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Clinical Trials
Melissa Spencer, Ph.D.
   
 
Affiliations
Associate Professor, Neurology
Member, ACCESS Program: Dept. of Molecular, Cell & Integrative Physiology

Education:
Degree: Ph.D.


Contact Information:
Email Address: mspencer@mednet.ucla.edu
Office Address: Office
635 Charles Young Dr. So
mail code 703422
Los Angeles, CA 90095
UNITED STATES
Work Address: Laboratory
635 Charles E. Young Dr. So
mail code 733422
Los Angeles, CA 90095
UNITED STATES
Home Page: http://www.uclaaccess.ucla.edu/cfm/access_faculty.cfm?FacultyKey=881


Direct Contact Information:
Fax Number: 310-206-1998
Work Phone Number: (310) 267-4582 Laboratory
310-794-5225 Office


Additional Information:

Melissa Spencer is an Associate Professor of Neurology and the Co-Director of the Center for Duchenne Muscular Dystrophy at UCLA. Dr. Spencer’s research expertise is in the area of pathogenesis of muscular dystrophy using genetically modified mouse models. She received her Ph.D. in 1994 at UCLA in which she used a biochemical approach to study the role of calpain proteases in mdx muscle. Her post-doctoral training focused on the role of T cells in mdx pathology. She has had a career long interest in pathogenesis of muscular dystrophy (DMD and LGMD) and has extensive experience in generating and phenotyping genetically modified mouse models (transgenic, knock out and knock in models). A particular strength of the Spencer lab is the longitudinal and multidisciplinary approach used to study these muscular dystrophies that ranges from the generation of genetically modified mice to use of biochemical, cell biological, immunological and functional approaches for analyzing phenotypic outcomes. One of these studies was carried into two clinical trials at UCLA, in which Dr. Spencer was the principal investigator, with Dr. Fowler who was a co-investigator; thus, the researchers at the UCLA MDCC are truly performing "bench-to-bedside translational research". Dr. Spencer was the recipient of a PECASE (Presidential Early Career Award For Scientists and Engineers) in 2001. She has participated in numerous NIH advisory committees including as a regular standing member of the SMEP study section. She participated in the generation of the Muscular Dystrophy and Education plan for the NIH as well as the report on the NIH Workshop on Translational Research in Muscular Dystrophy.

Publications:
Cohen, N, Kudryashova, E, Kramerova, I, Anderson,L.V.B. Beckmann, J.S., Bushby, KM and Spencer, M.J. Identification of putative in vivo substrates of calpain 3 by comparative proteomics of over-expressing transgenic and non-transgenic mice. . Proteomics (with cover) 2006; Nov;6(22): 6075-84.
Kramerova, I., Kudryashova, E. and Spencer, M.J. Regulation of M-cadherin-beta-catenin complex by calpain 3 during terminal stages of myogenic differentiation.. Molecular Cellular Biology Nov;26(22) 2006; Nov;26(22): 8437-47.
Kudryashova, E Kudryashov, D Kramerova, I Spencer, MJ Trim32 is a ubiquitin ligase mutated in limb girdle muscular dystrophy type 2H that binds to skeletal muscle myosin and ubiquitinates actin.. Journal of molecular biology.. 2005; 354(2): 413-24.
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Huebsch, KA Kudryashova, E Wooley, CM Sher, RB Seburn, KL Spencer, MJ Cox, GA Mdm muscular dystrophy: interactions with calpain 3 and a novel functional role for titin's N2A domain.. Human molecular genetics.. 2005; 14(19): 2801-11.
Kramerova, I Kudryashova, E Venkatraman, G Spencer, MJ Calpain 3 participates in sarcomere remodeling by acting upstream of the ubiquitin-proteasome pathway.. Human molecular genetics. . 2005; 14(15): 2125-34.
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Kramerova, I Kudryashova, E Tidball, JG Spencer, MJ Null mutation of calpain 3 (p94) in mice causes abnormal sarcomere formation in vivo and in vitro.. Human molecular genetics. . 2004; 13(13): 1373-88.
Fowler, EG Graves, MC Wetzel, GT Spencer, MJ Pilot trial of albuterol in Duchenne and Becker muscular dystrophy.. Neurology. . 2004; 62(6): 1006-8.
Tidball, J.G. and Spencer, M.J. Skipping to new gene therapies for muscular dystrophy.. Nature Medicine 2003; 9(8): 997-998.
Guyon, JR Kudryashova, E Potts, A Dalkilic, I Brosius, MA Thompson, TG Beckmann, JS Kunkel, LM Spencer, MJ Calpain 3 cleaves filamin C and regulates its ability to interact with gamma- and delta-sarcoglycans.. Muscle & nerve. . 2003; 28(4): 472-83.
Spencer, M.J., Guyon, J.R., Sorimachi, H., Potts, A., Richard, I., Herasse, M., Chamberlain, J., Dalkilic, I., Kunkel, L.M., and Beckmann, J.S. Stable expression of calpain 3 from a muscle transgene in vivo; immature muscle in transgenic mice suggests a role for calpain 3 in muscle maturation.. Proceedings of the National Academy of Sciences. 2002; 99(3): 8874-8879.
Tidball, JG Spencer, MJ Expression of a calpastatin transgene slows muscle wasting and obviates changes in myosin isoform expression during murine muscle disuse.. The Journal of physiology. . 2002; 545(Pt 3): 819-28.
Spencer, MJ Mellgren, RL Overexpression of a calpastatin transgene in mdx muscle reduces dystrophic pathology.. Human molecular genetics. . 2002; 11(21): 2645-55.
Spencer, MJ Montecino-Rodriguez, E Dorshkind, K Tidball, JG Helper (CD4(+)) and cytotoxic (CD8(+)) T cells promote the pathology of dystrophin-deficient muscle.. Clinical immunology (Orlando, Fla.) . 2001; 98(2): 235-43.
Spencer, MJ Marino, MW Winckler, WM Altered pathological progression of diaphragm and quadriceps muscle in TNF-deficient, dystrophin-deficient mice.. Neuromuscular disorders : NMD. . 2000; 10(8): 612-9.


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