@phdthesis{oai:ir.kagoshima-u.ac.jp:00006077,
 author = {有村, 博史 and Arimura, Hiroshi},
 month = {2016-10-28, 2016-10-28},
 note = {博士論文全文, 博士論文要旨, Abcb10, member 10 of the ABC transporter family, is reportedly a part of a complex in the mitochondrial inner membrane with mitoferrin-1 (Slc25a37) and ferrochelatase (Fech) and is responsible for heme biosynthesis in utero. However, it is unclear whether loss of Abcb10 causes pathological changes in adult mice. Here, we show that Abcb10−/− mice lack heme biosynthesis and erythropoiesis abilities and die in midgestation. Moreover, we generated Abcb10F/−; Mx1-Cre mice, with Abcb10 in hematopoietic cells deleted, which showed accumulation of protoporphyrin IX and maturation arrest in reticulocytes. Electron microscopy images of Abcb10−/− hematopoietic cells showed a marked increase of iron deposits at the mitochondria. These results suggest a critical role for Abcb10 in heme biosynthesis and provide new insights into the pathogenesis of erythropoietic protoporphyria and sideroblastic anemia.

Masatatsu Yamamoto, Hiroshi Arimura, Tomoko Fukushige, Kentarou Minami, Yukihiko Nishizawa, Akihide Tanimoto, Takuro Kanekura, Masayuki Nakagawa, Shin-ichi Akiyama, Tatsuhiko Furukawa
Abcb10 Role in Heme Biosynthesis In Vivo: Abcb10 Knockout in Mice Causes Anemia with Protoporphyrin IX and Iron Accumulation
Molecular and Cellular Biology Vol. 34, No. 6 p. 1077–1084 (2014)
https://doi.org/10.1128/MCB.00865-13},
 school = {鹿児島大学},
 title = {Abcb10 knockout mice causes anemia with protoporphyrin IX and iron accumulation: Abcb10 is essential for heme biosynthesis in vivo},
 year = {},
 yomi = {アリムラ, ヒロシ}
}