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首页> 外文期刊>Biochimica et biophysica acta. Molecular cell research >Recruitment and activation of SLK at the leading edge of migrating cells requires Src family kinase activity and the LIM-only protein 4
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Recruitment and activation of SLK at the leading edge of migrating cells requires Src family kinase activity and the LIM-only protein 4

机译：在迁移细胞的前沿招募和激活SLK需要Src家族激酶活性和仅LIM蛋白4

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摘要

The Ste20-like kinase SLK plays a pivotal role in cell migration and focal adhesion turnover and is regulated by the LIM domain-binding proteins Ldb1 and Ldb2. These adapter proteins have been demonstrated to interact with LMO4 in the organization of transcriptional complexes. Therefore, we have assessed the ability of LMO4 to also interact and regulate SLK activity. Our data show that LMO4 can directly bind to SLK and activate its kinase activity in vitro and in vivo. LMO4 can be co-precipitated with SLK following the induction of cell migration by scratch wounding and Cre-mediated deletion of LMO4 in conditional LMO4(fl/fl) fibroblasts inhibits cell migration and SLK activation. Deletion of LMO4 impairs Ldb1 and SLK recruitment to the leading edge of migrating cells. Supporting this, Src/Yes/Fyn-deficient cells (SYF) expressing very low levels of LMO4 do not recruit SLK to the leading edge. Re-expression of wildtype Myc-LMO4 in SYF cells, but not a mutant version, restores SLK localization and kinase activity. Overall, our data suggest that activation of SLK by haptotactic signals requires its recruitment to the leading edge by LMO4 in a Src-dependent manner. Furthermore, this establishes a novel cytosolic role for the transcriptional co-activator LMO4. (C) 2015 Elsevier B.V. All rights reserved.
机译：Ste20样激酶SLK在细胞迁移和粘着粘附转换中起关键作用，并受LIM域结合蛋白Ldb1和Ldb2的调节。已经证明这些衔接蛋白在转录复合物的组织中与LMO4相互作用。因此，我们评估了LMO4相互作用和调节SLK活性的能力。我们的数据表明，LMO4可以直接与SLK结合并在体内和体外激活其激酶活性。 LMO4可以与SLK共同沉淀，然后通过刮擦伤诱导细胞迁移，并且在条件LMO4（fl / fl）成纤维细胞中Cre介导的LMO4缺失抑制细胞迁移和SLK活化。 LMO4的缺失会损害Ldb1和SLK募集到迁移细胞的前沿。支持这一点的是，表达非常低水平的LMO4的Src / Yes / Fyn缺陷细胞（SYF）不会将SLK募集到最前沿。在SYF细胞中重新表达野生型Myc-LMO4，而不是突变体版本，可以恢复SLK定位和激酶活性。总体而言，我们的数据表明，通过触觉信号激活SLK需要LMO4以Src依赖性方式将其募集到最前沿。此外，这为转录共激活因子LMO4建立了新的胞质作用。 （C）2015 Elsevier B.V.保留所有权利。

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