Julia Haupt, Ph.D.
University of Pennsylvania
Hometown: Freiberg, Germany
Education: Post-Doctoral Fellow, University of Pennsylvania, Philadelphia, PA; Dr.rer.nat.(Doctor of Science), 2012, Free University of Berlin, Berlin, Germany; Diploma Biology, 2006, Friedrich-Schiller University Jena, Germany
Areas of Special Interest:
Fibrodysplasia ossificans progressive (FOP): biomechanical force sensing in progenitor cells and its implication in ectopic bone formation
Julia joined our lab in the spring of 2012 as a post-doctoral fellow. In her doctoral work she focused on the functional characterization of different FOP mutations.
Peer Reviewed Publications:
Haupt J, Deichsel A, Stange K, Ast C, Bocciardi R, Ravazzolo R, Di Rocco M, Ferrari P, Landi A, Kaplan FS, Shore EM, Reissner C, Seemann P. (2014). ACVR1 p.Q207E causes classic fibrodysplasia ossificans progressiva and is functionally distinct from the engineered constitutively active ACVR1 p.Q207D variant. Hum Mol Genet. 23 (20), 5364-5377.
Stricker S, Mathia S, Haupt J, Seemann P, Meier J, Mundlos S. (2011). Odd-skipped related genes regulate differentiation of embryonic limb mesenchyme and bone marrow mesenchymal stromal cells. Stem Cells Dev.; 21(4):623-33.
Kaplan FS, Seemann P, Haupt J, Xu M, Lounev VY, Mullins M, Shore EM. (2010). Investigations of activated ACVR1/ALK2, a bone morphogenetic protein type I receptor, that causes fibrodysplasia ossificans progressiva. Methods Enzymol.;484:357-73.
Villavicencio-Lorini P, Kuss P, Friedrich J, Haupt J, Farooq M, TÃ¼rkmen S, Duboule D, Hecht J, Mundlos S. (2010). Homeobox genes d11-d13 and a13 control mouse autopod cortical bone and joint formation. J Clin Invest.;120(6):1994-2004.
Seemann P, Brehm A, Konig J, Reissner C, Stricker S, Kuss P, Haupt J, Renninger S, Nickel J, Sebald W, Groppe JC, Ploger F, Pohl J, Schmidt-von Kegler M, Walther M, Gassner I, Rusu C, Janecke AR, Dathe K, Mundlos S. (2010). Mutations in GDF5 reveal a key residue mediating BMP inhibition by NOGGIN. PLoS Genet.;5(11):e1000747.
Shen Q, Little SC, Xu M, Haupt J, Ast C, Katagiri T, Mundlos S, Seemann P, Kaplan FS, Mullins MC, Shore EM. (2009). The fibrodysplasia ossificans progressiva R206H ACVR1 mutation activates BMP-independent chondrogenesis and zebrafish embryo ventralization. J Clin Invest.;119(11):3462-72.
Stricker S, Brieske N, Haupt J, Mundlos S. (2006). Comparative expression pattern of Odd-skipped related genes Osr1 and Osr2 in chick embryonic development. Gene Expr Patterns.;6(8):826-34.
Conferences Presentations and Abstracts:
Altered force sensing and cell-cell adhesion by mutant ACVR1/ALK2 FOP progenitor cells – implications for heterotopic ossification. American Society for Bone Mineral Research Annual Meeting, September 2014, Houston, Texas.
Regulation of cell differentiation by mechanical signals. Department of Genetics Postdoctoral & Graduate Student Research Talks, May 2013; University of Pennsylvania, Philadelphia, USA.
Haupt, J., A. Deichsel, K. Stange, E. Kajikhina, C. Ast, N. Souidi, F.S. Kaplan, E.M. Shore, P. Seemann. Functional consequences of fibrodysplasia ossificans progressiva-associated mutations ACVR1R206H and ACVR1Q207E in comparison to constitutive active ACVR1Q207D. Presented at the American Society for Bone and Mineral Research Annual Meeting; Minneapolis, MN, October, 2012.
Haupt J, Cosgrove B, McLeod C, Culbert A, Mauck RL, Shore EM. Altered force sensing and cell-cell adhesion by mutant ACVR1/ALK2 FOP progenitor cells – implications for heterotopic ossification. Presented at the National Bone Health Alliance (NBHA) Rare Bone Disease Workshop; Houston, TX, September, 2014.
2014 ASBMR Young Investigator Award
2014 Penn Center of Musculoskeletal Disorders (PCMD) First Place Poster Award, Bioengineering category.