PtdIns(3,4)P2 instigates focal adhesions to generate podosomes
PtdIns(3,4)P2 instigates focal adhesions to generate podosomes
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DOI：
10.4161/cam.3.2.7510
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发表时间：
2009-04-01
影响因子：
3.2
通讯作者：
Takenawa, Tadaomi
中科院分区：
文献类型：
--
作者：
Oikawa, Tsukasa;Takenawa, Tadaomi
细胞与细胞外基质（ECM）的粘附在细胞增殖、分化和迁移等生物学过程中起着重要作用。与其他类型的粘附结构（局灶性复合体、局灶性粘附等）不同，认为足体和侵入伪足具有除附着之外的其他功能，可能包括侵入ECM。为了使足体和侵入足侵入ECM，参与粘附、肌动蛋白聚合和ECM降解的分子必须被募集到作用位点。我们最近的研究表明，通过最低表达的磷酸肌醇PtdIns（3，4）P2介导的Tks 5-Grb 2支架的募集，随后是N-WASP的积累，在新形成的局灶性粘连附近形成足小体。虽然这项研究证明了在局部粘附转化过程中分子相互作用的细节，但其在体内侵袭过程中的调节仍有待澄清。在这里，我们讨论了局部粘连的转换为podosomes/invadopodia基于目前的理解的分子基础。
Cell-to-extracellular matrix (ECM) adhesion plays important roles in various biological events, such as proliferation, differentiation and migration. Distinct from other types of adhesion structures (focal complexes, focal adhesions and so on), podosomes and invadopodia are thought to have additional functions beyond attachment, possibly including invasion into the ECM. For podosomes and invadopodia to invade into the ECM, molecules involved in adhesion, actin polymerization and ECM degradation must be recruited to sites of action. Our recent study demonstrated that podosomes form near newly formed focal adhesions via the minimally expressed phosphoinositide PtdIns(3,4) P2-mediated recruitment of the Tks5-Grb2 scaffold, followed by the accumulation of N-WASP. Although this study demonstrated details of molecular interplay during the transformation of focal adhesion, its regulation in the in vivo invasion process remains to be clarified. Here, we discuss the molecular bases of the transformation of focal adhesions to podosomes/invadopodia based on current understanding.