-019-39686-1, 9, 2019.03. |
12. | Harada, Takeshi; Matsumoto, Shinji; Hirota, Suguru; Kimura, Hirokazu; Fujii, Shinsuke; Kasahara, Yuuya; Gon, Hidetoshi; Yoshida, Toshihiko; Itoh, Tomoo; Haraguchi, Naotsugu; Mizushima, Tsunekazu; Noda, Takehiro; Eguchi, Hidetoshi; Nojima, Satoshi; Morii, Eiichi; Fukumotol, Takumi; Obika, Satoshi; Kikuchi, Akira, Chemically Modified Antisense Oligonucleotide Against ARL4C Inhibits Primary and Metastatic Liver Tumor Growth, MOLECULAR CANCER THERAPEUTICS, 10.1158/1535-7163.MCT-18-0824, 18, 3, 602-612, 2019.03. |
13. | Yurie Mikami, Shinsuke Fujii, Kenichi Kouhashi, Yuichi Yamada, Masafumi Moriyama, Shintarou Kawano, Seiji Nakamura, Yoshinao Oda, Tamotsu Kiyoshima, Low grade myofibroblastic sarcoma arising in the tip of the tongue with intravascular invasion A case report, Oncology Letters, 10.3892/ol.2018.9115, 16, 3, 3889-3894, 2018.09, [URL]. |
14. | Mikami Yurie, Fujii Shinsuke, Kengo Nagata, Hiroko Wada, Kana Hasegawa, Misaki Abe, Reiko U. Yoshimoto, Shintaro Kawano, Seiji Nakamura, Tamotsu Kiyoshima, GLI-mediated Keratin 17 expression promotes tumor cell growth through the anti-apoptotic function in oral squamous cell carcinomas., J Cancer Res Clin Oncol, 10.1007/s00432-017-2398-2, 143, 8, 1381-1393, 2017.03. |
15. | Fujii S, Shinjo K, Matsumoto S, Harada T, Nojima S, Sato S, Usami Y, Toyosawa S, Morii E, Kondo Y, Kikuchi A, Epigenetic upregulation of ARL4C, due to DNA hypomethylation in the 3’-untranslated region, promotes tumorigenesis of lung squamous cell carcinoma, Oncotarget, doi: 10.18632/oncotarget.13147., 6, 49, 81571-81587, 2016.10. |
16. | Matsumoto S, Kurimoto T, Taketo M, Fujii S, Kikuchi A, The Wnt-Myb pathway suppresses KIT expression to control the timing of salivary proacinar differentiation and duct formation., Development., 143(13): 2311-24, 2016.04. |
17. | Fujii S, Matsumoto S, Nojima S, Morii E, Kikuchi A, Arl4c expression in colorectal and lung cancers promotes tumorigenesis and may represent a novel therapeutic target., Oncogene, 34, 4834-4844, 2015.09. |
18. | Ibuka S, Matsumoto S, Fujii S, Kikuchi A, The P2Y2 receptor promotes Wnt3a- and EGF-induced epithelial tubular formation by IEC6 cells by binding to integrins., J Cell Sci., 10.1242/jcs.169060., 128, 11, 2156-2158, 2015.06. |
19. | Matsumoto S, Fujii S, Sato A, Ibuka S, Kagawa Y, Ishii M, Kikuchi A, A combination of Wnt and growth factor signaling induces Arl4c expression to form epithelial tubular structures. , EMBO J, 33, 702-718, 2014.04. |
