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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

BH3-Mimetic Drugs: Blazing the Trail for New Cancer Medicines.

Delphine Merino, +6 more
- 10 Dec 2018 - 
TL;DR: The BCL-2 inhibitor venetoclax has been approved for treatment of refractory chronic lymphocytic leukemia and this drug and inhibitors of pro-survival MCL-1 and B CL-XL are being tested in diverse malignancies.
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The anti-apoptotic activities of Rel and RelA required during B-cell maturation involve the regulation of Bcl-2 expression.

Mathis Grossmann, +5 more
- 01 Dec 2000 - 
TL;DR: Findings indicate that Rel and RelA serve essential, albeit redundant, functions during the later antigen‐independent stages of B‐ and T‐cell maturation, with these transcription factors promoting the survival of peripheral B cells in part by upregulating Bcl‐2.
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Puma cooperates with Bim, the rate-limiting BH3-only protein in cell death during lymphocyte development, in apoptosis induction

Miriam Erlacher, +9 more
- 25 Dec 2006 - 
TL;DR: Hyperplasia of lymphatic organs is comparable with that observed in mice overexpressing Bcl-2 in all hemopoietic cells exceeding the hyperplasia observed in bim−/− mice and Bim and Puma have clearly overlapping functions in p53-dependent and -independent apoptosis.
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Two molecular pathways initiate mitochondria-dependent dopaminergic neurodegeneration in experimental Parkinson's disease.

Celine Perier, +11 more
- 08 May 2007 - 
TL;DR: It is shown that the tumor suppressor p53 mediates Bax transcriptional induction after PD-related complex I blockade in vivo, but it does not participate in Bax mitochondrial translocation in this model, either by a transcription-independent mechanism or through the induction of BH3-only proteins Puma or Noxa.
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bcl-2 transgene expression inhibits apoptosis in the germinal center and reveals differences in the selection of memory B cells and bone marrow antibody-forming cells.

Kenneth G. C. Smith, +5 more
- 07 Feb 2000 - 
TL;DR: The inability of BCL-2 to alter selection of bone marrow AFCs is consistent with these cells being selected within the germinal center on the basis of their affinity being above some threshold rather than their survival being due to a selective competition for an antigen-based signal.