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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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Hrk/DP5 contributes to the apoptosis of select neuronal populations but is dispensable for haematopoietic cell apoptosis

TL;DR: It is demonstrated that HRK contributes to apoptosis signalling elicited by trophic factor withdrawal in certain neuronal populations but is dispensable for apoptosis of haematopoietic cells.
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The BH3-Only Proteins Bim and Puma Cooperate to Impose Deletional Tolerance of Organ-Specific Antigens

TL;DR: The data show that Puma cooperates with Bim to impose a thymic-deletion checkpoint to peripheral self-antigens and cement the notion that defects in apoptosis alone are sufficient to cause autoimmune disease.
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What do we know about the mechanisms of elimination of autoreactive T and B cells and what challenges remain.

TL;DR: The roles of the proapoptotic Bcl‐2 family member Bim and the small family of Nur77‐related transcriptional regulators in lymphocyte negative selection are discussed and the processes that may lead to the activation of Bim are speculated on.
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BH3-only proapoptotic Bcl-2 family members Noxa and Puma mediate neural precursor cell death.

TL;DR: It is found that genotoxic injury induces a rapid p53-dependent increase in expression of Noxa and Puma mRNA in telencephalic NPCs, identified as important regulators of genotoxin-induced telENCEphalic NPC death.
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CD45 links the B cell receptor with cell survival and is required for the persistence of germinal centers

TL;DR: These results show mechanistic differences in B cell survival during germinal center initiation and propagation; CD40 signaling is sufficient for the former, whereas the latter requires signaling from the BCR.