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Romina M. Wiedmann

Researcher at Ludwig Maximilian University of Munich

Publications -  7
Citations -  414

Romina M. Wiedmann is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Cancer cell & Anoikis. The author has an hindex of 7, co-authored 7 publications receiving 384 citations. Previous affiliations of Romina M. Wiedmann include University of British Columbia.

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The V-ATPase-inhibitor Archazolid abrogates tumor metastasis via inhibition of endocytic activation of the Rho-GTPase Rac1

TL;DR: The results indicate that archazolid effectively decreases metastatic dissemination of breast tumors by impairing the trafficking and spatially restricted activation of EGFR and Rho-GTPase Rac1, which are pivotal for directed movement of cells.
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Mode of Cell Death Induction by Pharmacological Vacuolar H+-ATPase (V-ATPase) Inhibition

TL;DR: It is concluded that archazolid leads to energy stress which activates adaptive mechanisms like autophagy mediated by HIF1α and finally leads to apoptosis which is proposed as a promising drugable target in cancer therapy caught up at the interplay of apoptosis, Autophagy, and cellular/metabolic stress.
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Hsp27 promotes insulin-like growth factor-I survival signaling in prostate cancer via p90Rsk-dependent phosphorylation and inactivation of BAD.

TL;DR: It is reported that Hsp27 expression and phosphorylation levels correlate with IGF-I signaling and castrate-resistant progression in human prostate cancer specimens and cell lines and support targeting HSp27 as a therapeutic strategy for castrate -resistant prostate cancer.
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Cotargeting Stress-Activated Hsp27 and Autophagy as a Combinatorial Strategy to Amplify Endoplasmic Reticular Stress in Prostate Cancer

TL;DR: Findings identify autophagy as a cytoprotective, stress-induced adaptive pathway, activated following disruption of protein homeostasis and ER stress induced by Hsp27 silencing, which illustrates potential benefits of blocking activation of adaptive pathways to improve treatment outcomes in cancer.
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Pretubulysin: from hypothetical biosynthetic intermediate to potential lead in tumor therapy.

TL;DR: Pretubulysin induces apoptosis and inhibits cancer cell migration and tubulin assembly in vitro and appears to be an ideal candidate for future development in preclinical trials and a very promising early lead structure in cancer therapy.