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      START-GAP3/DLC3 is a GAP for RhoA and Cdc42 and is localized in focal adhesions regulating cell morphology

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      Biochemical and Biophysical Research Communications
      Elsevier BV

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          Abstract

          In the human genome there are three genes encoding RhoGAPs that contain the START (steroidogenic acute regulatory protein (StAR)-related lipid transfer)-domain. START-GAP3/DLC3 is a tumor suppressor gene similar to two other human START-GAPs known as DLC1 or DLC2. Although expression of START-GAP3/DLC3 inhibits the proliferation of cancer cells, its molecular function is not well understood. In this study we carried out biochemical characterization of START-GAP3/DLC3, and explored the effects of its expression on cell morphology and intracellular localization. We found that START-GAP3/DLC3 serves as a stimulator of PLCdelta1 and as a GAP for both RhoA and Cdc42 in vitro. Moreover, we found that the GAP activity is responsible for morphological changes. The intracellular localization of endogenous START-GAP3/DLC3 was explored by immunocytochemistry and was revealed in focal adhesions. These results indicate that START-GAP3/DLC3 has characteristics similar to other START-GAPs and the START-GAP family seems to share common characteristics.

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          Author and article information

          Journal
          Biochemical and Biophysical Research Communications
          Biochemical and Biophysical Research Communications
          Elsevier BV
          0006291X
          December 2007
          December 2007
          : 364
          : 4
          : 783-789
          Article
          10.1016/j.bbrc.2007.10.052
          17976533
          06754c35-9ff0-4d16-afb0-e48e12a82d3c
          © 2007

          https://www.elsevier.com/tdm/userlicense/1.0/


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