Search

A dual-band circularly polarized four-arm Spidron fractal antenna is proposed for Ku-band satellite communication. The dual-band characteristic is realized using two-crossed dipole antennas of different lengths. Each dipole arm includes a Spidron fractal patch to generate circular polarization and a printed meander-line to reduce the size. The proposed antenna is fed by a 50-coaxial cable, and a conducting cavity is utilized to obtain a directional circularly polarized radiation pattern. The experiments demonstrate that the fabricated antenna exhibits −10 dB reflection bandwidths ranging from 10.75 GHz to 12.65 GHz and from 13.33 GHz to more than 15 GHz with a broad 3 dB axial ratio bandwidth covering a frequency range of 10.66–14.46 GHz. The measured peak gains are 8.76 dBic in the lower band and 7.43 dBic in the upper band. [ABSTRACT FROM PUBLISHER]

We performed chromatin immunoprecipitation (ChIP) analyses of developmentally staged solid tissues isolated from wild-type and p53-null mice to determine specific histone N-terminal modifications, histone-modifying proteins, and transcription factor interactions at the developmental repressor region (-850) and core promoter of the hepatic tumor marker alpha-fetoprotein (AFP) gene. Both repression of AFP during liver development and silencing in the brain, where AFP is never expressed, are associated with dimethylation of histone H3 lysine 9 (DiMetH3K9) and the presence of heterochromatin protein 1 (HP1). These heterochromatic markers remain localized to AFP during developmental repression but spread to the upstream albumin gene during silencing. Developmentally regulated decreases in levels of acetylated H3 (AcH3K9) and H4 (AcH4) and of di- and trimethylated H3K4 (DiMetH3K4 and TriMetH3K4) occur at both the core promoter and distal repressor regions of AFP. Hepatic expression of AFP correlates with FoxA interaction at the repressor region and the binding of RNA polymerase II and TATA-binding protein to the core promoter, p53 acts as a developmental repressor of AFP in the liver by binding to chromatin, excluding FoxA interaction and targeting mSin3A/HDAC1 to the distal repressor region, p53-null mice exhibit developmentally delayed AFP repression, concomitant with acetylation of H3K9, methylation of H3K4, and loss of DiMetH3K9, mSin3A/ HDAC1, and HP1 interactions. [ABSTRACT FROM AUTHOR]

We purified the oncoprotein SnoN and found that it functions as a corepressor of the tumor suppressor p53 in the regulation of the hepatic α-fetoprotein (AFP) tumor marker gene. p53 promotes SnoN and histone deacetylase interaction at an overlapping Smad binding, p53 regulatory element (SBE/p53RE) in AFP. Comparison of wild-type and p53-null mouse liver tissue by using chromatin immunoprecipitation (CHIP) reveals that the absence of p53 protein correlates with the disappearance of SnoN at the SBE/p53RE and loss of AFP developmental repression. Treatment of AFP-expressing hepatoma cells with transforming growth factor-βl (TGF-β1) induced SnoN transcription and Smad2 activation, concomitant with AFP repression. ChIP assays show that TGF-β1 stimulates p53, Smad4, P-Smad2 binding, and histone H3K9 deacetylation and methylation, at the SBE/p53RE. Depletion, by small interfering RNA, of SnoN and/or p53 in hepatoma cells disrupted repression of AFP transcription. These findings support a model of cooperativity between p53 and TGF-β effectors in chromatin modification and transcription repression of an oncodevelopmental tumor marker gene. [ABSTRACT FROM AUTHOR]