近日，最新一期美国在线科学杂志《PLoS综合》上刊登的一项研究成果称，日本一个研究小组最新研究发现，一种名为CALM的基因对于红细胞吸收铁和造血必不可少，这种基因一旦出现缺陷，将导致极度贫血。
奈良女子大学研究人员的最新实验发现，CALM基因的缺陷会导致红细胞吸收铁的能力降低，结果红细胞数量减少，形态也出现异常，从而引起极度贫血。
研究还发现，体内CALM基因不发挥作用的小鼠还会出现脑室偏大和大脑皮质萎缩的症状。这种症状与阿尔茨海默氏症非常相似，对这一症状的研究将有助于弄清阿尔茨海默氏症的发病机制。
之前的研究曾发现，CALM基因如果出现异常，细胞内外的物质就没有办法正常运输，一些物质就会滞留在细胞内，导致阿尔茨海默氏症和白血病。通过此次研究，研究小组发现CALM基因对红细胞来说也极为重要。(生物谷 Bioon.com)
doi:10.1371/journal.pone.0031854
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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.
