David L. Allen - US grants
Affiliations: | University of Colorado, Boulder, Boulder, CO, United States |
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The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, David L. Allen is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 2004 — 2008 | Allen, David L [⬀] | K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Matrix Metalloproteinases, Exercise, and Muscle Damage @ University of Colorado At Boulder DESCRIPTION (provided by applicant): Candidate. The candidate, David L. Allen, Ph.D., is a research associate with extensive experience in both physiology and molecular biology. Dr. Allen's past and current research has focused on the cellular and molecular mechanisms underlying skeletal muscle adaptation in animals. His immediate career goal is to acquire any and all research and professional skills necessary for achieving his long-term goal of developing an independent, extramurally-funded translational research program focusing on the molecular mechanisms underlying exercise adaptation in both animals and humans. The proposed development plan will provide Dr. Allen with the additional experience and training necessary to achieve this goal. Career Development plan. Dr. Allen's proposed training activities consist of: (1) acquiring new research skills associated with the proposed research plan; (2) structured activities including attendance and presentation at journal clubs, colloquia, and national and local scientific meetings, and regular interactions with his mentoring team. Environment. The primary sponsor, Dr. Douglas Seals, is an extramurally funded scientist with a record of mentoring and two decades of experience in human exercise research; the co-sponsors provide guidance in specific components of the research plan, including muscle physiology, molecular biology, and genetics. Research. The hypotheses to be tested in this proposal are the following: (1) increased expression of matrix metalloproteinases (MMPs) is a central component of eccentric exercise-induced muscle damage and/or repair; (2) variations in transcription as a consequence of promoter polymorphisms in the MMP genes are responsible for at least part of the variation in muscle damage and soreness in humans following eccentric exercise. Systemic and muscle MMP levels will be assessed in human subjects following a bout of eccentric exercise and will be correlated with indices of muscle damage and muscle soreness. In addition, pharmacological and genetic manipulations will be used in mice to directly evaluate the causal role of MMPs in muscle damage and repair. Finally, subjects will be genotyped for known functional MMP promoter polymorphisms, which will be correlated with MMP levels and muscle damage and soreness following eccentric exercise. |
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| 2008 — 2010 | Allen, David L [⬀] Allen, David L [⬀] | R03Activity Code Description: To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
Regulation of Exercise-Induced Il-6 Expression in Skeletal Muscle @ University of Colorado DESCRIPTION (provided by applicant): Interleukin-6 (IL-6) is a cytokine secreted by many cell types, including skeletal muscle. Under basal conditions, skeletal muscle IL-6 expression is minimal, but its mRNA expression and secretion increase up to a hundredfold in response to a single bout of endurance exercise. Secreted IL-6 appears to act as a sensor linking increased muscle activity with mobilization of substrate stores from liver and fat, as it increases liver glycogenolysis and adipose lipolysis. Currently the molecular mechanisms governing exercise-induced IL-6 expression in skeletal muscle are poorly defined. The purpose of this proposal is to develop an integrative, translational program of research using animal models and human studies to elucidate the mechanisms underlying exercise-induced IL-6 expression in skeletal muscle. The major aims of this research are threefold: (1) to develop a mouse model of IL-6 exercise responsiveness with which we will test the effects of different exercise paradigms on IL-6 expression in vivo;(2) to examine whether increased transcription is responsible for the increase in IL-6 mRNA expression in mouse and human muscle in response to exercise;(3) to determine whether specific IL-6 promoter polymorphisms affect muscle IL-6 expression in human subjects undergoing a single bout of endurance exercise. IL-6 pre-mRNA, mature IL-6 mRNA, and luciferase activity will be quantified in response to a single bout of endurance exercise in mice containing an IL-6 promoter- reporter transgene. In addition, we will compare the effects of different exercise modalities (voluntary vs. forced running), different exercise variables (intensity and duration), and muscle fiber type on the exercise IL-6 response. Finally, human subjects will be genotyped for the IL-6 -174 G/C polymorphism and will be exercised to determine whether exercise-induced IL-6 transcription differs in subjects with different IL-6 genotypes. Together these data should provide insights into the mechanisms governing exercise-induced IL-6 expression in muscle that may assist in the development of optimally effective training programs for persons suffering from conditions such as obesity and diabetes which are characterized by defects in substrate mobilization. The proposed research seeks to understand how a gene called interleukin-6 (IL-6) is regulated in skeletal muscle in response to exercise. IL-6 released by skeletal muscle during exercise signals the fat and the liver to release their stores of sugars and fats for use by the contracting muscle, and thus understanding how IL-6 is regulated, and how this gene is turned on during exercise, may provide insights into how to design better exercise regimens to optimize fat and sugar utilization during exercise. This in turn may help prevent the development of disorders such as obesity and diabetes, and may help people who already have these conditions to improve their metabolism and reduce the negative effects of these conditions on their health and well-being. |
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