M
Marina Schorpp-Kistner
Researcher at German Cancer Research Center
Publications - 43
Citations - 4939
Marina Schorpp-Kistner is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: JUNB & Cellular differentiation. The author has an hindex of 26, co-authored 43 publications receiving 4604 citations. Previous affiliations of Marina Schorpp-Kistner include Heidelberg University.
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Journal ArticleDOI
AP-1 subunits: quarrel and harmony among siblings
TL;DR: AP-1-mediated regulation of processes such as proliferation, differentiation, apoptosis and transformation should be considered within the context of a complex dynamic network of signalling pathways and other nuclear factors that respond simultaneously.
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Altered endochondral bone development in matrix metalloproteinase 13-deficient mice
Dominique Stickens,Danielle J. Behonick,Nathalie Ortega,Babette Heyer,Bettina Hartenstein,Ying Yu,Amanda J. Fosang,Marina Schorpp-Kistner,Peter Angel,Zena Werb +9 more
TL;DR: The hypothesis that proper ECM remodeling is the dominant rate-limiting process for programmed cell death, angiogenesis and osteoblast recruitment during normal skeletal morphogenesis is supported.
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c-Jun and JunB Antagonistically Control Cytokine-Regulated Mesenchymal–Epidermal Interaction in Skin
Axel Szabowski,Nicole Maas-Szabowski,Sven Andrecht,Andrea Kolbus,Marina Schorpp-Kistner,Norbert E. Fusenig,Peter Angel +6 more
TL;DR: It is suggested that the relative activation state of these AP-1 subunits in a non-cell-autonomous, transregulatory fashion directs regeneration of the epidermis and maintenance of tissue homeostasis in skin.
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Function and regulation of AP-1 subunits in skin physiology and pathology
TL;DR: The mouse skin has become the model of choice to study the regulation and function of AP-1 subunits in many physiological and pathological processes in vivo and in vitro, and regulates expression of important components of the cytokine network, cell surface receptors and proteases, which orchestrate the process of wound healing.
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JunB is essential for mammalian placentation
TL;DR: Injection of junB−/− embryonic stem (ES) cells into tetraploid wild‐type blastocysts resulted in a partial rescue, in which the ES cell‐derived fetuses were no longer growth retarded and displayed a normal placental labyrinth.