|My Research Interest in RESIST|
Our research focus in RESIST is to gain a detailed understanding of adenoviral replication strategies and manipulation of the host cell nuclear processes as a basis to further develop novel antiviral intervention therapies.
Human adenoviruses cause conjunctivitis, gastrointestinal illnesses and pneumonia, among other things. In most cases however an infection exhibits no symptoms or only mild symptoms in healthy adults. However, for individuals with immune system deficiencies the course of the infection can have serious effects or even be fatal. An infection is particularly dangerous for children following a stem cell transplant. In this case, we need to block virus replication and lower the mortality rate for infected patients.
Within this research program, we are investigating how the virus reproduces in the cell with a special focus on marked changes in what are called PML nuclear complexes made up of several proteins within the cell. These structures, which are round in the uninfected cell, dissolve after adenovirus infection and form elongated fibrils. This pathogenic process will be modulated and blocked to hinder the virus making use of this cellular manipulation for their own reproduction and benefit. Same strategies will be also validated for other human pathogenic viruses to develop broad spectrum intervention therapies.
Prof. Schreiner about her scientific work
Prof. Dr. Sabrina Schreiner – Curriculum Vitae
Undergraduate and Postgraduate Training
Academic and Research Posts
Other Scientific Roles
Awards and Prizes
10 Selected Publications
Stubbe M, Mai J, Stubbe HC, Berscheminski J, Karimi M, Hofmann S, Weber E, Hadian K, Hay RT, Groitl P, Dobner T, Schreiner S. 2020. HAdV E2A SUMOylation prevents antiviral response promoted by host PML-NB components. mBio. Mar 17;11(2):e00049-20.
Hofmann S, Mai J, Masser S, Groitl P, Hermann A, Brack-Werner R, Sternsdorf T and Schreiner S. 2020. ATO (Arsenic Trioxide) effects on PML nuclear bodies reveals antiviral intervention capacity. manuscript in press Advanced Science.
Müncheberg S, Hay TR, Ip HW, Meyer T, Weiß C, Brenke J, Masser S, Hadian K, Dobner T, Schreiner S. 2018. E1B-55K mediated regulation of RNF4 STUbL promotes HAdV gene expression. J Virol. Jun 13;92(13).
Freudenberger N, Hay R T, Groitl P, Dobner T, Schreiner S. 2018. HAdV pV core protein is targeted by the host SUMOylation machinery to pursue essential viral functions. J Virol. Jan 30;92(4).
Wimmer P, Berscheminski J, Blanchette P, Groitl P, Branton PE, Hay RT, Dobner T, Schreiner S. 2016. PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor suppressor p53. Oncogene. 35(1):69-82.
Bürck C, Mund A, Berscheminski J, Kieweg L, Müncheberg S, Dobner T* and Schreiner S*. 2015. KAP1 is a host restriction factor that promotes HAdV E1B-55K SUMO modification. J. Virol. Nov;90(2):930-46.
Berscheminski J, Brun J, Speiseder T, Wimmer P, Ip WH, Terzic M, Dobner T, Schreiner S. 2015. Sp100A is a tumor suppressor that activates p53-dependent transcription and countercats E1A/E1B-55K-mediated transformation. Oncogene. doi: 10.1038/onc.2015.378.
Schreiner S, Kinkley S, Bürck C, Mund A, Wimmer P, Schubert T, Groitl P and Dobner T. 2013. SPOC1-mediated antiviral host cell responses antagonized early in Human Adenovirus type 5 infection. PLoS Pathog. 9(11):e1003775.
Schreiner S, Bürck C, Glass M, Groitl P, Wimmer P, Kinkley S, Mund A, Everett RD and Dobner T. 2013. Control of human adenovirus type 5 gene expression by cellular Daxx/ATRX chromatin-associated complexes. Nucleic Acids Res. 41(6):3532-50.
Schreiner S, Martinez R, Groitl P, Rayne F, Vaillant R, Wimmer P, Bossis G, Sternsdorf T, Ruzsics Z, Dobner T, Wodrich H. 2012. Transcriptional activation of the adenoviral genome is mediated by capsid protein VI. Plos Path. 8(2). e1002549.