ABSTRACT
The cadmium copper hydroxide nitrate, CdCu(3)(OH)(6)(NO(3))(2).0.5H(2)O, is furnished from oxygenated suspensions of Cu(2)O in aqueous Cd(NO(3))(2). The compound possesses the kagome structural motif and shows no evidence of magnetic ordering to temperatures as low as 5 K, despite exhibiting a Curie-Weiss temperature of Theta = -114 +/- 27 K, thus giving a spin frustration parameter, f = 22.8.
ABSTRACT
The syntheses and magnetic susceptibilities of a pure series of rare copper minerals from the atacamite family with general formula ZnxCu4-x(OH)6Cl2 (0 = x = 1) are reported. The structure of these compounds features a corner-sharing triangular kagomé lattice of antiferromagnetically coupled Cu(II) ions. We correlate the onset of magnetic ordering with the mole fraction of paramagnetic Cu(II) ions located between kagomé layers and demonstrate that the fully Zn-substituted compound shows no magnetic ordering down to 2 K, resulting in a highly spin-frustrated S = 1/2 lattice.
ABSTRACT
The tumor suppressor protein BRCA1 has been shown to enhance p53 transcription, whereas activated p53 represses BRCA1 transcription. To further understand the functional interaction of these proteins, we investigated the role of BRCA1 in p53-induced phenotypes. We found that BRCA1 when subjected to forced expression acts synergistically with wild-type p53, resulting in irreversible growth arrest, as shown by VhD mouse fibroblast cells expressing a temperature-sensitive mutant of p53. Furthermore, reintroduction of both BRCA1 and p53 into BRCA1(-/-)/p53(-/-) mouse embryonic fibroblasts markedly increased the senescence phenotype compared to that induced by p53 alone. In particular, we found that BRCA1 expression attenuated p53-mediated cell death in response to gamma-irradiation. Moreover, microarray screening of 11 000 murine genes demonstrated that a set of genes upregulated by p53 is enhanced by coexpression of BRCA1 and p53, suggesting that BRCA1 and p53 exert a promoter selectivity leading to a specific phenotype. Taken together, our results provide evidence that BRCA1 is involved in p53-mediated growth suppression rather than apoptosis.