Grant number: | 11/12050-7 |
Support Opportunities: | Scholarships in Brazil - Doctorate |
Effective date (Start): | October 01, 2011 |
Effective date (End): | January 31, 2015 |
Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
Principal Investigator: | Antonio Carlos Boschiero |
Grantee: | Sandra Mara Ferreira |
Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
Abstract ARHGAP21 is a Rho-GAP that, like Cdc42 and FAK, modulates the activity of proteins involved with rearrangement of actin cytoskeleton in pancreatic beta cell, leading the inhibition of insulin secretion. Furthermore, glucose modulates the ARHGAP21/FAK and ARHGAP21/Cdc42 interactions, which may explain, at least in part, the control of insulin secretion by ARHGAP21. However, the pathways by which glucose control ARHGAP21 remain unknowns. In addition, despite of ARHGAP21 is related with protein involved with rearrangement of actin cytoskeleton, and, therefore, extrusion of insulin granule, still not known the role of ARHGAP21 on secretory machinery and release of insulin granule. Therefore, the aim of study is assessed in MIN6 cells and isolated islets of mice, the possible pathways of glucose signalization modulate the ARHGAP21 activity and the possible control of secretory machinery and insulin release in that Rho-GAP. | |
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