研究等業績 - 原著論文 - 藤田　香里

p53 isoforms in cellular senescence- and ageing-associated biological and physiological functions.

Kaori FUJITA

International Journal of Molecular Sciences   20 ( 23 ) 6023   2019年11月  [査読有り]  [招待有り]

研究論文（学術雑誌）   単著

Positive feedback between p53 and TRF2 during telomere-damage signaling and cellular senescence.

Kaori FUJITA, Izumi Horikawa, Abdul M Mondal, Lisa M Miller Jenkins, et al.

Nature Cell Biology   12 ( 12 ) 1205 - 1212   2010年12月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

p53 isoforms Δ133p53 and p53β are endogenous regulators of replicative cellular senescence.

Kaori FUJITA, Abudal M Mondal, Izumi Horikawa, Giang H Nguyễn, et al.

Nature Cell Biology   11 ( 9 ) 1135 - 1142   2009年09月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Autophagic degradation of the inhibitory p53 isoform Δ133p53α as a regulatory mechanism for p53-mediated senescence.

Izumi Horikawa, Kaori FUJITA, Lisa M Miller Jenkins, Yukiharu Hiyoshi, et al.

Nature Communications   5   4706   2014年08月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes.

Abdul M Mondal, Izumi Horikawa, Sharon R Pine, Kaori FUJITA, et al.

International Journal of Clinical Investigation   123 ( 12 ) 5247 - 5257   2013年12月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Downregulation of splicing factor SRF3 induces p53β, and alternatively spliced isoform of p53 that promotes cellular senescence.

Yizhe Tang, Izumi Horikawa, Masahiko Ajiro, Ana I Robles, Kaori FUJITA, et al.

Oncogene   32 ( 22 ) 2792 - 2798   2013年05月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

p53 governs telomere regulation feedback too, via TRF2.

Izumi Horikawa, Kaori FUJITA, Curtis C. Harris

Aging (Albany NY)   3 ( 1 ) 26 - 32   2011年01月  [査読有り]  [招待有り]

研究論文（学術雑誌）   国際共著

DOI

Δ133p53 represses p53-inducible senescence genes and enhances the generation of human induced pluripotent stem cells.

Izumi Horikawa, Key-yoon Park, Kazunobu Isogaya, Yukiharu Hiyoshi, Han Li, Katsuhiro Anami, Ana I Robles, Abudal M Mondal, Kaori FUJITA, et al.

Cell Death and Differentiation   24 ( 6 ) 1017 - 1028   2017年01月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Evaluation of FGFR inhibitor ASP5878 as a drug candidate for achondroplasia.

Tomonori Ozaki, Tatsuya Kawamoto, Yuki Iimori, Nobuaki Takeshita, Yukiko Yamagishi, Hiroaki Nakamura, Masazumi Kamohara, Kaori FUJITA, Masayuki Tanahashi, Noriyuki Tsumaki

Scientific Reports   10 ( 1 ) 20915   2020年12月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

P53 isoforms in cellular senescence-and ageing-associated biological and physiological functions

Fujita K.

International Journal of Molecular Sciences ( International Journal of Molecular Sciences )  20 ( 23 ) 6023 - 6023   2019年12月  [査読有り]  [招待有り]

研究論文（学術雑誌）  

Cellular senescence, a term originally used to define the characteristics of normal human fibroblasts that reached their replicative limit, is an important factor for ageing, age-related diseases including cancer, and cell reprogramming. These outcomes are mediated by senescence-associated changes in gene expressions, which sometimes lead to the secretion of pro-inflammatory factors, or senescence-associated secretory phenotype (SASP) that contribute to paradoxical pro-tumorigenic effects. p53 functions as a transcription factor in cell-autonomous responses such as cell-cycle control, DNA repair, apoptosis, and cellular senescence, and also non-cell-autonomous responses to DNA damage by mediating the SASP function of immune system activation. The human TP53 gene encodes twelve protein isoforms, which provides an explanation for the pleiotropic p53 function on cellular senescence. Recent reports suggest that some short isoforms of p53 may modulate gene expressions in a full-length p53-dependent and -independent manner, in other words, some p53 isoforms cooperate with full-length p53, whereas others operate independently. This review summarizes our current knowledge about the biological activities and functions of p53 isoforms, especially Δ40p53, Δ133p53α, and p53β, on cellular senescence, ageing, age-related disorder, reprogramming, and cancer. Numerous cellular and animal model studies indicate that an unbalance in p53 isoform expression in specific cell types causes age-related disorders such as cancer, premature ageing, and degenerative diseases.

