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Web Desc
Diabetes Mellitus: Molecular Signaling, Genes and Therapeutics
joint with Molecular Control of Adipogenesis and Obesity
Organizer(s): Michael P. Czech and Douglas A. Melton
Date: March 04 - 10, 2004
Location: Fairmont Banff Springs, Banff, AB, Canada
Sponsored by Biovitrum AB and Lilly Research Laboratories
Summary of Meeting:
The current worldwide epidemic of Diabetes Mellitus has fueled intensive efforts to understand the basic genetic and molecular mechanisms of cell signaling in a variety of relevant tissues. These research efforts by both basic and clinical scientists have successfully utilized the technologies of genomics, proteomics and chemical biology as well as the traditional tools of genetics, physiology and molecular and cell biology to yield exciting new insights into this disease. Particularly novel findings relate to the interface between insulin signaling and membrane trafficking; beta cell development and apoptosis; adipocyte signaling to brain, beta cells, liver and muscle; and the role of cytokines in insulin resistance. The goal of the conference (to be held jointly with the Molecular Control of Adipogenesis and Obesity conference organized by Stephen Farmer and Sheila Collins) is to bring together scientists working in several intersecting areas of the field, e.g., the application of new technologies to diabetes; stem cell and developmental biology; regulated membrane trafficking; integration of metabolism and gene expression; and chemistry and therapeutics. The conference will also explore the integration and utility of information derived from recently obtained gene and protein databases, as well as repositories of protein-protein interactions. Half of the sessions will be jointly held with the concurrent meeting on adipogenesis in order to optimize the information flow between researchers in the fields of the related syndromes of diabetes and obesity. Identify key intracellular and intercellular signaling elements that function to: 1. Regulate and coordinate metabolic pathways among tissues, 2. Provide control switches for proliferation, differentiation, apoptosis of diabetes-related tissues, 3. Control neuroendocrine pathways that regulate appetite and metabolism, and 4. Regulate nuclear factors that control glucose and lipid homeostasis. Analyze data derived from genomic and proteomic technologies combined with bioinformatics for probing gene functions in the etiology of diabetes syndromes. Initiate collaborative efforts with other investigators who use complementary approaches and/or techniques to study the molecular and physiological bases of diabetes, and to develop novel therapeutic initiatives.
Discounted Abstract Deadline: November 3 2003
Discounted Registration Deadline: January 5 2004
We gratefully acknowledge additional support for this conference from:
Biovitrum ABEducational grant from Lilly USA, LLCJDRF
TestDiet division Purina Mills LLC
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Grant No. 1R13DK067026-01
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

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Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

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