Fibroblast and hematopoietic cell transformation by the fms oncogene (CSF-1 receptor).
Fibroblast and hematopoietic cell transformation by the fms oncogene (CSF-1 receptor).
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fms 癌基因（CSF-1 受体）对成纤维细胞和造血细胞的转化。
DOI：
10.1002/jcp.1041330416
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Sherr,CJ
中科院分区：
文献类型：
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作者：
Sherr,CJ
c-fms原癌基因编码单核吞噬细胞集落刺激因子（CSF-1）的受体。尽管CSF-1受体的酪氨酸激酶活性受到其配体的刺激，但病毒癌基因v-fms编码一种组成型受体激酶，可通过非自分泌机制转化成纤维细胞和造血细胞。c-fms基因的突变以及远端3 ′编码序列的关键改变似乎是完全激活其潜在转化潜力的原因。v-fms基因可以将CSF-1或IL-3依赖性造血细胞系转化为因子独立性并使其致瘤。v-fms基因产物的表达不反式调节CSF-1或IL-3的正常受体，并且既不影响它们的亲和力、数量，也不影响它们被其配体或佛波醇酯独立下调的潜力。v-fms转化造血靶细胞的能力表明，c-fms原癌基因的关键改变可能类似地导致白血病。
The c‐fmsproto‐oncogene encodes the receptor for the mononuclear phagocyte colony stimulating factor, CSF‐1. Although the tyrosine kinase activity of the CSF‐1 receptor is stimulated by its ligand, the viral oncogene, v‐fms, encodes a constitutive receptor kinase that can transform both fibroblasts and hematopoietic cells by a nonautocrine mechanism. Mutations in the c‐fmsgene as well as a critical alteration of the distal 3′ coding sequences appear to be responsible for fully activating its latent transforming potential. The v‐fmsgene can convert CSF‐1 or IL‐3 dependent hematopoietic cell lines to factor independence and render them tumorigenic. Expression of the v‐fmsgene product does not transmodulate the normal receptors for CSF‐1 or IL‐3 and affects neither their affinity, number, nor potential to be independently down‐regulated by their ligands or by phorbol esters. The ability of v‐fmsto transform hematopoietic target cells suggests that critical alterations in the c‐fmsproto‐oncogene might similarly contribute to leukemia.