Academic Title: Dr.
First Name: Ulrike
Last Name: Baschant
Academic Degree: PhD
Member Since: May 2017
City: Dresden (Germany)
Institution: Department of Endocrinology, Diabetes and Bone Diseases; University Hospital Dresden
Ulrike studied biochemistry in Jena (Germany) and received her PhD in 2011 in the field of osteoimmunolgy at the Institute for Age Research in the group of Prof. Jan Tuckermann. During her PhD thesis she studied the mechanisms of glucocorticoid-induced osteoporosis and of glucocorticoid therapy in inflammatory bone diseases.
After her PhD she continued for another two years in the lab of Prof. Jan Tuckermann and moved with his group to Ulm (University Ulm, Germany) where she further elucidated glucocorticoid effects in bone.
In 2013, Ulrike joined the lab of Prof. Lorenz Hofbauer in Dresden (Germany) to study molecular mechanisms of osteohematological bone diseases in preclinical models. One of her main projects she is currently working on is to assess the consequences of iron-overload on bone and the hematopoietic stem cell niche.
Recently she became also interested in understanding age-related alterations of the osteohematopoietic niche and to decipher mechanisms how osteoblast-targeted and lifestyle interventions slow down age-related pathological processes
- Eva-Luise Köhler Award
- Copp Prize
- DFG Grant "Glucocorticoids and HSCs"
List of 5 Best Publications
- Transferrin receptor 2 controls bone mass and pathological bone formation via BMP and Wnt signalinghttps://www.nature.com/articles/s42255-018-0005-8
- Glucocorticoid receptor in stromal cells is essential for Glucocorticoid-mediated suppression of inflammation in arthritishttps://ard.bmj.com/content/77/11/1610
- Wnt5a is a key target for the pro-osteogenic effects of iron chelation on osteoblast progenitorshttps://haematologica.org/article/view/7906
- The multiple facets of Glucocorticoid action in rheumatoid arthritishttps://www.nature.com/articles/nrrheum.2012.166
- Dicer ablation in osteoblasts by Runx2 driven cre-loxP recombination affects bone integrity, but not Glucocorticoid-induced suppression of bone formationhttps://www.nature.com/articles/srep32112