Hilton D J, Nicola N A, Metcalf D
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Proc Natl Acad Sci U S A. 1988 Aug;85(16):5971-5. doi: 10.1073/pnas.85.16.5971.
Leukemia inhibitory factor (LIF), a glycoprotein capable of suppressing the clonogenicity and inducing the differentiation of the murine myeloid leukemia cell line M1, was radioiodinated to a high specific radioactivity with retention of full biological activity. Binding of 125I-labeled LIF to M1 cells reached a steady state at 37 degrees C after approximately equal to 40 min and was in competition with unlabeled LIF but not granulocyte colony-stimulating factor or a range of other cytokines or differentiation-inducing agents. Specific binding was demonstrable to cells from a range of murine hemopoietic tissues including the bone marrow, the spleen, and the peritoneal cavity. Autoradiography revealed macrophages, monocytes, and their precursors to be the major cell types responsible for 125I-labeled LIF binding within these tissues. Receptors on M1 cells were of high affinity (apparent Kd, 100-200 pM) and few in number (300-500 per cell).
白血病抑制因子(LIF)是一种糖蛋白,能够抑制克隆形成并诱导小鼠髓性白血病细胞系M1分化。它被放射性碘化至高比放射性,同时保留了全部生物活性。125I标记的LIF与M1细胞的结合在37℃下约40分钟后达到稳态,并且与未标记的LIF存在竞争,但与粒细胞集落刺激因子或一系列其他细胞因子及分化诱导剂不存在竞争。在包括骨髓、脾脏和腹腔在内的一系列小鼠造血组织的细胞中可证明存在特异性结合。放射自显影显示巨噬细胞、单核细胞及其前体是这些组织中负责125I标记的LIF结合的主要细胞类型。M1细胞上的受体具有高亲和力(表观解离常数Kd为100 - 200 pM)且数量较少(每个细胞300 - 500个)。