20. | Fujii S, Maeda H, Tomokiyo A, Monnouchi S, Hori K, Wada N, Akamine A, The effects of TGF-β1 on the proliferation and differentiation of human periodontal ligament cells and a human periodontal ligament stem/progenitor cell line., Cell Tissue Res., 2011.11. |
21. | Fujii S, Maeda H, Wada N, Tomokiyo A, Saito M, Akamine A, Investigating a clonal human periodontal ligament progenitor/stem cell line in vitro and in vivo., J Cell Physiol, 215(3):743-749, 2008.03. |
22. | Shinsuke Fujii., Hidefumi Maeda., Naohisa Wada., Yoshio Kano., Akifumi Akamine. , Establishing and characterizing human periodontal ligament fibroblasts immortalized by SV40T-antigen and hTERT gene transfer., Cell and tissue research, 324巻 117-125頁, 2006.01. |
主要総説, 論評, 解説, 書評, 報告書等
1. | Matsumoto S, Fujii S, Kikuchi A, Arl4c is a key regulator of tubulogenesis and tumorigenesis as a target gene of Wnt–β-catenin and growth factor–Ras signaling, J Biochem, 2016.10. |
主要学会発表等
学会活動
所属学会名
日本臨床口腔病理学会
日本歯科医学教育学会
日本臨床細胞学会
歯科基礎医学会
日本癌学会
日本病理学会
日本歯科保存学会
日本歯内療法学会
Japan Asssociation of Dental Research
International Association of Dental Research
学術論文等の審査
年度 | 外国語雑誌査読論文数 | 日本語雑誌査読論文数 | 国際会議録査読論文数 | 国内会議録査読論文数 | 合計 |
---|---|---|---|---|---|
2023年度 | 5 | 5 | |||
2022年度 | 5 | 5 | |||
2021年度 | 2 | 2 | |||
2019年度 | 2 | 2 | |||
2017年度 | 1 | 1 | |||
2016年度 | 1 | 1 |
その他の研究活動
外国人研究者等の受入れ状況
2019.12~2020.03, 1ヶ月以上, Faculty of Dentistry, University of Medicine and Pharmacy - Ho Chi Minh City, Vietnam, .
受賞
第63回学術奨励賞, 公益財団法人 UBE学術振興財団, 2023.06.
Jeremy Jass Prize for Research Excellence in Pathology in 2021 , The Journal of Pathology, 2023.01.
九大歯学優秀研究者賞(IF部門), 九州大学歯学研究院等, 2022.06.
第67回日本病理学会秋期特別総会 学術研究賞(A演説), 日本病理学会, 2021.02.
Dentsply賞, 日本歯科保存学会, 2009.10.
優秀論文賞, 日本歯内療法学会, 2007.05.
藤野賞, 九州大学歯学府, 2007.04.
デンツプライ賞, 株式会社デンツプライ, 2006.05.
日本歯科保存学会奨励賞, 日本歯科保存学会, 2006.04.
研究資金
科学研究費補助金の採択状況(文部科学省、日本学術振興会)
2024年度~2027年度, 基盤研究(B), 代表, 口腔腫瘍実質がもたらす間質転換による顎骨破壊機序の解明と治療標的分子の探索.
2023年度~2025年度, 国際共同研究強化(A), 代表, シングルセル解析を用いた口腔腫瘍間質由来破骨細胞形成因子(SODF)の同定.
2023年度~2026年度, 基盤研究(B), 分担, 超早期癌発見戦略に向けた変異細胞-隣接正常細胞-間質細胞における不安定性出現解明.
2023年度~2026年度, 基盤研究(C), 分担, 口腔細胞診における遺伝子検査法(GSC)の創出とその臨床応用.
2022年度~2024年度, 基盤研究(C), 分担, Compressed sensingを用いた正確な口腔癌深達度の三次元的取得.
2021年度~2023年度, 基盤研究(C), 分担, 早期癌に認められる異型におけるHippo-YAPシグナルの機能解析.
2020年度~2022年度, 基盤研究(C), 代表, エナメル上皮腫を引き起こす新しい分子基盤の解明とがんゲノム医療に向けた臨床応用.
2019年度~2021年度, 基盤研究(C), 分担, 癌微小環境の機械侵襲と新規癌遺伝子シグナル制御の相互強化による新たな癌治療戦略.
2019年度~2022年度, 基盤研究(B), 分担, オミックス解析を用いた歯根膜発生機構の解明と幹細胞誘導型組織再生技術への応用.
2017年度~2019年度, 基盤研究(C), 分担, メカノセンサーを基盤とした歯の発生メカニズムの解明.
2016年度~2018年度, 基盤研究(C), 分担, TRPチャネルを介したがん組織微小環境ストレスによる癌細胞形質への影響の解明.
2016年度~2018年度, 一般研究(C), 分担, エナメル質形成における分子シャペロンGRP78の関与
.
.
2016年度~2019年度, 基盤研究(C), 代表, Arl4cを標的とした核酸医薬による口腔がんの新規分子標的治療法の開発.
