p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53.

By K. Oda, H. Arakawa, Tomoaki Tanaka, K. Matsuda, C. Tanikawa, Toshiki Mori, H. Nishimori, K. Tamai, T. Tokino, Yusuke Nakamura and 1 more. Cell, 2000

1,233 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e1eb8275e4dc82d687cc19fb424d725e6c33d777

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Citations in the corpus

Tumor suppressive functions of p53. (2009, background): “For example, the phosphorylation of p53 at serine 46 has been shown to correlate with apoptosis, and may be partially explained by the ability of this phosphorylation to regulate expression of at least one p53 apoptotic target, p53AIP1 (Oda et al. 2000).”
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].”
The expanding role of mitochondria in apoptosis. (2001, background): “Two proapoptotic gene products, Noxa and Puma, were identified recently as BH3-only members of the Bcl-2 family that are induced in a p53-dependent manner in primary mouse cells exposed to X-ray irradiation (E. Oda et al. 2000; Nakano and Vousden 2001; Yu et al. 2001).”
The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Phosphorylation of p53 S46 promotes the induction of proapoptotic target gene p53AIP1, thus favoring the induction of Cite this article as Cold Spring Harb Perspect Med 2016;6:a026104 5 w w w .p er sp ec ti ve si n m ed ic in e. o rg apoptosis (Oda et al. 2000).”
p53: death star. (2000, neutral): “(Oda et al., 2000a) ,”
Transcriptional control of human p53-regulated genes (2008, background): “Investigators found that the induction of p53AIP1 (p53-regulated apoptosis-inducing protein-1) depends on the phosphorylation of the Ser46 residue of p53 (Ref”
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”
PUMA, a novel proapoptotic gene, is induced by p53. (2001, background): “Cleavage of procaspase 9 and procaspase 3 to the smaller active forms indicates activation of this apoptotic pathway. b-actin expression was assessed to ensure equal protein loading. sense oligonucleotides to inhibit PUMA expression re- PUMA-a and PUMA-b in a group with Bax and Noxa as BH3 domain–co”
Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation. (2003, background): “Of these, Ser46 seems to be specifically important in UV-induced apoptosis through the activation of the gene p53AIP1 [48].”
Control of apoptosis by p53 (2003, background): “These include the ‘multidomain’ Bcl-2 family member Bax (Miyashita et al., 1994), as well as the ‘BH3-only’ members Puma (Nakano and Vousden, 2001), Noxa (Oda et al., 2000a), and Bid (Sax et al., 2002).”
Acetylation of the p53 DNA-binding domain regulates apoptosis induction. (2006, background): “These modifications include the phosphorylation of serines 20 and 46 and the acetylation of lysine 373 (Bulavin et al., 1999; Jack et al., 2002; Knights et al., 2006; Oda et al., 2000).”
Live or let die: the cell's response to p53 (2002, background): “cgi?l=63970"> p53AIP1 , but not mediators of cell-cycle arrest such as CDKN1A (Ref”