Agency Fact Sheet, Department of Commerce: Insurance Division, FY2010

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Agency Fact Sheet, Department of Commerce: Professional Licensure Division, FY2010

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Agency Fact Sheet, Department of Commerce: Alcoholic Beverages Division, FY2011

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Agency Fact Sheet, Department of Commerce: Banking Division, FY2011

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Agency Fact Sheet, Department of Commerce: Credit Union Division, FY2011

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Agency Fact Sheet, Department of Commerce: Insurance Division, FY2011

This document produced by the Iowa Department of Administrative Services has been developed to provide a multitude of information about executive branch agencies/department on a single sheet of paper. The facts provides general information, contact information, workforce data, leave and benefits information and affirmative action data.

Agency Fact Sheet, Department of Commerce: Professional Licensure Division, FY2011

This document produced by the Iowa Department of Administrative Services has been developed to provide a multitude of information about executive branch agencies/department on a single sheet of paper. The facts provides general information, contact information, workforce data, leave and benefits information and affirmative action data.

Agency Fact Sheet, Department of Commerce: Banking Division, FY2002

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Agency Fact Sheet, Department of Commerce: Credit Union Division, FY2002

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Agency Fact Sheet, Department of Commerce: Insurance Division, FY2002

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Agency Fact Sheet, Department of Commerce: Professional Licensure Division, FY2002

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Insulin and insulin-like growth factor I receptors utilize different G protein signaling components.

We examined the role of heterotrimeric G protein signaling components in insulin and insulin-like growth factor I (IGF-I) action. In HIRcB cells and in 3T3L1 adipocytes, treatment with the Galpha(i) inhibitor (pertussis toxin) or microinjection of the Gbetagamma inhibitor (glutathione S-transferase-betaARK) inhibited IGF-I and lysophosphatidic acid-stimulated mitogenesis but had no effect on epidermal growth factor (EGF) or insulin action. In basal state, Galpha(i) and Gbeta were associated with the IGF-I receptor (IGF-IR), and after ligand stimulation the association of IGF-IR with Galpha(i) increased concomitantly with a decrease in Gbeta association. No association of Galpha(i) was found with either the insulin or EGF receptor. Microinjection of anti-beta-arrestin-1 antibody specifically inhibited IGF-I mitogenic action but had no effect on EGF or insulin action. beta-Arrestin-1 was associated with the receptors for IGF-I, insulin, and EGF in a ligand-dependent manner. We demonstrated that Galpha(i), betagamma subunits, and beta-arrestin-1 all play a critical role in IGF-I mitogenic signaling. In contrast, neither metabolic, such as GLUT4 translocation, nor mitogenic signaling by insulin is dependent on these protein components. These results suggest that insulin receptors and IGF-IRs can function as G protein-coupled receptors and engage different G protein partners for downstream signaling.

Agency Fact Sheet, Department of Commerce: Credit Union Division, FY2003

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Agency Fact Sheet, Department of Commerce: Alcoholic Beverages Division, FY2003

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Agency Fact Sheet, Department of Commerce: Banking Division, FY2003

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