Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins

By H. Puthalakath, A. Strasser. Cell Death and Differentiation, 2002

763 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Toxicology

View Paper: https://www.semanticscholar.org/paper/5dfdad2ed3cc1b3b4f46306a140934e28c180882

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Guido Kroemer
2. Jerry M. Adams
3. L. Galluzzi
4. Suzanne Cory
5. A. Strasser
6. A. Letai
7. Christoph Borner
8. Peter Vandenabeele

In Oncology

1. Jerry M. Adams
2. Guido Kroemer
3. A. Strasser
4. L. Galluzzi
5. Suzanne Cory
6. A. Letai
7. Christoph Borner
8. Shizuo Akira

In Toxicology

1. A. Letai
2. Christoph Borner
3. Jerry M. Adams
4. A. Strasser

Citations in the corpus

• Bcl-2 family members: intracellular targeting, membrane-insertion, and changes in subcellular localization (2004, background): “Translocation is initiated by a variety of mechanisms, which include transcriptional regulation, posttranslational modification and/or conformational change [2,48,49].”
• Dicer ablation affects antibody diversity and cell survival in the B lymphocyte lineage. (2008, neutral): “The Em-bcl-2 transgene was chosen for this purpose, as Bim and Bcl-2 are known to be key players in balancing death and survival in B cell development (Hughes et al., 2006; Puthalakath and Strasser, 2002; Strasser et al., 1990).”
• ER stress triggers apoptosis by activating BH3-only protein Bim. (2007, background): “The proapoptotic activity of BH3-only proteins can be regulated by a variety of transcriptional as well as posttranslational control mechanisms (Puthalakath and Strasser, 2002).”
• The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “The multiplicity of mammalian BH3-only proteins presumably allows more precise control over apoptosis, and indeed the regulation of these proteins is complex, involving both transcriptional and diverse post-translational mechanisms (Puthalakath and Strasser, 2002; Cory et al., 2003).”
• Molecular mechanisms of cell death in neurological diseases (2021, background): “growth factor deprivation, DNA damage, ER stress), the BH3-only proteins (BIM, PUMA, BID, BMF, BAD, HRK, BIK, NOXA), the critical initiators of apoptosis, are transcriptionally or post-transcriptionally upregulated [22].”
• Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. (2007, background): “In response to a wide range of death and derangement signals, BH3-only members are activated (3, 4).”
• JNK Signaling in Apoptosis (2008, background): “Alternatively, phosphorylated Bim can bind and neutralize the antiapoptotic activities of Bcl2 and Bcl XL, thereby promoting apoptosis (Puthalakath et al., 1999; Puthalakath and Strasser, 2002).”