Phosphatidylinositol 3-kinase activity in murine erythroleukemia cells during DMSO-induced differentiation.
Phosphatidylinositol 3-kinase activity in murine erythroleukemia cells during DMSO-induced differentiation.
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DMSO 诱导分化过程中鼠红白血病细胞中磷脂酰肌醇 3-激酶的活性。
DOI：
10.1006/excr.1995.1252
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Cohen,CM
中科院分区：
文献类型：
--
作者：
Ai,Z;Misra,S;Susa,M;Varticovski,L;Cohen,CM
我们用小鼠红白血病细胞（MEL细胞）研究磷脂酰肌醇3-激酶（PI 3-激酶）在红系分化中的作用。当用二甲基亚砜（DMSO）处理时，在纤连蛋白基质上生长的MEL细胞异步地定型为红系分化，其中90%的细胞在处理的第3天定型。我们发现，在前3天的DMSO处理MEL细胞显示出总PI 3-激酶活性的两倍增加和高度磷酸化的PI 3-激酶产物，PIP 3的四倍增加。同时，PI 3-激酶调节亚基p85的含量没有变化。第3天后，PI 3-激酶活性下降，同时细胞中p85抗原消失。PI 3-激酶抑制剂渥曼青霉素在培养基中的列入导致细胞PI 3-激酶活性的抑制和DMSO诱导的红系分化的延迟。这些数据表明PI 3-激酶可能在MEL细胞向红系分化的过程中起关键作用。
We have used murine erythroleukemia cells (MEL cells) to investigate the role of phosphatidylinositol 3-kinase (PI 3-kinase) in erythroid differentiation. When treated with dimethyl sulfoxide (DMSO), MEL cells grown on a fibronectin matrix become committed to erythroid differentiation asynchronously, with 90% of cells becoming committed by Day 3 of treatment. We found that during the first 3 days of DMSO treatment MEL cells showed a twofold increase in total PI 3-kinase activity and a fourfold increase in the highly phosphorylated PI 3-kinase product, PIP3. At the same time there was no change in the content of p85, the PI 3-kinase regulatory subunit. After Day 3, PI 3-kinase activity declined, in parallel with a disappearance of p85 antigen from the cells. Inclusion of the PI 3-kinase inhibitor Wortmannin in the culture medium resulted in an inhibition of cellular PI 3-kinase activity and a delay in DMSO-induced erythroid differentiation. These data suggest that PI 3-kinase may play a critical role during commitment of MEL cells to erythroid differentiation.