Regulation of the G2/M transition by p53

By W. Taylor, G. Stark. Oncogene, 2001

1,635 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2130b7a0bdd2839c47da88297719626769faee88

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. Guido Kroemer
2. J. Bartek
3. N. Holbrook
4. J. Martindale
5. R. Medema
6. M. Kastan
7. G. Somero
8. R. Kaufman

In Molecular Biology

1. Guido Kroemer
2. J. Bartek
3. M. Castedo
4. G. Somero
5. M. Guo
6. Haolan Wang
7. Yongheng Chen
8. Anindya Dutta

In Oncology

1. Guido Kroemer
2. J. Bartek
3. M. Castedo
4. M. Guo
5. Haolan Wang
6. Yongheng Chen
7. N. Holbrook
8. J. Martindale

Citations in the corpus

• cDNA microarray analysis reveals the capacity of the cold-adapted Antarctic fish Trematomus bernacchii to alter gene expression in response to heat stress (2009, background): “Consistent with this hypothesis, the growth arrest and DNA-damage inducible protein GADD45, a marker of stress-related inhibition of the cell cycle (Taylor and Stark 2001), was induced in heat-stressed individuals, immediately following heat shock and at the 4-h recovery time point.”
• 53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers (2010, background): “p53 has a major role in the surveillance of chromosome integrity at the G1/S transition, although evidence for a relatively weaker p53-dependent checkpoint at the G2/M transition has also been reporte”
• Cell death by mitotic catastrophe: a molecular definition (2004, background): “For instance, p53 negatively regulates the transcription of Cdk1 (Yun et al., 1999) and cyclin B1 (Taylor et al., 1999), while enhancing the transcription of three Cdk1 inhibitors (Gadd45, p21 and 14-3-3s) (Taylor and Stark, 2001).”
• p21 in cancer: intricate networks and multiple activities (2009, background): “CDC2 , CHEK1 and TERT are repressed by p21 through the inhibition of CDK2-mediated phosphorylation of RB- and E2f-dependent transcriptio”
• The cell cycle: a review of regulation, deregulation and therapeutic targets in cancer (2003, background): “Increased binding of cyclin B to 14-3-3 σ actively excludes it from the nucleus. p53 also mediates the dissociation of CDK1-cyclin B1 complexes by induction of Gadd45 (growth arrest and DNA damage inducible gene) (Hermeking et al. 1997; Taylor & Stark 2001).”
• Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “As for many checkpoint genes, p53 is not essential for cell viability yet plays key roles in at least two response pathways after DNA damage: G1 arrest and apoptosis [reviewed in (186)].”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “In addition, p53 represses CDKs and cyclin B, which are required for entry into mitosis and are involved in G2/M phase block.(62,63) p53 induces transcription of 14-3-3 sigma and represses the cell cycle protein-dependent kinase Cdc2.”
• Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury (2010, neutral): “For example, p53 has a key role at the G2 checkpoint that regulates the G2/M transition in response to stress and DNA damag”
• Cellular response to oxidative stress: Signaling for suicide and survival * (2002, background): “…kinase inhibitor, p21(Waf1), important in mediating G1 arrest, and GADD45 and 14-3-3s, which are important in mediating G2/M phase arrest (Taylor and Stark, 2001). p53 and its downstream target p21 are believed to play a role in hydrogen peroxide-induced growth arrest and replicative…”
• Cell-cycle checkpoints and cancer (2004, background): “The maintenance phase of the G2 checkpoint probably partly relies on the transcriptional programmes regulated by BRCA1 and p53, leading to the upregulation of cell-cycle inhibitors such as the CDK inhibitor p21, GADD45a (growth arrest and DNA-damage-inducible 45 alpha) and 14–3–3 sigma protein”