p53: death star.

By Karen H. Vousden. Cell, 2000

779 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/5d217d30b802ae4a7cbf4dab0b15a01f570d53f4

How researchers see this paper

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

In Cell Biology

1. K. Nakano
2. P. Johnston
3. D. Longley
4. Yosef Shiloh
5. Karen H. Vousden
6. Eyal Gottlieb
7. M. Kastan

In Molecular Biology

1. Yosef Shiloh
2. M. Kastan
3. Moshe Oren
4. K. Nakano
5. P. Johnston
6. D. Longley
7. Karen H. Vousden
8. Eyal Gottlieb

In Oncology

1. Yosef Shiloh
2. Moshe Oren
3. K. Nakano
4. M. Kastan
5. Karen H. Vousden
6. P. Johnston
7. D. Longley
8. Eyal Gottlieb

Citations in the corpus

• Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes. (2001, background): “The products of both p53 and p19(Arf) genes have been implicated in some apoptotic pathways (Lowe 1999; Sherr and Weber 2000; Vousden 2000).”
• ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage. (2001, background): “The cellular levels of the p53 protein significantly increase in response to stress such as DNA damage, activation of oncogenes, and hypoxia (for review, see Giaccia and Kastan 1998; Oren 1999; Prives and Hall 1999; Vousden 2000).”
• TIGAR, a p53-inducible regulator of glycolysis and apoptosis. (2006, background): “In particular, the ability to induce expression of cell-cycle arrest targets without induction of the apoptotic target genes may allow for the resolution of damage in a stressed cell without recourse to permanent cell-cycle arrest or cell death (Vousden, 2000).”
• PUMA, a novel proapoptotic gene, is induced by p53. (2001, background): “…now been identified that encode proteins with apoptotic potential, and the apoptotic response totion from 2 mg/ml to 0.03 mg/ml (PUMA protein could no longer be detected by Western blot at concentration p53 is likely to reflect the coordinate effect of activation of several genes (Vousden, 2000).”
• Molecular mechanisms of drug resistance (2005, background): “One model suggests that more profound DNA damage induces higher and prolonged activation of p53, which increases the chances of apoptosis over arrest [117].”