期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 21, 期 2, 页码 595-602出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.21.2.595-602.2001
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资金
- NATIONAL CANCER INSTITUTE [R29CA046677, R01CA046677] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [G12RR003037] Funding Source: NIH RePORTER
- NCI NIH HHS [CA46677, R01 CA046677] Funding Source: Medline
- NCRR NIH HHS [G12 RR003037, RR-03037] Funding Source: Medline
In response to epidermal growth factor (EGF), the EGF receptor is endocytosed and degraded. A substantial lag period exists between endocytosis and degradation, suggesting that endocytosis is more than a simple negative feedback Phospholipase D (PLD), which has been implicated in vesicle formation in the Golgi, is activated in response to EGF and other growth factors. We report here that EGF receptor endocytosis is dependent upon PLD and the PLD1 regulators, protein kinase C alpha and RalA. EGF-induced receptor degradation is accelerated by overexpression of either wild-type PLD1 or PLD2 and retarded by overexpression of catalytically inactive mutants of either PLD1 or PLD2, EGF-induced activation of mitogen-activated protein kinase, which is dependent upon receptor endocytosis, is also dependent upon PLD. These data suggest a role for PLD in signaling that facilitates receptor endocytosis.
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