Articles with the keyword: 
jerry submitted, created time 3 months 2 weeks (www.genesdev.org)
Osteosarcoma is the most common primary malignant tumor of bone. Analysis of familial cancer syndromes and sporadic cases has strongly implicated both p53 and pRb in its pathogenesis. This research provided a valuable platform for addressing the molecular genetics of osteosarcoma and for developing novel therapeutic strategies. 
DNA Damage Signals for p53 Pulses
jerry submitted, created time 4 months 2 weeks (www.sciencedirect.com)
A major challenge of systems biology is to understand how network topology affects protein dynamics in living cells. A new study show that p53 pulses are driven by pulses in the upstream signaling kinases, ATM and Chk2, and that a negative feedback mediated by the phosphatase Wip1 is essential for maintaining the uniform shape of p53 pulses.
Acetylation Is Indispensable for p53 Activation
kavin submitted, created time 4 months 2 weeks (www.cell.com)
The activation of the tumor suppressor p53 facilitates the cellular response to genotoxic stress; however, the p53 response can only be executed if its interaction with its inhibitor Mdm2 is abolished. This study identifies p53 acetylation as an indispensable event that destabilizes the p53-Mdm2 interaction and enables the p53-mediated stress response.
p53 Activation: A Case against Sir
jerry submitted, created time 4 months 3 weeks (www.cancercell.org)
The p53 tumor suppressor is a critical transcription factor for controlling cell growth and apoptosis during times of cellular stress.
In this issue, the researchers screened small-molecule activators of p53 that could potentially reduce tumor growth Tenovin-6 was identified as a potent SIRT1 and SIRT2 inhibitor that indirectly activated p53 at single-digit micromolar concentrations.
The identification of a specific sirtuin inhibitor has broad implications in understanding sirtuin-p53 signaling and the development of novel chemotherapeutics
Cancer Drug -- Promising New Design Found
DanyC submitted, created time 6 months 4 weeks (health.usnews.com)
A drug that targets a protein interaction involved in many types of cancer has been created by University of Michigan researchers.
PS:
Many traditional cancer drugs also activate p53, but they do so by causing DNA damage.
Updates on p53: modulation of p53 degradation as a therapeutic approach
DanyC submitted, created time 8 months 3 weeks (www.nature.com)
"The p53 pathway is aberrant in most human tumors with over 50% expressing mutant p53 proteins. The pathway is critically controlled by protein degradation. Here, we discuss the latest developments in the search for small molecules that can modulate p53 pathway protein stability and restore p53 activity for cancer therapy."
Cancer Fighter May Be Fertility Helper
Eric wu submitted, created time 10 months 1 week (sciencenow.sciencemag.org)
A protein known primarily for its role in fighting cancer also helps embryos implant in the womb, according to a study in mice. The find may explain why some women have difficulty becoming pregnant.
Type I phosphatidylinositol-4,5-bisphosphate 4-phosphatase regulates stress-induced apoptosis
carly submitted, created time 11 months 2 weeks (www.pnas.org)
A recently discovered phosphatidylinositol monophosphate, phosphatidylinositol 5-phosphate (PtdIns-5-P), plays an important role in nuclear signaling by influencing p53-dependent apoptosis. It interacts with a plant homeodomain finger of inhibitor of growth protein-2, causing an increase in the acetylation and stability of p53.
sumsung submitted, created time 11 months 4 weeks (www.pnas.org)
Cancer is a disease of aging. The accumulation of mutations in individual cells over a lifetime is thought to be the reason. In this work, we explored an additional hypothesis: could p53 function decline with age, which would contribute to an enhanced mutation frequency and tumorigenesis in the aging process.
Heat Shock Factor 1 Is a Powerful Multifaceted Modifier of Carcinogenesis
DanyC submitted, created time 1 year 3 days (www.cell.com)
"Researchers report that eliminating HSF1 protects mice from tumors induced by mutations of the RAS oncogene or a hot spot mutation in the tumor suppressor p53. In cell culture, HSF1 supports malignant transformation by orchestrating a network of core cellular functions including proliferation, survival, protein synthesis, and glucose metabolism
june submitted, created time 1 year 6 days (www.medicalnewstoday.com)
UroToday.com- Antiproliferative factor (APF) is a sialoglycopeptide elevated in the urine of patients with interstitial cystitis. APF is detectable in the urine of 95% of IC patients as compared to approximately 9% of controls and is also a low molecular weight glycosylated peptide related to the membrane receptor frizzled 8
Key to longer life (in flies) lies in just 14 brain cells
carly submitted, created time 1 year 2 weeks (www.eurekalert.org)
Fruit flies live significantly longer when the activity of the protein p53 is reduced in just 14 insulin-producing cells in their brains, new Brown University research shows. The results put scientists one step closer to understanding caloric restriction, a biochemical process proven to slow aging. Results appear in the Proceedings of the National Academy of Sciences.
Study details regulation of vital tumor suppressor gene p53
lewis submitted, created time 1 year 1 month (www.eurekalert.org)
So vital is the p53 tumor suppressor gene in controlling cancer that its dysfunction is linked to more than half of human cancers. Now, a just-published study reveals new levels of subtlety in the body's management of this all-important tumor suppressor gene and the protein it produces.
Nrf2 and p53 cooperatively protect against BBN-induced urinary bladder carcinogenesis
jiangyun submitted, created time 1 year 1 month (carcin.oxfordjournals.org)
These results thus reveal potential interactions between p53 and Nrf2 and their gene batteries, and indicate that both factors cooperatively contribute to tumor prevention.
jiangyun submitted, created time 1 year 1 month (carcin.oxfordjournals.org)
DNA mismatch repair (MMR) is a highly conserved system that repairs DNA adducts acquired during replication, as well as some forms of exogenous/endogenous DNA damage. Our results support the hypothesis that p53 and Msh6 are functionally interrelated and that, with concomitant mutation, these tumor suppressors act together to accelerate tumorigenesis.
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