The administrative core of the Senator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center will coordinate the activities within and outside the Center as well as promote an interactive and collaborative research environment. The responsibilities of Core A include the following: organization of the flow of project information, distribution of research effort, allocation of budgetary and other resources, preparing annual budgets and projections, scheduling and facilitating regular Muscle Disease Neuropathology Conference meetings, and consulting the Dean regarding progress, scientific direction, administrative issues and concerns, and future plans. The scientific responsibilities of Core A include the following: scientific integration, coordination, and direction of research projects as needed, consultation with advisors and consultants concerning importance and progress of the research as it relates to other current and developing muscular dystrophy research, identifying seminar speakers and coordinating their participation and contributions to the Center, and holding an annual retreat for the Center Investigators. This core will also facilitate expansion of our collaboration with national and international leaders in the field of congenital/limbgirdle muscular dystrophy. The Core A Administrator coordinates an annual open house for the Muscular Dystrophy Association located in Cedar Rapids, lowa which hosts seminars for approximately 100 patients/families to discuss current and upcoming research and advancements in muscular dystrophy. The Administrator is also responsible for coordinating the Wellstone Steering Committee Face to Face Meeting when hosted by the University of lowa, coordinating meetings among Core Directors and Project Leaders, and coordinating patient/family tours.
The administrative core of our MDCRC renewal will coordinate the overall mission of the MDCRC by providing essential administrative support (for example tracking the budget and coordinating patient visits) for the two two projects and other cores in order to accelerate the tempo of discovery in preclinical translational research and the achievement of clinical trial readiness.
|Clements, Reena; Turk, Rolf; Campbell, Kevin P et al. (2017) Dystroglycan Maintains Inner Limiting Membrane Integrity to Coordinate Retinal Development. J Neurosci 37:8559-8574|
|Brun, Brianna N; Mockler, Shelley R H; Laubscher, Katie M et al. (2017) Comparison of brain MRI findings with language and motor function in the dystroglycanopathies. Neurology 88:623-629|
|Brun, Brianna N; Mockler, Shelley R H; Laubscher, Katie M et al. (2017) Childhood Activity on Progression in Limb Girdle Muscular Dystrophy 2I. J Child Neurol 32:204-209|
|Shaw, Natalie D; Brand, Harrison; Kupchinsky, Zachary A et al. (2017) SMCHD1 mutations associated with a rare muscular dystrophy can also cause isolated arhinia and Bosma arhinia microphthalmia syndrome. Nat Genet 49:238-248|
|Rader, Erik P; Turk, Rolf; Willer, Tobias et al. (2016) Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle. Proc Natl Acad Sci U S A 113:10992-7|
|Praissman, Jeremy L; Willer, Tobias; Sheikh, M Osman et al. (2016) The functional O-mannose glycan on ?-dystroglycan contains a phospho-ribitol primed for matriglycan addition. Elife 5:|
|Turk, Rolf; Hsiao, Jordy J; Smits, Melinda M et al. (2016) Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy. Mol Cell Proteomics 15:2169-85|
|de Greef, Jessica C; Hamlyn, Rebecca; Jensen, Braden S et al. (2016) Collagen VI deficiency reduces muscle pathology, but does not improve muscle function, in the ?-sarcoglycan-null mouse. Hum Mol Genet 25:1357-69|
|Inamori, Kei-Ichiro; Beedle, Aaron M; de Bernabé, Daniel Beltrán-Valero et al. (2016) LARGE2-dependent glycosylation confers laminin-binding ability on proteoglycans. Glycobiology 26:1284-1296|
|Jerber, Julie; Zaki, Maha S; Al-Aama, Jumana Y et al. (2016) Biallelic Mutations in TMTC3, Encoding a Transmembrane and TPR-Containing Protein, Lead to Cobblestone Lissencephaly. Am J Hum Genet 99:1181-1189|
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