Volgelstein et al. went on to suggest that loss of the DCC gene and of p53 result in a malignant adenocarcinoma.
Yasuhiro Suzuki has modeled various systems such as membrane systems, signaling pathways (P53), ecosystems, and enzyme systems by using his method, abstract rewriting system on multisets (ARMS).
The p53 protein was discovered 10 years earlier by several groups, including that of David Lane and Lionel Crawford, Arnold Levine, and Lloyd Old.
Downstream molecules that are activated by JNK include c-Jun, ATF2, ELK1, SMAD4, p53 and HSF1.
The test looks at 23 individual DNA alterations, including 21 specific point alterations in the APC, KRAS and p53 genes, as well as testing BAT26, a gene involved in microsatellite instability (MSI).
The biology of HPV+ OPC is distinct of HPV- OPC with P53 degradation (inactivated by E6 instead of by genetic mutation), pRB pathway inactivation (by E7 instead of Cyclin D1 amplification), and P16 upregulation (over-expression of p16 instead of inactivation due to reduced negative feedback from pRB).
At low nM concentrations, Leptomycin B blocks the nuclear export of many proteins including HIV-1 Rev, MAPK/ERK, and NF-κB/IκB, and it inhibits the inactivation of p53.
Altered expression of multiple genes is observed with miR-885-5p, including the CDK2 and MCM5 genes encoding cyclin-dependent kinase 2 and mini-chromosome maintenance protein MCM5, and also with several p53 target genes.
They form a classic group for the study of medullablastoma and other cancers and include mice lines that are KO for p53, Ptch1, and Ink4c.
Overexpression of several enzymes of the NAD+ salvage pathway, including nicotinate phosphoribosyltransferase (PNC1) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) have been shown to extend lifespan in rat models by activating SIRT1 and promoting p53 deacetylation (van der Veer et al., 2007; Porcu and Chiarugi, 2005; Arraki et al., 2004; Berger et al., 2004; Bedalov and Simon, 2004).
p14ARF inhibits mdm2, thus promoting p53, which promotes p21 activation, which then binds and inactivates certain cyclin-CDK complexes, which would otherwise promote transcription of genes that would carry the cell through the Pier Paolo Pandolfi
Dr. Pandolfi and colleagues characterized the function of the fusion oncoproteins of APL, of the genes involved in the chromosomal translocations of APL, as well as of major tumor suppressors such PTEN, PML, and p53.
Primary peritoneal carcinoma shows similar rates of tumor suppressor gene dysfunction (p53, BRCA, WT1) as ovarian cancer and can also show an increased expression of HER-2/neu.
He has a long-running collaboration with Tyler Jacks and Robert Weinberg, starting with the characterization of tumors in p53 knockout mice.
It is believed that estrogen promotes growth by up-regulating IGF-1, EGFR, TGF-beta1, TGF-beta3 and PDGF, and promotes aberrant survival of leiomyoma cells by down-regulating p53, increasing expression of the anti-apoptotic factor PCP4 and antagonizing PPAR-gamma signalling.