p53- and Mdm2-Independent Repression of NF-κB Transactivation by the ARF Tumor Suppressor
By S. Rocha, K. Campbell, N. Perkins. 2003
197 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f50950865a2ae45a04df8df39c7b0775ff9b6aae
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- N. Perkins
- T. Gilmore
- Jamie E. Hoberg
- Catherine S. Ramsey
- H. Nakano
- Marty W. Mayo
- D. Tuveson
- R. DePinho
In Immunology
- N. Perkins
- T. Gilmore
- Jamie E. Hoberg
- Catherine S. Ramsey
- H. Nakano
- Marty W. Mayo
- R. DePinho
- N. Bardeesy
In Molecular Biology
- N. Perkins
- N. Bardeesy
- T. Gilmore
- R. DePinho
- Jamie E. Hoberg
- Catherine S. Ramsey
- Marty W. Mayo
- D. Tuveson
Citations in the corpus
- To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis (2003, background): “ARF inhibited NF-kB-mediated transcription in a promoter-specific manner and downregulated expression of the antiapoptotic Bcl-xL protein (Rocha et al., 2003a).”
- Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “…has p53-independent functions—including the repression of ribosomal RNA synthesis, the inhibition of NF- B activity, and the targeting of E2F for degradation—suggesting that a number of other pathways are impaired by INK4A/ARF loss (Martelli et al. 2001; Rocha et al. 2003; Sugimoto et al. 2003).”
- Good cop, bad cop: the different faces of NF-κB (2006, background): “In addition to p53, the ARF tumor suppressor also regulates RelA activity.(51,71) ARF expression, which is induced by oncogenes, results in activation of p53 through binding to and inactivation of Hdm2/Mdm2.”
- IκB Kinase α-Mediated Derepression of SMRT Potentiates Acetylation of RelA/p65 by p300 (2006, background): “The transactivation potential of RelA/p65 is repressed by phosphorylation at threonine 502 by p14 or by glycogen synthase kinase 3 -induced phosphorylation of RelA/p65 at S468 (11, 51, 52).”
- Integrating cell-signalling pathways with NF-κB and IKK function (2007, background): “By contrast, phosphorylation at Thr505 by the CHK1 checkpoint kinase, which can be activated by ATM- and Rad3-related (ATR) kinase in response to ARF tumour suppressor induction or DNA damage following cisplatin treatment, inhibits RelA transactivation and results in its increased association with H”
- Transient and Selective NF-κB p65 Serine 536 Phosphorylation Induced by T Cell Costimulation Is Mediated by IκB Kinase β and Controls the Kinetics of p65 Nuclear Import 1 (2004, background): “p14-mediated repression of p65 trans activation requires threonine 502 phosphorylation (28) within p65 trans activation domain 2 (TA2).”