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禽肉瘤病毒UR2的转化蛋白与磷脂酰肌醇激酶活性相关：在肿瘤发生中的可能作用。

Transforming protein of avian sarcoma virus UR2 is associated with phosphatidylinositol kinase activity: possible role in tumorigenesis.

作者信息

Macara I G, Marinetti G V, Balduzzi P C

出版信息

Proc Natl Acad Sci U S A. 1984 May;81(9):2728-32. doi: 10.1073/pnas.81.9.2728.

DOI:10.1073/pnas.81.9.2728
PMID:6326140
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC345143/
Abstract

The transforming protein of avian sarcoma virus UR2, p68v-ros, has an associated tyrosine-specific protein kinase activity similar to that of p60v-src and several other oncogene products. However, this activity has not been linked unequivocally to transformation, and the physiological action of these proteins remains in doubt. We now have found that immunoprecipitated p68v-ros also is associated with phosphatidylinositol (PtdIns) kinase (ATP:PtdIns 4-phosphotransferase, EC 2.7.1.67) activity. PtdIns 4,5-bisphosphate [PtdIns(4,5)P2] specifically inhibits both this activity and the autophosphorylation of p68v-ros. Moreover, cells transformed by UR2 showed significant increases in 32P-labeling of PtdIns 4-phosphate (PtdIns4P) and PtdIns(4,5)P2 and in the formation of their catabolites, inositol 1,4-bisphosphate and inositol 1,4,5-trisphosphate, as compared to uninfected cells. These results suggest that a physiologically relevant function of oncogene kinases might be the phosphorylation of PtdIns and that increased turnover of PtdIns4P and PtdIns(4,5)P2 might play a role in transformation by increasing the formation of diacylglycerol, a catabolite of polyphosphoinositides that activates kinase C. This protein copurifies with the phorbol ester receptor, and its activation is likely to be intimately linked with mitogenesis. This hypothesis suggests a mechanism whereby certain oncogene proteins might cause the unrestricted growth typical of transformed cells and could explain why tumor promoters mimic many of the effects of transformation.

摘要

禽肉瘤病毒UR2的转化蛋白p68v-ros具有一种相关的酪氨酸特异性蛋白激酶活性，类似于p60v-src及其他几种癌基因产物的活性。然而，这种活性尚未明确与转化相关联，这些蛋白的生理作用仍存在疑问。我们现在发现，免疫沉淀的p68v-ros也与磷脂酰肌醇（PtdIns）激酶（ATP：PtdIns 4-磷酸转移酶，EC 2.7.1.67）活性相关。磷脂酰肌醇4,5-二磷酸[PtdIns(4,5)P2]特异性抑制这种活性以及p68v-ros的自身磷酸化。此外，与未感染细胞相比，由UR2转化的细胞中磷脂酰肌醇4-磷酸（PtdIns4P）和PtdIns(4,5)P2的32P标记以及它们的分解代谢产物肌醇1,4-二磷酸和肌醇1,4,5-三磷酸的形成均显著增加。这些结果表明，癌基因激酶的一种生理相关功能可能是磷脂酰肌醇的磷酸化，并且PtdIns4P和PtdIns(4,5)P2周转的增加可能通过增加二酰基甘油的形成在转化中发挥作用，二酰基甘油是激活蛋白激酶C的多磷酸肌醇的一种分解代谢产物。这种蛋白与佛波酯受体共同纯化，其激活可能与有丝分裂密切相关。这一假说提出了一种机制，据此某些癌基因蛋白可能导致转化细胞典型的无限制生长，并可以解释为什么肿瘤启动子模拟了许多转化效应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/d055c90a7e87/pnas00610-0137-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/f9829ed3f21c/pnas00610-0136-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/9c80a521dad6/pnas00610-0136-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/820e7944a06a/pnas00610-0136-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/72e46d30a2cd/pnas00610-0136-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/908d101b6091/pnas00610-0136-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/d055c90a7e87/pnas00610-0137-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/f9829ed3f21c/pnas00610-0136-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/9c80a521dad6/pnas00610-0136-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/820e7944a06a/pnas00610-0136-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/72e46d30a2cd/pnas00610-0136-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/908d101b6091/pnas00610-0136-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1636/345143/d055c90a7e87/pnas00610-0137-a.jpg

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