2014年度~2016年度, 若手研究(B), 代表, 唾液腺上皮組織の発生および再生におけるWntシグナルの役割の解明.
2010年度~2012年度, 基盤研究(C), 代表, 歯周靭帯の再生を主軸にした新規歯周組織再生療法の開発.
2010年度~2012年度, 基盤研究(B), 分担, 歯根膜を有した次世代型人工歯根の開発.
2009年度~2011年度, 基盤研究(B), 分担, 歯根膜はその再生に何を必要とするか?.
2009年度~2010年度, 若手研究(B), 代表, ヒト歯根膜組織再生に関連した遺伝子の同定.
2008年度~2009年度, 若手研究(B), 代表, ヒト歯根膜組織再生に関連した遺伝子の同定.
2007年度~2009年度, 基盤研究(B), 分担, ヒト歯根膜前駆細胞クローン株を用いた歯根膜再生機構の解明.
2007年度~2007年度, 若手研究(スタートアップ), 代表, ヒト歯根膜前駆細胞株の分化メカニズム解明.
競争的資金(受託研究を含む)の採択状況
2016年度~2016年度, 国立研究開発法人日本医療研究開発機構(AMED)創薬支援ネットワーク, 分担, 低分子量Gタンパク質を標的とする新規がん治療のための核酸医薬の探索.
2015年度~2015年度, 国立研究開発法人日本医療研究開発機構(AMED)創薬支援ネットワーク, 分担, 低分子量Gタンパク質を標的とする新規がん治療のための核酸医薬の探索.
学内資金・基金等への採択状況
2023年度~2024年度, 公益財団法人 UBE 学術振興財団 第63回学術奨励賞, 代表, 唾液腺悪性腫瘍(腺様嚢胞癌)における「癌細胞-神経連関」による腫瘍形成機構の解明
.
.
2022年度~2023年度, 公益財団法人 テルモ生命科学振興財団 研究助成, 代表, 口腔腫瘍における腫瘍実質-間質連関による顎骨破壊機構の解明.
2022年度~2024年度, 公益財団法人新日本先進医療研究財団, 代表, シングルセル RNA-seq 解析を用いた口腔腫瘍における間質由来破骨細胞形成因子(SODF)の同定.
2022年度~2023年度, 公益財団法人 持田記念医学薬学振興財団, 代表, シングルセル解析を用いた口腔腫瘍における腫瘍-間質連関による顎骨吸収機構の解明.
2020年度~2021年度, 公益財団法人SGH財団 SGHがん研究助成, 代表, 口腔腺扁平上皮癌におけるエピゲノム異常に関する研究:癌の悪性度に関与する扁平上皮-腺上皮分化転換機構の解明
.
.
2019年度~2020年度, 公益財団法人新日本先進医療研究財団: , 代表, Wntシグナル下流癌抑制遺伝子を分子標的とした新規唾液腺腫瘍治療法の開発.
2019年度~2019年度, 武田科学振興財団 医学系研究助成(基礎), 代表, 新規オルガノイド培養法を用いた歯数を決定する分子基盤の解明.
2016年度~2018年度, 公益財団法人福岡県すこやか健康事業団 がん研究助成金, 代表, Arl4cを分子標的とする核酸医薬を応用した新規エナメル上皮腫治療法の開発.
2015年度~2015年度, 大阪大学未来戦略機構・第二部門・生体統御ネットワーク医学教育プログラム・異分野融合教育研究推進プロジェクト
, 代表, 肺がん治療を目指した新規核酸医薬品の創出.
, 代表, 肺がん治療を目指した新規核酸医薬品の創出.
2015年度~2015年度, 大阪大学橋渡し研究支援推進プログラム, 分担, Arl4cを標的としたがん治療を目的とする新規医薬品の創出.
2014年度~2014年度, 大阪大学橋渡し研究支援推進プログラム, 分担, Arl4cを標的としたがん治療を目的とする新規医薬品の創出.
2013年度~2013年度, 大阪大学未来戦略機構・第二部門・生体統御ネットワーク医学教育プログラム・異分野融合教育研究推進プロジェクト, 代表, 唾液腺の発生および再生におけるWntシグナルの役割の解明.
本データベースの内容を無断転載することを禁止します。