Mammalian phospholipase D physiological and pathological roles.

Mammalian phospholipase D physiological and pathological roles.
复制标题

DOI:
10.1111/j.1748-1716.2011.02298.x
复制
发表时间:
2012-02
期刊:
Acta physiologica (Oxford, England)
影响因子:
--
通讯作者:
Frohman MA
Frohman MA
中科院分区:
其他
文献类型:
--
作者:
Peng X;Frohman MA

文献摘要

参考文献

被引文献

相似文献

磷脂酶D(PLD)是一个信号传导酶超家族,最常产生脂质第二信使磷脂酸(PA),存在于从细菌到人的多种生物体中,并在多种细胞途径中发挥作用。自20世纪80年代初首次描述哺乳动物PLD活性以来,大多数关于PLD功能的重要见解都是从细胞模型的研究中获得的。哺乳动物PLD超家族成员的生理和病理生理作用的报告现在开始出现通过遗传模型。在这篇综述中,我们总结了PLD功能在这些模型系统的最新研究结果,突出了新认识的超家族的癌症,神经元病理生理学,心血管疾病,精子发生和传染病的连接。
Phospholipase D (PLD), a superfamily of signaling enzymes that most commonly generate the lipid second messenger Phosphatidic Acid (PA), is found in diverse organisms from bacteria to man and functions in multiple cellular pathways. Since the early 1980’s when mammalian PLD activities were first described, most of the important insights concerning PLD function have been gained from studies on cellular models. Reports on physiological and pathophysiological roles for members of the mammalian PLD superfamily are now starting to emerge through from genetic models. In this review, we summarize recent findings on PLD functions in these model systems, highlighting newly appreciated connections of the superfamily to cancer, neuronal pathophysiology, cardiovascular topics, spermatogenesis, and infectious disease.
缺乏磷脂酶D1的小鼠中的α(IIB)β(3)整联蛋白活化和剪切依赖性血栓形成。
DOI: 10.1126/scisignal.2000551
发表时间: 2010-01-05
期刊: Science signaling
影响因子: 7.3
作者:
Elvers M;Stegner D;Hagedorn I;Kleinschnitz C;Braun A;Kuijpers ME;Boesl M;Chen Q;Heemskerk JW;Stoll G;Frohman MA;Nieswandt B
通讯作者: Nieswandt B
DOI: 10.1093/hmg/ddp326
发表时间: 2009-10-15
影响因子: 3.5
作者:
Chen H;Chan DC
通讯作者: Chan DC
DOI: 10.1126/science.1066015
发表时间: 2001-11-30
期刊: SCIENCE
影响因子: 56.9
作者:
Fang, YM;Vilella-Bach, M;Chen, J
通讯作者: Chen, J
DOI: 10.1091/mbc.e03-09-0673
发表时间: 2004-03-01
影响因子: 3.3
作者:
Du, GW;Huang, P;Frohman, MA
通讯作者: Frohman, MA
DOI: 10.1091/mbc.12.4.943
发表时间: 2001-04-01
影响因子: 3.3
作者:
Freyberg, Z;Sweeney, D;Shields, D
通讯作者: Shields, D