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Andreas Strasser
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 537
Citations - 75592
Andreas Strasser is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 128, co-authored 509 publications receiving 66903 citations. Previous affiliations of Andreas Strasser include University of Alabama at Birmingham & Basel Institute for Immunology.
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Journal ArticleDOI
Eliminating Legionella by inhibiting BCL-XL to induce macrophage apoptosis
Mary Speir,Kate E. Lawlor,Kate E. Lawlor,Stefan P Glaser,Stefan P Glaser,Gilu Abraham,Seong Hoong Chow,Adam Vogrin,Keith E. Schulze,Ralf Schuelein,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Kylie D. Mason,Elizabeth L. Hartland,Trevor Lithgow,Andreas Strasser,Andreas Strasser,Guillaume Lessene,Guillaume Lessene,David C.S. Huang,David C.S. Huang,James E Vince,James E Vince,Thomas Naderer +23 more
TL;DR: Results indicate that repurposing BH3-mimetic compounds, originally developed to induce cancer cell apoptosis, may have efficacy in treating Legionnaires' and other diseases caused by intracellular microbes.
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Transgenic Expression of Dominant-Negative Fas-Associated Death Domain Protein in β Cells Protects against Fas Ligand-Induced Apoptosis and Reduces Spontaneous Diabetes in Nonobese Diabetic Mice
TL;DR: Data support a role for death receptors in β cell destruction in NOD mice, but blocking the perforin/granzyme pathway would also be necessary for dominant-negative FADD to have a beneficial clinical effect.
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Transgenic overexpression of human Bcl-2 in islet β cells inhibits apoptosis but does not prevent autoimmune destruction
Janette Allison,H. E. Thomas,Dianne Beck,Jamie L. Brady,Andrew M. Lew,Andrew G. Elefanty,Andrew G. Elefanty,Hiro Kosaka,Thomas W. H. Kay,David C.S. Huang,Andreas Strasser +10 more
TL;DR: Transgenic mice expressing human Bcl-2 alone could not prevent or ameliorate cytotoxic or autoimmune beta cell damage in vivo, and the anti-apoptotic protein, B cl-2, might protect against some of these stimuli.
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Differential regulation of macrophage differentiation in response to leukemia inhibitory factor/oncostatin-M/interleukin-6: the effect of enforced expression of the SCL transcription factor.
TL;DR: Examination of growth factor-induced macrophage differentiation in M1 leukemia cells that simultaneously display receptors for interleukin-6, leukemia inhibitory factor and Oncostatin-M suggests that LIF receptor/gp130 heterodimers utilize an SCL-inhibitable pathway while gp130 homodIMers do not and demonstrates differential-regulation of components of the mature macrophages phenotype.
Journal ArticleDOI
A portrait of the Bcl-2 protein family: life, death, and the whole picture.
Marc Pellegrini,Andreas Strasser +1 more
TL;DR: The Bcl-2 family of proteins are important regulators of cell death and are comprised of two opposing factions, the proapoptotic versus the antiap optotic members.