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癌基因与磷脂酰肌醇代谢

Oncogenes and phosphatidylinositol turnover.

作者信息

Cantley L C, Whitman M, Chahwala S, Fleischman L, Kaplan D R, Schaffhausen B S, Roberts T M

出版信息

Ann N Y Acad Sci. 1986;488:481-90. doi: 10.1111/j.1749-6632.1986.tb46580.x.

DOI:10.1111/j.1749-6632.1986.tb46580.x
PMID:2437850
Abstract

Products of phosphatidylinositol turnover have recently been implicated as regulators of cell growth and differentiation. Transformation of cells in culture by infection with certain viruses (Rous sarcoma virus, Kirsten sarcoma virus, and polyoma virus) or by transfection with the oncogenes carried by these viruses affect the steady-state level of intermediates in the PI turnover pathway. In addition, immunoprecipitates of the transforming gene products of Rous sarcoma virus and polyoma virus contain activities of certain enzymes in the PI turnover pathway. We have previously reported that polyoma middle T immunoprecipitates can catalyze phosphorylation of PI to phosphatidylinositol-4-phosphate (PIP). This activity is not intrinsic to middle T or c-src but is due to a cellular enzyme that specifically associates with this complex. The PI kinase is found in immunoprecipitates of the middle T protein from polyoma viruses that are capable of cell transformation but does not associate with mutants of middle T defective in transformation suggesting that this association may be important for transformation.

摘要

磷脂酰肌醇代谢产物最近被认为是细胞生长和分化的调节因子。通过感染某些病毒(劳氏肉瘤病毒、柯斯顿肉瘤病毒和多瘤病毒)或转染这些病毒携带的癌基因来转化培养中的细胞,会影响磷脂酰肌醇(PI)代谢途径中中间体的稳态水平。此外,劳氏肉瘤病毒和多瘤病毒转化基因产物的免疫沉淀物含有PI代谢途径中某些酶的活性。我们之前报道过,多瘤病毒中T抗原免疫沉淀物可以催化PI磷酸化为磷脂酰肌醇-4-磷酸(PIP)。这种活性并非中T抗原或c-src所固有,而是由于一种与该复合物特异性结合的细胞酶。PI激酶存在于能够进行细胞转化的多瘤病毒中T蛋白的免疫沉淀物中,但不与转化缺陷的中T抗原突变体结合,这表明这种结合可能对转化很重要。

相似文献

1
Oncogenes and phosphatidylinositol turnover.癌基因与磷脂酰肌醇代谢
Ann N Y Acad Sci. 1986;488:481-90. doi: 10.1111/j.1749-6632.1986.tb46580.x.
2
Phosphatidylinositol kinases and cell transformation.
Symp Fundam Cancer Res. 1986;39:165-72.
3
Phosphoinositide kinase activity and transformation.磷酸肌醇激酶活性与转化
Fed Proc. 1986 Oct;45(11):2647-52.
4
Association of phosphatidylinositol kinase activity with polyoma middle-T competent for transformation.磷脂酰肌醇激酶活性与具有转化能力的多瘤病毒中T抗原的关联。
Nature. 1985;315(6016):239-42. doi: 10.1038/315239a0.
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Transformation by polyoma virus middle T antigen.多瘤病毒中T抗原介导的转化
Cancer Surv. 1986;5(2):173-82.
6
Phosphatidylinositol metabolism and polyoma-mediated transformation.磷脂酰肌醇代谢与多瘤病毒介导的转化
Proc Natl Acad Sci U S A. 1986 Jun;83(11):3624-8. doi: 10.1073/pnas.83.11.3624.
7
Common elements in growth factor stimulation and oncogenic transformation: 85 kd phosphoprotein and phosphatidylinositol kinase activity.生长因子刺激与致癌转化中的共同要素:85kd磷蛋白和磷脂酰肌醇激酶活性。
Cell. 1987 Sep 25;50(7):1021-9. doi: 10.1016/0092-8674(87)90168-1.
8
Transformation-defective mutants of polyomavirus middle T antigen associate with phosphatidylinositol 3-kinase (PI 3-kinase) but are unable to maintain wild-type levels of PI 3-kinase products in intact cells.多瘤病毒中T抗原的转化缺陷型突变体与磷脂酰肌醇3激酶(PI 3激酶)相关联,但无法在完整细胞中维持PI 3激酶产物的野生型水平。
J Virol. 1992 Mar;66(3):1702-8. doi: 10.1128/JVI.66.3.1702-1708.1992.
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An 81 kd protein complexed with middle T antigen and pp60c-src: a possible phosphatidylinositol kinase.一种与中T抗原和pp60c-src复合的81kd蛋白质:一种可能的磷脂酰肌醇激酶。
Cell. 1987 Sep 25;50(7):1031-7. doi: 10.1016/0092-8674(87)90169-3.
10
Induction of tumor formation and cell transformation by polyoma middle T antigen in the absence of Src.在缺乏Src的情况下,多瘤病毒中T抗原诱导肿瘤形成和细胞转化。
Oncogene. 1993 Sep;8(9):2521-9.

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