Dr. rer. nat. Katja Stange

+49 38208 68-852
Research Institute for Farm Animal Biology (FBN)
Institute of Muscle Biology and Growth
Growth and Development Unit
Wilhelm-Stahl-Allee 2
18196 Dummerstorf

Research interests

  • Skeletal muscle development
  • Physiological role of myogenic cells in the mammalian system
  • Differentiation of mesenchymal stem cells and myogenic precursor cells
  • Possibilities to influence skeletal muscle growth

Curriculum Vitae

  • 2015-present: Scientist, Research Institute for Farm Animal Biology (FBN) Dummerstorf, Institute of Muscle Biology and Growth
  • 2015: Dr. rer. nat., Humboldt University Berlin and completion of Docotral Studies in „Regenerative Therapies“ at Charité Universitätsmedizin Berlin
  • 2012-2014: Doctoral fellowship of the Sonnenfeld-Stiftung
  • 2011-2015: Doctoral studies at Berlin Brandenburg Center for Regenerative Therapies (BCRT), Model Systems for Cell Differentiation, and member of the Berlin Brandenburg School for Regenerative Therapies (BSRT)
  • 2011: Dipl.-Ing., Technical University Berlin
  • 2005-2011: Study of Medical Biotechnology, Technical University Berlin


Stange, K.; Schumacher, T.; Miersch, C.; Whelan, R.; Klünemann, M.; Röntgen, M. (2023):
Methionine Sources Differently Affect Production of Reactive Oxygen Species, Mitochondrial Bioenergetics, and Growth of Murine and Quail Myoblasts In Vitro. CURR ISSUES MOL BIOL 45 (4): 2661-2680
Stange, K.; Keric, A.; Friese, A.; Röntgen, M. (2022):
Preparation of spheroids from primary pig cells in a mid-scale bioreactor retaining their myogenic potential. Cells-Basel 11 (9): 1453, 1-18
Grunow, B.; Stange, K.; Bochert, R.; Tönißen, K. (2021):
Histological and biochemical evaluation of skeletal muscle in the two salmonid species Coregonus maraena and Oncorhynchus mykiss. Plos One 16: e0255062, 1-17
Zhao, Y.; Albrecht, E.; Stange, K.; Li, Z.; Schregel, J.; Sciascia, Q. L.; Metges, C. C.; Maak, S. (2021):
Glutamine supplementation stimulates cell proliferation in skeletal muscle and cultivated myogenic cells of low birth weight piglets. Sci Rep-UK 11: 13432, 1-15
Stange, K.; Ahrens, H. E.; von Maltzahn, J.; Röntgen, M. (2020):
Isolation and ex vivo cultivation of single myofibers from porcine muscle. IN VITRO CELL DEV-AN 56 (8): 585-592
Stange, K.; Miersch, C.; Sponder, G.; Röntgen, M. (2020):
Low birth weight influences the postnatal abundance and characteristics of satellite cell subpopulations in pigs. Sci Rep-UK 10: 6149, 1-14
Hildebrand, L.; Schmidt-von Kegler, M.; Walther, M.; Seemann, P.; Stange, K. (2019):
Limb specific Acvr1-knockout during embryogenesis in mice exhibits great toe malformation as seen in Fibrodysplasia Ossificans Progressiva (FOP). Dev Dynam 248 (5): 396-403
Miersch, C.; Stange, K.; Röntgen, M. (2018):
Effects of trypsinization and of a combined trypsin, collagenase, and DNase digestion on liberation and in vitro function of satellite cells isolated from juvenile porcine muscles. IN VITRO CELL DEV-AN 54 (6): 406-412
Miersch, C.; Stange, K.; Röntgen, M. (2018):
Separation of functionally divergent muscle precursor cell populations from porcine juvenile muscles by discontinuous Percoll density gradient centrifugation. BMC Cell Biol 19: 2, 1-12
Miersch, C.; Stange, K.; Hering, S.; Kolisek, M.; Viergutz, T.; Röntgen, M. (2017):
Molecular and functional heterogeneity of early postnatal porcine satellite cell populations is associated with bioenergetic profile. Sci Rep-UK 7: 45052, 1-14
Hildebrand, L.; Stange, K.; Deichsel, A.; Gossen, M.; Seemann, P. (2017):
The Fibrodysplasia Ossificans Progressiva (FOP) mutation p.R206H in ACVR1 confers an altered ligand response. CELL SIGNAL 29: 23-30
Stange, K.; Ott, C.E.; Schmidt-von Kegler, M.; Gillesen-Kaesbach, G.; Mundlos, S.; Dathe, K.; Seemann, P. (2015):
Brachydactyly Type C patient with compound heterozygosity for p.Gly319Val and p.Ile358Thr variants in the GDF5 proregion: benign variants or mutations?. J Hum Genet 60 (8): 419-425
Stange, K.; Désir, J.; Kakar, N.; Müller, T.D.; Budde, B.S.; Gordon, C.T.; Horn, D.; Seemann, P.; Borck, G. (2015):
A hypomorphic BMPR1B mutation causes du Pan acromesomelic dysplasia. Orphanet J Rare Dis 10: 84, 1-6