DOI

Changes in acetyl-CoA mediate Sik3-induced maturation of chondrocytes in endochondral bone formation.

Azuma Kosai, Nanao Horike, Yoshiaki Takei, Akihiro Yamashita, Kaori FUJITA, Takashi Kamatani, Noriyuki Tsumaki

Biochemical and Biophysical Research Communications   516 ( 4 ) 1097 - 1102   2019年09月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

A-674563 increases chondrocyte marker expression in cultured chondrocytes by inhibiting Sox9 degradation.

Tomohito Kobayashi, Kaori FUJITA, Takashi Kamatani, Shuichi Matsuda, Noriyuki Tsumaki

Biochemical and Biophysical Research Communications   495 ( 1 ) 1468 - 1475   2018年01月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Petrosin B prevents chondrocyte hypertrophy and osteoarthritis in mice by inhibiting Sik3.

Yasuhiro Yahara, Hiroshi Takemori, Minoru Okada, Azuma Kosai, Akihiro Yamashita, Tomohito Kobayashi, Kaori FUJITA, et al.

Nature Communications   7   10959   2016年05月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Statin treatment rescues FGFR3 skeletal dysplasia phenotypes.

Akihiro Yamashita, Miho Morioka, Hiromi Kishi, Takeshi Kimura, Yasuhiro Yahara, Minoru Okada, Kaori FUJITA, et al.

Nature   513 ( 7519 ) 507 - 511   2014年09月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Stem cell aging and the implications for stem cell-based therapies for aging-related diseases and aged tissues.

Kaori FUJITA, Noriyuki Tsumaki

Clinical Calcium   23 ( 1 ) 65 - 73   2013年01月  [招待有り]

研究論文（学術雑誌）   国内共著

NIH3T3 cells overexpressing CD98 heavy chain resist early G1 arrest and apoptosis induced by serum starvation.

Kaori Hara, Shiho Ueda, Yoshiya Ohno, Toshiyuki Tanaka, et al.

Cancer Science   103 ( 8 ) 1469 - 1466   2012年08月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Tetrahydrouridine inhibits cell proliferation through cell cycle regulation regardless of cytidine deaminase expression levels.

Naotake Funamizu, Curtis Ray Lacy, Kaori FUJITA, Kenei Furukawa, et al.

PLoS One   7 ( 5 ) e37424   2012年05月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

ING2 is upregulated in colon cancer and increases invasion by enhanced MMP13 expression.

Kensuke Kumamoto, Kaori FUJITA, Reiko Kurotani, Motonobu Saito, et al.

International Journal of Cancer   125 ( 6 ) 1306 - 1315   2009年09月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Nutlin-3a activates p53 to both down-regulate inhibitor of growth 2 and up-regulate mi-34a, mir-34b, and mir-34c expression, and induce senescence.

Kensuke Kumamoto, Elisa A Spillare, Kaori FUJITA, Izumi Horikawa, et al.

Cancer Research   69 ( 9 ) 3194 - 3203   2008年05月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Functional diversity of human protection of telomeres 1 isoforms in telomere protection and cellular senescence.

Qin Yang, Ran Zhang, Izumi Horikawa, Kaori FUJITA, Yalda Afshar, et al.

Cancer Research   67 ( 24 ) 11677 - 11686   2007年12月  [査読有り]

研究論文（学術雑誌）   国際共著

DOI

Induction of abnormal nuclear shape in two distinct modes by overexpression of serine/threonine protein phosphatase 5 in HeLa cells.

Hirokazu Fukuda, Naoto Tsuchiya, Kaori Hara-Fujita, Sachiyo Takagi, Minako Nagao, Hitoshi Nakagama

Journal of Cellular Biochemistry   101 ( 2 ) 321 - 330   2007年05月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Enhanced tumorigenicity caused by truncation of the extracellular domain of GP125/CD98 heavy chain.

Kaori Hara, Hiroshi Kudoh, Takemi Enomoto, Yoshiyuki Hashimoto, Takashi Masuko

Oncogene   19 ( 54 ) 6209 - 6215   2000年12月  [査読有り]

研究論文（学術雑誌）   国内共著

DOI

Malignant transformation of NIH3T3 cells by overexpression of early lymphocyte activation antigen CD98.

Kaori Hara, Hiroshi Kudoh, Takemi Enomoto, Yoshiyuki Hashimoto, Takashi Masuko

Biochemical and Biophysical Research Communications   262 ( 3 ) 720 - 725   1999年09月  [査読有り]

研究論文（学術雑誌）   国内共著