二酰基甘油激酶θ结合和负RhoA受活跃。
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Houssa B, de Widt J, Kranenburg O, Moolenaar WH,范Blitterswijk WJ
二酰基甘油激酶θ结合和负RhoA受活跃。
J生物化学杂志。1999年3月12日,274 (11):6820 - 2。
- PubMed ID
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10066731 (在PubMed]
- 文摘
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二酰基甘油激酶(DGK)磷酸化第二信使产生磷脂酸甘油二酯。到目前为止,很少有人了解DGK活动的监管。我们以前确认DGKtheta同形像,主要是表现在大脑(Houssa B。Schaap D。van der细胞膜,J。Goto, K。近藤,H。Yamakawa,。柴田则M。Takenawa, T。,范Blitterswijk w . j .(1997)生物。272年化学,10422 - 10428)。我们现在报告专门DGKtheta绑定激活RhoA在nontransfected转染COS细胞以及神经n1e - 115细胞。 Binding is abolished by a point mutation (Y34N) in the effector loop of RhoA. DGKtheta does not bind to inactive RhoA, nor to the other Rho-family GTPases, Rac or Cdc42. Like active RhoA, DGKtheta localizes to the plasma membrane. Strikingly, the binding of activated RhoA to DGKtheta completely inhibits DGK catalytic activity. Our results suggest that DGKtheta is a downstream effector of RhoA and that its activity is negatively regulated by RhoA. Through accumulation of newly produced diacylglycerol, RhoA-mediated inhibition of DGKtheta may lead to enhanced PKC activity in response to external stimuli.