近日,，最新一期美國在線科學雜志《PLoS綜合》上刊登的一項研究成果稱,，日本一個研究小組最新研究發(fā)現(xiàn),，一種名為CALM的基因?qū)τ诩t細胞吸收鐵和造血必不可少,，這種基因一旦出現(xiàn)缺陷,，將導致極度貧血,。
奈良女子大學研究人員的最新實驗發(fā)現(xiàn)，CALM基因的缺陷會導致紅細胞吸收鐵的能力降低,，結(jié)果紅細胞數(shù)量減少,，形態(tài)也出現(xiàn)異常，從而引起極度貧血,。
研究還發(fā)現(xiàn),，體內(nèi)CALM基因不發(fā)揮作用的小鼠還會出現(xiàn)腦室偏大和大腦皮質(zhì)萎縮的癥狀。這種癥狀與阿爾茨海默氏癥非常相似,，對這一癥狀的研究將有助于弄清阿爾茨海默氏癥的發(fā)病機制,。
之前的研究曾發(fā)現(xiàn)，CALM基因如果出現(xiàn)異常,，細胞內(nèi)外的物質(zhì)就沒有辦法正常運輸,，一些物質(zhì)就會滯留在細胞內(nèi)，導致阿爾茨海默氏癥和白血病,。通過此次研究,，研究小組發(fā)現(xiàn)CALM基因?qū)t細胞來說也極為重要。(生物谷 Bioon.com)
doi:10.1371/journal.pone.0031854
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PMID:
The Clathrin Assembly Protein PICALM Is Required for Erythroid Maturation and Transferrin Internalization in Mice
Mai Suzuki, Hirokazu Tanaka, Akira Tanimura, Kenji Tanabe, Natsuko Oe, Shinya Rai, Syunsuke Kon, Manabu Fukumoto, Kohji Takei, Takaya Abe, Itaru Matsumura, Yuzuru Kanakura, Toshio Watanabe*
Phosphatidylinositol binding clathrin assembly protein (PICALM), also known as clathrin assembly lymphoid myeloid leukemia protein (CALM), was originally isolated as part of the fusion gene CALM/AF10, which results from the chromosomal translocation t(10;11)(p13;q14). CALM is sufficient to drive clathrin assembly in vitro on lipid monolayers and regulates clathrin-coated budding and the size and shape of the vesicles at the plasma membrane. However, the physiological role of CALM has yet to be elucidated. Here, the role of CALM in vivo was investigated using CALM-deficient mice. CALM-deficient mice exhibited retarded growth in utero and were dwarfed throughout their shortened life-spans. Moreover, CALM-deficient mice suffered from severe anemia, and the maturation and iron content in erythroid precursors were severely impaired. CALM-deficient erythroid cells and embryonic fibroblasts exhibited impaired clathrin-mediated endocytosis of transferrin. These results indicate that CALM is required for erythroid maturation and transferrin internalization in mice.
