Stt4磷脂酰肌醇4-激酶定位于质膜，并在Pkc1介导的丝裂原活化蛋白激酶级联反应中发挥作用。

Stt4 PI 4-kinase localizes to the plasma membrane and functions in the Pkc1-mediated MAP kinase cascade.

作者信息

Audhya Anjon, Emr Scott D

机构信息

Division of Cellular and Molecular Medicine, The Howard Hughes Medical Institute, School of Medicine, University of California San Diego, La Jolla, CA 92093, USA.

出版信息

Dev Cell. 2002 May;2(5):593-605. doi: 10.1016/s1534-5807(02)00168-5.

DOI:10.1016/s1534-5807(02)00168-5

PMID:12015967

Abstract

Production of the essential phospholipid PI4P at the Golgi by the Pik1 kinase is required for protein secretion, while a distinct pool of PI4P generated by the Stt4 kinase is critical for normal actin cytoskeleton organization. We identify a transmembrane protein that stabilizes Stt4 at the plasma membrane where it directs synthesis of PI4P, which is required for activation of the Rho1/Pkc1-mediated MAP kinase cascade. Inactivation of Stt4 or the PI4P 5-kinase Mss4 results in mislocalization of the Rho-GTPase GEF Rom2. Rom2 binds PI4,5P(2) through its PH domain and represents the first identified effector in the Stt4-Mss4 pathway. Based on these results, we propose that Stt4-Mss4 generates PI4,5P(2) at the plasma membrane, required to recruit/activate effector proteins such as Rom2.

摘要

Pik1激酶在高尔基体产生必需磷脂PI4P是蛋白质分泌所必需的，而由Stt4激酶产生的不同的PI4P池对于正常肌动蛋白细胞骨架组织至关重要。我们鉴定出一种跨膜蛋白，它在质膜上稳定Stt4，在那里Stt4指导PI4P的合成，这是激活Rho1/Pkc1介导的MAP激酶级联反应所必需的。Stt4或PI4P 5-激酶Mss4的失活导致Rho-GTPase GEF Rom2的定位错误。Rom2通过其PH结构域结合PI4,5P(2)，是Stt4-Mss4途径中第一个被鉴定的效应器。基于这些结果，我们提出Stt4-Mss4在质膜上产生PI4,5P(2)，这是招募/激活诸如Rom2等效应蛋白所必需的。