ASPP proteins specifically stimulate the apoptotic function of p53.
By Yardena Samuels-Lev, D. J. O’Connor, D. Bergamaschi, G. Trigiante, J. Hsieh, S. Zhong, Isabelle Campargue, L. Naumovski, T. Crook, Xin Lu. Molecules and Cells, 2001
702 citations recorded by the source corpus.
Subfields: Biotechnology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/c0a433aab6e4d441e754b2562a583e081291841a
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Citations in the corpus
- Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “307 Unlike ASPP2, iASPP preferentially binds p53-PRD 283 and interacts with the DBD through the L1 loop, helix H2 and N-terminal loop 308 (Fig.”
- The role of p53 in determining sensitivity to radiotherapy (2003, background): “The third model claims that the choice between apoptosis and growth arrest depends on the availability of p53 co-factors that differentially regulate the ability of p53 to bind to specific subsets of target gene”
- The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “ASPP1/2 proteins interact with the p53 core domain and stimulate p53 binding to the promoters of apoptotic genes (Samuels-Lev et al. 2001).”
- Role of p53 in Cell Death and Human Cancers (2011, background): “ASPP1 and ASPP2 which contain ankylin repeats, SH3 domain and Pro-rich domain, interact with p53 and specifically enhance pro-apoptotic activity of p53 through the inhibition of pro-survival Bcl2 [113].”
- Apoptosis - the p53 network (2003, background): “…apoptosis stimulating proteins of p53 (ASPP), for example, increases the DNA binding and transactivation activity of p53 on the promoters of apoptotic genes (e.g. Baxand PIG3), while failing to promote binding to the p21 promoter by a mechanism that remains to be defined (Samuels-Lev et al., 2001).”
- Functional diversity of protein phosphatase-1, a cellular economizer and reset button. (2004, background): “genes by p53 (310), but addition of PP1 dissociated p53”
- Molecular mechanisms of drug resistance (2005, background): “A third model proposes that the availability of transcriptional co-factors determines the ability of p53 to activate different subsets of genes [119,120].”
- Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation. (2003, background): “For example, with the assistance of ASPP proteins, p53 exhibits a striking preference for the promoters of proapoptotic genes [47 ].”